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Scientifica  2013 

HIV-1 Trans Infection of CD4+ T Cells by Professional Antigen Presenting Cells

DOI: 10.1155/2013/164203

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Abstract:

Since the 1990s we have known of the fascinating ability of a complex set of professional antigen presenting cells (APCs; dendritic cells, monocytes/macrophages, and B lymphocytes) to mediate HIV-1 trans infection of CD4+ T cells. This results in a burst of virus replication in the T cells that is much greater than that resulting from direct, cis infection of either APC or T cells, or trans infection between T cells. Such APC-to-T cell trans infection first involves a complex set of virus subtype, attachment, entry, and replication patterns that have many similarities among APC, as well as distinct differences related to virus receptors, intracellular trafficking, and productive and nonproductive replication pathways. The end result is that HIV-1 can sequester within the APC for several days and be transmitted via membrane extensions intracellularly and extracellularly to T cells across the virologic synapse. Virus replication requires activated T cells that can develop concurrently with the events of virus transmission. Further research is essential to fill the many gaps in our understanding of these trans infection processes and their role in natural HIV-1 infection. 1. Introduction The uptake of human immunodeficiency virus 1 (HIV-1) by professional antigen presenting cells (APCs) and subsequent transfer of virus to CD4+ T cells can result in explosive levels of virus replication in the T cells. This could be a major pathogenic process in HIV-1 infection and development of acquired immunodeficiency syndrome (AIDS). This process of trans (Latin; to the other side) infection of virus going across from the APC to the T cell is in contrast to direct, cis (Latin; on this side) infection of T cells by HIV-1. Note that this is a narrow definition of trans infection, as direct, cell-to-cell spread of virus is a classic phenomenon in viral infections [1], including HIV-1 [2, 3]. In fact, T cell-to-T cell infection involves many factors that are part of APC-to-T cell trans infection, including expression of CD4 on T cells and formation of a virologic synapse [4, 5] and evasion of neutralizing antibody [6] and the viral inhibitory effects of antiretroviral treatment (ART) [7, 8]. The use of trans infection in this review, however, refers to the in vitro model where infection of APC with low levels of HIV-1 leads to replication of virus in T cells, that is, orders of magnitude more than cis infection of either APC or T cells, and T cell-to-T cell or APC-to-APC trans infections. The outcome of the APC-to-T cell trans infection process has been considered to be

 References

[1]  W. Mothes, N. M. Sherer, J. Jin, and P. Zhong, “Virus cell-to-cell transmission,” Journal of Virology, vol. 84, no. 17, pp. 8360–8368, 2010.
[2]  W. Hübner, G. P. McNerney, P. Chen et al., “Quantitative 3D video microscopy of HIV transfer across T cell virological synapses,” Science, vol. 323, no. 5922, pp. 1743–1747, 2009.
[3]  B. K. Chen, “T cell virological synapses and HIV-1 pathogenesis,” Immunologic Research, vol. 54, no. 1–3, pp. 133–139, 2012.
[4]  N. Martin, S. Welsch, C. Jolly, J. A. G. Briggs, D. Vaux, and Q. J. Sattentau, “Virological synapse-mediated spread of human immunodeficiency virus type 1 between T cells is sensitive to entry inhibition,” Journal of Virology, vol. 84, no. 7, pp. 3516–3527, 2010.
[5]  Q. J. Sattentau, “Cell-to-cell spread of retroviruses,” Viruses, vol. 2, no. 6, pp. 1306–1321, 2010.
[6]  P. Gupta, R. Balachandran, M. Ho, A. Enrico, and C. Rinaldo, “Cell-to-cell transmission of human immunodeficiency virus type 1 in the presence of azidothymidine and neutralizing antibody,” Journal of Virology, vol. 63, no. 5, pp. 2361–2365, 1989.
[7]  A. Sigal, J. T. Kim, A. B. Balazs et al., “Cell-to-cell spread of HIV permits ongoing replication despite antiretroviral therapy,” Nature, vol. 477, no. 7362, pp. 95–98, 2011.
[8]  A. Sigal and D. Baltimore, “As good as it gets? The problem of HIV persistence despite antiretroviral drugs,” Cell Host & Microbe, vol. 12, no. 2, pp. 132–138, 2012.
[9]  J. Wilkinson and A. L. Cunningham, “Mucosal transmission of HIV-1: first stop dendritic cells,” Current Drug Targets, vol. 7, no. 12, pp. 1563–1569, 2006.
[10]  G. Morrow, L. Vachot, P. Vagenas, and M. Robbiani, “Current concepts of HIV transmission,” Current HIV/AIDS Reports, vol. 4, no. 1, pp. 29–35, 2007.
[11]  M. A. W. P. de Jong and T. B. H. Geijtenbeek, “Human immunodeficiency virus-1 acquisition in genital mucosa: langerhans cells as key-players,” Journal of Internal Medicine, vol. 265, no. 1, pp. 18–28, 2009.
[12]  D. McDonald, “Dendritic cells and HIV-1 trans-infection,” Viruses, vol. 2, no. 8, pp. 1704–1717, 2010.
[13]  K. Waki and E. O. Freed, “Macrophages and cell-cell spread of HIV-1,” Viruses, vol. 2, no. 8, pp. 1603–1620, 2010.
[14]  E. R. Wonderlich and S. M. Barratt-Boyes, “A dendrite in every pie: myeloid dendritic cells in HIV and SIV infection,” Virulence, vol. 3, no. 7, pp. 647–653, 2012.
[15]  N. Teleshova, N. Derby, E. Martinelli, P. Pugach, G. Calenda, and M. Robbiani, “Simian immunodeficiency virus interactions with macaque dendritic cells,” Advances in Experimental Medicine and Biology, vol. 762, pp. 155–181, 2013.
[16]  N. Romani, B. E. Clausen, and P. Stoitzner, “Langerhans cells and more: langerin-expressing dendritic cell subsets in the skin,” Immunological Reviews, vol. 234, no. 1, pp. 120–141, 2010.
[17]  A. W. Mesman and T. B. Geijtenbeek, “Pattern recognition receptors in HIV transmission,” Frontiers in Immunology, vol. 3, p. 59, 2012.
[18]  A. N. Harman, C. R. Bye, N. Nasr et al., “Identification of lineage relationships and novel markers of blood and skin human dendritic cells,” The Journal of Immunology, vol. 190, no. 1, pp. 66–79, 2013.
[19]  D. V. Belsito, M. R. Sanchez, R. L. Baer, F. Valentine, and G. J. Thorbecke, “Reduced Langerhans' cell Ia antigen and ATPase activity in patients with the acquired immunodeficiency syndrome,” The New England Journal of Medicine, vol. 310, no. 20, pp. 1279–1282, 1984.
[20]  E. Tschachler, V. Groh, and M. Popovic, “Epidermal Langerhans cells—a target for HTLV-III/LAV infection,” Journal of Investigative Dermatology, vol. 88, no. 2, pp. 233–237, 1987.
[21]  J. Kanitakis, C. Marchand, H. Su et al., “Immunohistochemical study of normal skin of HIV-1-infected patients shows no evidence of infection of epidermal Langerhans cells by HIV,” AIDS Research and Human Retroviruses, vol. 5, no. 3, pp. 293–302, 1989.
[22]  J. Kanitakis and J. Thivolet, “Infection of human epidermal Langerhans' cells by HIV,” AIDS, vol. 4, no. 3, pp. 266–268, 1990.
[23]  D. C. Kalter, J. J. Greenhouse, J. M. Orenstein, S. M. Schnittman, H. E. Gendelman, and M. S. Meltzer, “Epidermal Langerhans cells are not principal reservoirs of virus in HIV disease,” The Journal of Immunology, vol. 146, no. 10, pp. 3396–3404, 1991.
[24]  N. Dusserre, C. Dezutter-Dambuyant, F. Mallet et al., “In vitro HIV-1 entry and replication in Langerhans cells may clarify the HIV-1 genome detection by PCR in epidermis of seropositive patients,” Journal of Investigative Dermatology, vol. 99, no. 5, pp. 99S–102S, 1992.
[25]  C. C. Compton, T. S. Kupper, and K. B. Nadire, “HIV-infected Langerhans cells constitute a significant proportion of the epidermal Langerhans cell population throughout the course of HIV disease,” Journal of Investigative Dermatology, vol. 107, no. 6, pp. 822–826, 1996.
[26]  M. Henry, A. Uthman, C. Ballaun, G. Stingl, and E. Tschachler, “Epidermal Langerhans cells of AIDS patients express HIV-1 regulatory and structural genes,” Journal of Investigative Dermatology, vol. 103, no. 4, pp. 593–596, 1994.
[27]  C. Dezutter-Dambuyant, “In vivo and in vitro infection of human Langerhans cells by HIV-1,” Advances in Experimental Medicine and Biology, vol. 378, pp. 447–451, 1995.
[28]  A. Giannetti, G. Zambruno, A. Cimarelli et al., “Direct detection of HIV-1 RNA in epidermal Langerhans cells of HIV-infected patients,” Journal of Acquired Immune Deficiency Syndromes, vol. 6, no. 4, pp. 329–333, 1993.
[29]  A. Cimarelli, G. Zambruno, A. Marconi, G. Girolomoni, U. Bertazzoni, and A. Giannetti, “Quantitation by competitive PCR of HIV-1 proviral DNA in epidermal Langerhans cells of HIV-infected patients,” Journal of Acquired Immune Deficiency Syndromes, vol. 7, no. 3, pp. 230–235, 1994.
[30]  D. McIlroy, B. Autran, R. Cheynier et al., “Infection frequency of dendritic cells and CD4+ T lymphocytes in spleens of human immunodeficiency virus-positive patients,” Journal of Virology, vol. 69, no. 8, pp. 4737–4745, 1995.
[31]  B. Ludewig, J. Holzmeister, M. Gentile et al., “Replication pattern of human immunodeficiency virus type 1 in mature Langerhans cells,” Journal of General Virology, vol. 76, part 6, pp. 1317–1325, 1995.
[32]  M. T. Dittmar, G. Simmons, S. Hibbitts et al., “Langerhans cell tropism of human immunodeficiency virus type 1 subtype A through F isolates derived from different transmission groups,” Journal of Virology, vol. 71, no. 10, pp. 8008–8013, 1997.
[33]  M. Zaitseva, A. Blauvelt, S. Lee et al., “Expression and function of CCR5 and CXCR4 on human Langerhans cells and macrophages: implications for HIV primary infection,” Nature Medicine, vol. 3, no. 12, pp. 1369–1375, 1997.
[34]  P. R. Gorry and P. Ancuta, “Coreceptors and HIV-1 pathogenesis,” Current HIV/AIDS Reports, vol. 8, no. 1, pp. 45–53, 2011.
[35]  T. Kawamura, F. O. Gulden, M. Sugaya et al., “R5 HIV productively infects langerhans cells, and infection levels are regulated by compound CCR5 polymorphisms,” Proceedings of the National Academy of Sciences of the United States of America, vol. 100, no. 14, pp. 8401–8406, 2003.
[36]  F. O. Nestle, P. di Meglio, J. Z. Qin, and B. J. Nickoloff, “Skin immune sentinels in health and disease,” Nature Reviews Immunology, vol. 9, no. 10, pp. 679–691, 2009.
[37]  F. O. Nestle, X. G. Zheng, C. B. Thompson, L. A. Turka, and B. J. Nickoloff, “Characterization of dermal dendritic cells obtained from normal human skin reveals phenotypic and functionally distinctive subsets,” The Journal of Immunology, vol. 151, no. 11, pp. 6535–6545, 1993.
[38]  K. L. Summers, B. D. Hock, J. L. McKenzie, and D. N. J. Hart, “Phenotypic characterization of five dendritic cell subsets in human tonsils,” American Journal of Pathology, vol. 159, no. 1, pp. 285–295, 2001.
[39]  E. Segura, J. Valladeau-Guilemond, M. H. Donnadieu, X. Sastre-Garau, V. Soumelis, and S. Amigorena, “Characterization of resident and migratory dendritic cells in human lymph nodes,” The Journal of Experimental Medicine, vol. 209, no. 4, pp. 653–660, 2012.
[40]  D. Gibbings and A. D. Befus, “CD4 and CD8: an inside-out coreceptor model for innate immune cells,” Journal of Leukocyte Biology, vol. 86, no. 2, pp. 251–259, 2009.
[41]  T. Hirbod, R. C. Bailey, K. Agot et al., “Abundant expression of HIV target cells and C-type lectin receptors in the foreskin tissue of young Kenyan men,” American Journal of Pathology, vol. 176, no. 6, pp. 2798–2805, 2010.
[42]  T. Hirbod, T. Kaldensj？, L. Lopalco et al., “Abundant and superficial expression of C-type lectin receptors in ectocervix of women at risk of HIV infection,” Journal of Acquired Immune Deficiency Syndromes, vol. 51, no. 3, pp. 239–247, 2009.
[43]  T. Hirbod, T. Kaldensjo, and K. Broliden, “In situ distribution of HIV-binding CCR5 and C-type lectin receptors in the human endocervical mucosa,” PLoS One, vol. 6, no. 9, Article ID e25551, 2011.
[44]  T. Kaldensj？, P. Petersson, A. Tolf, G. Morgan, K. Broliden, and T. Hirbod, “Detection of intraepithelial and stromal langerin and CCR5 positive cells in the human endometrium: potential Targets for HIV infection,” PLoS One, vol. 6, no. 6, Article ID e21344, 2011.
[45]  J. P. Zoeteweij, H. Golding, H. Mostowski, and A. Blauvelt, “Cutting edge: cytokines regulate expression and function of the HIV coreceptor CXCR4 on human mature dendritic cells,” The Journal of Immunology, vol. 161, no. 7, pp. 3219–3223, 1998.
[46]  I. Tohou, L. Misery, O. Sabido et al., “Functional HIV CXCR4 coreceptor on human epithelial Langerhans cells and infection by HIV strain X4,” Journal of Leukocyte Biology, vol. 70, no. 2, pp. 313–321, 2001.
[47]  A. Blauvelt, H. Asada, M. W. Saville et al., “Productive infection of dendritic cells by HIV-1 and their ability to capture virus are mediated through separate pathways,” Journal of Clinical Investigation, vol. 100, no. 8, pp. 2043–2053, 1997.
[48]  T. Kawamura, M. Qualbani, E. K. Thomas, J. M. Orenstein, and A. Blauvelt, “Low levels of productive HIV infection in Langerhans cell-like dendritic cells differentiated in the presence of TGF-beta1 and increased viral replication with CD40 ligand-induced maturation,” European Journal of Immunology, vol. 31, no. 2, pp. 360–368, 2001.
[49]  P. Sivard, W. Berlier, B. Picard, O. Sabido, C. Genin, and L. Misery, “HIV-1 infection of langerhans cells in a reconstructed vaginal mucosa,” Journal of Infectious Diseases, vol. 190, no. 2, pp. 227–235, 2004.
[50]  T. Kawamura, S. E. Bruse, A. Abraha et al., “PSC-RANTES blocks R5 human immunodeficiency virus infection of Langerhans cells isolated from individuals with a variety of CCR5 diplotypes,” Journal of Virology, vol. 78, no. 14, pp. 7602–7609, 2004.
[51]  M. Sugaya, K. Loré, R. A. Koup, D. C. Douek, and A. Blauvelt, “HIV-infected langerhans cells preferentially transmit virus to proliferating autologous CD4+ memory T cells located within langerhans cell-T cell clusters,” The Journal of Immunology, vol. 172, no. 4, pp. 2219–2224, 2004.
[52]  M. Prakash, M. S. Kapembwa, F. Gotch, and S. Patterson, “Chemokine receptor expression on mucosal dendritic cells from the endocervix of healthy women,” Journal of Infectious Diseases, vol. 190, no. 2, pp. 246–250, 2004.
[53]  M. A. W. P. de Jong, L. de Witte, M. J. Oudhoff, S. I. Gringhuis, P. Gallay, and T. B. H. Geijtenbeek, “TNF-α and TLR agonists increase susceptibility to HIV-1 transmission by human Langerhans cells ex vivo,” Journal of Clinical Investigation, vol. 118, no. 10, pp. 3440–3452, 2008.
[54]  Y. Ogawa, T. Kawamura, T. Kimura, M. Ito, A. Blauvelt, and S. Shimada, “Gram-positive bacteria enhance HIV-1 susceptibility in Langerhans cells, but not in dendritic cells, via Toll-like receptor activation,” Blood, vol. 113, no. 21, pp. 5157–5166, 2009.
[55]  M. A. W. P. de Jong, L. de Witte, M. E. Taylor, and T. B. H. Geijtenbeek, “Herpes simplex virus type 2 enhances HIV-1 susceptibility by affecting langerhans cell function,” The Journal of Immunology, vol. 185, no. 3, pp. 1633–1641, 2010.
[56]  L. de Witte, A. Nabatov, M. Pion et al., “Langerin is a natural barrier to HIV-1 transmission by Langerhans cells,” Nature Medicine, vol. 13, no. 3, pp. 367–371, 2007.
[57]  E. J. Platt, K. Wehrly, S. E. Kuhmann, B. Chesebro, and D. Kabat, “Effects of CCR5 and CD4 cell surface concentrations on infections by macrophagetropic isolates of human immunodeficiency virus type 1,” Journal of Virology, vol. 72, no. 4, pp. 2855–2864, 1998.
[58]  E. J. Platt, S. L. Kozak, J. P. Durnin, T. J. Hope, and D. Kabat, “Rapid dissociation of HIV-1 from cultured cells severely limits infectivity assays, causes the inactivation ascribed to entry inhibitors, and masks the inherently high level of infectivity of virions,” Journal of Virology, vol. 84, no. 6, pp. 3106–3110, 2010.
[59]  G. Girolomoni, M. T. Valle, V. Zacchi, M. G. Costa, A. Giannetti, and F. Manca, “Cultured human Langerhans' cells are superior to fresh cells at presenting native HIV-1 protein antigens to specific CD4+ T-cell lines,” Immunology, vol. 87, no. 2, pp. 310–316, 1996.
[60]  A. Blauvelt, S. Glushakova, and L. B. Margolis, “HIV-infected human Langerhans cells transmit infection to human lymphoid tissue ex vivo,” AIDS, vol. 14, no. 6, pp. 647–651, 2000.
[61]  K. M. Fahrbach, S. M. Barry, S. Ayehunie, S. Lamore, M. Klausner, and T. J. Hope, “Activated CD34-derived langerhans cells mediate transinfection with human immunodeficiency virus,” Journal of Virology, vol. 81, no. 13, pp. 6858–6868, 2007.
[62]  F. Hladik, G. Lentz, R. E. Akridge et al., “Dendritic cell-T-cell interactions support coreceptor-independent human immunodeficiency virus type 1 transmission in the human genital tract,” Journal of Virology, vol. 73, no. 7, pp. 5833–5842, 1999.
[63]  T. Kawamura, Y. Koyanagi, Y. Nakamura et al., “Significant virus replication in langerhans cells following application of HIV to abraded skin: Relevance to occupational transmission of HIV,” The Journal of Immunology, vol. 180, no. 5, pp. 3297–3304, 2008.
[64]  S. J. A. M. Santegoets, S. Gibbs, K. Kroeze et al., “Transcriptional profiling of human skin-resident Langerhans cells and CD1a+ dermal dendritic cells: Differential activation states suggest distinct functions,” Journal of Leukocyte Biology, vol. 84, no. 1, pp. 143–151, 2008.
[65]  J. Banchereau, L. Thompson-Snipes, S. Zurawski et al., “The differential production of cytokines by human Langerhans cells and dermal CD14+ DCs controls CTL priming,” Blood, vol. 119, no. 24, pp. 5742–5749, 2012.
[66]  W. H. Kwan, A. M. Helt, C. Mara？ón et al., “Dendritic cell precursors are permissive to dengue virus and human immunodeficiency virus infection,” Journal of Virology, vol. 79, no. 12, pp. 7291–7299, 2005.
[67]  L. de Witte, A. Nabatov, and T. B. H. Geijtenbeek, “Distinct roles for DC-SIGN+-dendritic cells and Langerhans cells in HIV-1 transmission,” Trends in Molecular Medicine, vol. 14, no. 1, pp. 12–19, 2008.
[68]  M. Peressin, V. Holl, S. Schmidt et al., “HIV-1 replication in langerhans and interstitial dendritic cells is inhibited by neutralizing and Fc-mediated inhibitory antibodies,” Journal of Virology, vol. 85, no. 2, pp. 1077–1085, 2011.
[69]  A. N. Harman, J. Wilkinson, C. R. Bye et al., “HIV induces maturation of monocyte-derived dendritic cells and Langerhans cells,” The Journal of Immunology, vol. 177, no. 10, pp. 7103–7113, 2006.
[70]  L. E. Soto-Ramirez, B. Renjifo, M. F. McLane et al., “HIV-1 Langerhans' cell tropism associated with heterosexual transmission of HIV,” Science, vol. 271, no. 5253, pp. 1291–1293, 1996.
[71]  M. Pope, S. S. Frankel, J. R. Mascola et al., “Human immunodeficiency virus type 1 strains of subtypes B and E replicate in cutaneous dendritic cell-T-cell mixtures without displaying subtype-specific tropism,” Journal of Virology, vol. 71, no. 10, pp. 8001–8007, 1997.
[72]  R. Berger, S. Gartner, K. Rappersberger, C. A. Foster, K. Wolff, and G. Stingl, “Isolation of human immunodeficiency virus type 1 from human epidermis: virus replication and transmission studies,” Journal of Investigative Dermatology, vol. 99, no. 3, pp. 271–277, 1992.
[73]  P. U. Cameron, P. S. Freudenthal, J. M. Barker, S. Gezelter, K. Inaba, and R. M. Steinman, “Dendritic cells exposed to human immunodeficiency virus type-1 transmit a vigorous cytopathic infection to CD4+ T cells,” Science, vol. 257, no. 5068, pp. 383–386, 1992.
[74]  M. Pope, M. G. H. Betjes, N. Romani et al., “Conjugates of dendritic cells and memory T lymphocytes from skin facilitate productive infection with HIV-1,” Cell, vol. 78, no. 3, pp. 389–398, 1994.
[75]  S. Ayehunie, R. W. Groves, A. M. Bruzzese, R. M. Ruprecht, T. S. Kupper, and E. Langhoff, “Acutely infected Langerhans cells are more efficient than T cells in disseminating HIV type 1 to activated T cells following a short cell-cell contact,” AIDS Research and Human Retroviruses, vol. 11, no. 8, pp. 877–884, 1995.
[76]  Y. Ganor, Z. Zhou, D. Tudor et al., “Within 1 h, HIV-1 uses viral synapses to enter efficiently the inner, but not outer, foreskin mucosa and engages Langerhans-T cell conjugates,” Mucosal Immunology, vol. 3, no. 5, pp. 506–522, 2010.
[77]  M. Sugaya, O. Hartley, M. J. Root, and A. Blauvelt, “C34, a membrane fusion inhibitor, blocks HIV infection of Langerhans cells and viral transmission to T cells,” Journal of Investigative Dermatology, vol. 127, no. 6, pp. 1436–1443, 2007.
[78]  F. Hladik, P. Sakchalathorn, L. Ballweber et al., “Initial events in establishing vaginal entry and infection by human immunodeficiency virus type-1,” Immunity, vol. 26, no. 2, pp. 257–270, 2007.
[79]  S. Patterson, N. R. English, H. Longhurst et al., “Analysis of human immunodeficiency virus type 1 (HIV-1) variants and levels of infection in dendritic and T cells from symptomatic HIV-1-infected patients,” Journal of General Virology, vol. 79, no. 2, pp. 247–257, 1998.
[80]  M. Otero, G. Nunnari, D. Leto et al., “Peripheral blood dendritic cells are not a major reservoir for HIV type 1 in infected individuals on virally suppressive HAART,” AIDS Research and Human Retroviruses, vol. 19, no. 12, pp. 1097–1103, 2003.
[81]  E. Langhoff and W. A. Haseltine, “Infection of accessory dendritic cells by human immunodeficiency virus type 1,” Journal of Investigative Dermatology, vol. 99, no. 5, pp. 89S–94S, 1992.
[82]  E. Langhoff, K. H. Kalland, and W. A. Haseltine, “Early molecular replication of human immunodeficiency virus type 1 in cultured-blood-derived T helper dendritic cells,” Journal of Clinical Investigation, vol. 91, no. 6, pp. 2721–2726, 1993.
[83]  J. Chehimi, K. Prakash, V. Shanmugam et al., “CD4-independent infection of human peripheral blood dendritic cells with isolates of human immunodeficiency virus type 1,” Journal of General Virology, vol. 74, part 7, pp. 1277–1285, 1993.
[84]  S. Patterson, J. Gross, N. English, A. Stackpoole, P. Bedford, and S. C. Knight, “CD4 expression on dendritic cells and their infection by human immunodeficiency virus,” Journal of General Virology, vol. 76, part 5, pp. 1155–1163, 1995.
[85]  L. M. Pinchuk, P. S. Polacino, M. B. Agy, S. J. Klaus, and E. A. Clark, “The role of CD40 and CD80 accessory cell molecules in dendritic cell-dependent HIV-1 infection,” Immunity, vol. 1, no. 4, pp. 317–325, 1994.
[86]  A. Smed-S？rensen, K. Loré, J. Vasudevan et al., “Differential susceptibility to human immunodeficiency virus type 1 infection of myeloid and plasmacytoid dendritic cells,” Journal of Virology, vol. 79, no. 14, pp. 8861–8869, 2005.
[87]  A. Granelli-Piperno, I. Shimeliovich, M. Pack, C. Trumpfheller, and R. M. Steinman, “HIV-1 selectively infects a subset of nonmaturing BDCA1-positive dendritic cells in human blood,” The Journal of Immunology, vol. 176, no. 2, pp. 991–998, 2006.
[88]  D. Weissman, J. Daucher, T. Barker, J. Adelsberger, M. Baseler, and A. S. Fauci, “Cytokine regulation of HIV replication induced by dendritic cell-CD4-positive T cell interactions,” AIDS Research and Human Retroviruses, vol. 12, no. 9, pp. 759–767, 1996.
[89]  P. U. Cameron, M. Pope, S. Gezelter, and R. M. Steinman, “Infection and apoptotic cell death of CD4+ T cells during an immune response to HIV-1-pulsed dendritic cells,” AIDS Research and Human Retroviruses, vol. 10, no. 1, pp. 61–71, 1994.
[90]  P. U. Cameron, M. G. Lowe, F. Sotzik, A. F. Coughlan, S. M. Crowe, and K. Shortman, “The interaction of macrophage and non-macrophage tropic isolates of HIV-1 with thymic and tonsillar dendritic cells in vitro,” Journal of Experimental Medicine, vol. 183, no. 4, pp. 1851–1856, 1996.
[91]  D. Weissman, Y. Li, J. M. Orenstein, and A. S. Fauci, “Both a precursor and a mature population of dendritic cells can bind HIV: however, only the mature population that expresses CD80 can pass infection to unstimulated CD4+ T cells,” The Journal of Immunology, vol. 155, no. 8, pp. 4111–4117, 1995.
[92]  A. Granelli-Piperno, B. Moser, M. Pope et al., “Efficient interaction of HIV-1 with purified dendritic cells via multiple chemokine coreceptors,” Journal of Experimental Medicine, vol. 184, no. 6, pp. 2433–2438, 1996.
[93]  J. Pudney and M. J. Song, “Electron microscopic analysis of HIV-host cell interactions,” Tissue and Cell, vol. 26, no. 4, pp. 539–550, 1994.
[94]  P. U. Cameron, M. G. Lowe, S. M. Crowe et al., “Susceptibility of dendritic cells to HIV-1 in vitro,” Journal of Leukocyte Biology, vol. 56, no. 3, pp. 257–265, 1994.
[95]  P. U. Cameron, A. J. Handley, D. C. Baylis et al., “Preferential infection of dendritic cells during human immunodeficiency virus type 1 infection of blood leukocytes,” Journal of Virology, vol. 81, no. 5, pp. 2297–2306, 2007.
[96]  T. B. H. Geijtenbeek, D. S. Kwon, R. Torensma et al., “DC-SIGN, a dendritic cell-specific HIV-1-binding protein that enhances trans-infection of T cells,” Cell, vol. 100, no. 5, pp. 587–597, 2000.
[97]  E. J. Soilleux, L. S. Morris, G. Leslie et al., “Constitutive and induced expression of DC-SIGN on dendritic cell and macrophage subpopulations in situ and in vitro,” Journal of Leukocyte Biology, vol. 71, no. 3, pp. 445–457, 2002.
[98]  B. Jameson, F. Baribaud, S. P？hlmann et al., “Expression of DC-SIGN by dendritic cells of intestinal and genital mucosae in humans and rhesus macaques,” Journal of Virology, vol. 76, no. 4, pp. 1866–1875, 2002.
[99]  A. Engering, S. J. van Vliet, T. B. H. Geijtenbeek, and Y. van Kooyk, “Subset of DC-SIGN+ dendritic cells in human blood transmits HIV-1 to T lymphocytes,” Blood, vol. 100, no. 5, pp. 1780–1786, 2002.
[100]  K. B. Gurney, J. Elliott, H. Nassanian et al., “Binding and transfer of human immunodeficiency virus by DC-SIGN+ cells in human rectal mucosa,” Journal of Virology, vol. 79, no. 9, pp. 5762–5773, 2005.
[101]  B. J. C. Macatangay and C. R. Rinaldo, “Regulatory T cells in HIV immunotherapy,” HIV Therapy, vol. 4, no. 6, pp. 639–647, 2010.
[102]  K. Wendelsdorf, G. Dean, S. Hu, S. Nordone, and H. T. Banks, “Host immune responses that promote initial HIV spread,” Journal of Theoretical Biology, vol. 289, pp. 17–35, 2011.
[103]  A. Granelli-Piperno, A. Golebiowska, C. Trumpfheller, F. P. Siegal, and R. M. Steinman, “HIV-1-infected monocyte-derived dendritic cells do not undergo maturation but can elicit IL-10 production and T cell regulation,” Proceedings of the National Academy of Sciences of the United States of America, vol. 101, no. 20, pp. 7669–7674, 2004.
[104]  M. E. Moreno-Fernandez, C. M. Rueda, L. K. Rusie, and C. A. Chougnet, “Regulatory T cells control HIV replication in activated T cells through a cAMP-dependent mechanism,” Blood, vol. 117, no. 20, pp. 5372–5380, 2011.
[105]  C. Barat, C. Gilbert, M. Imbeault, and M. J. Tremblay, “Extracellular ATP reduces HIV-1 transfer from immature dendritic cells to CD4+ T lymphocytes,” Retrovirology, vol. 5, article 30, 2008.
[106]  N. Derby, E. Martinelli, and M. Robbiani, “Myeloid dendritic cells in HIV-1 infection,” Current Opinion in HIV and AIDS, vol. 6, no. 5, pp. 379–384, 2011.
[107]  R. L. Sabado, M. O'Brien, A. Subedi et al., “Evidence of dysregulation of dendritic cells in primary HIV infection,” Blood, vol. 116, no. 19, pp. 3839–3852, 2010.
[108]  S. M. Dillon, K. B. Robertson, S. C. Pan et al., “Plasmacytoid and myeloid dendritic cells with a partial activation phenotype accumulate in lymphoid tissue during asymptomatic chronic HIV-1 infection,” Journal of Acquired Immune Deficiency Syndromes, vol. 48, no. 1, pp. 1–12, 2008.
[109]  M. Almeida, M. Cordero, J. Almeida, and A. Orfao, “Abnormal cytokine production by circulating monocytes and dendritic cells of myeloid origin in ART-treated HIV-1+ patients relates to CD4+ T-cell recovery and HCV Co-infection,” Current HIV Research, vol. 5, no. 3, pp. 325–336, 2007.
[110]  J. Huang, Y. Yang, M. Al-Mozaini et al., “Dendritic cell dysfunction during primary HIV-1 infection,” The Journal of Infectious Diseases, vol. 204, no. 10, pp. 1557–1562, 2011.
[111]  J. M. Vázquez-Guillén, P. J. García-Jacobo, P. Zapata-Benavides et al., “Expression of DC-SIGN in peripheral blood dendritic cells of patients with typical, slow, and rapid progression to AIDS,” Archives of Medical Research, vol. 40, no. 2, pp. 132–135, 2009.
[112]  A. Meier, G. Alter, N. Frahm et al., “MyD88-dependent immune activation mediated by human immunodeficiency virus type 1-encoded toll-like receptor ligands,” Journal of Virology, vol. 81, no. 15, pp. 8180–8191, 2007.
[113]  A. Meier, A. Bagchi, H. K. Sidhu et al., “Upregulation of PD-L1 on monocytes and dendritic cells by HIV-1 derived TLR ligands,” AIDS, vol. 22, no. 5, pp. 655–658, 2008.
[114]  O. T. Campbell-Yesufu and R. T. Gandhi, “Update on human immunodeficiency virus (HIV)-2 infection,” Clinical Infectious Diseases, vol. 52, no. 6, pp. 780–787, 2011.
[115]  M. G. Duvall, K. Loré, H. Blaak et al., “Dendritic cells are less susceptible to human immunodeficiency virus type 2 (HIV-2) infection than to HIV-1 infection,” Journal of Virology, vol. 81, no. 24, pp. 13486–13498, 2007.
[116]  P. Szabolcs, E. D. Feller, M. A. S. Moore, and J. W. Young, “Progenitor recruitment and in vitro expansion of immunostimulatory dendritic cells from human CD34+ bone marrow cells by c-kit-ligand, GM-CSF, and TNFα,” Advances in Experimental Medicine and Biology, vol. 378, pp. 17–20, 1995.
[117]  N. Romani, D. Reider, M. Heuer et al., “Generation of mature dendritic cells from human blood. An improved method with special regard to clinical applicability,” Journal of Immunological Methods, vol. 196, no. 2, pp. 137–151, 1996.
[118]  A. Sacchi, G. Cappelli, C. Cairo et al., “Differentiation of monocytes into CD1a- dendritic cells correlates with disease progression in HIV-infected patients,” Journal of Acquired Immune Deficiency Syndromes, vol. 46, no. 5, pp. 519–528, 2007.
[119]  B. Canque, Y. Bakri, S. Camus, M. Yagello, A. Benjouad, and J. C. Gluckman, “The susceptibility to X4 and R5 human immunodeficiency virus-1 strains of dendritic cells derived in vitro from CD34+ hematopoietic progenitor cells is primarily determined by their maturation stage,” Blood, vol. 93, no. 11, pp. 3866–3875, 1999.
[120]  M. K. Warren, W. L. Rose, J. L. Cone, W. G. Rice, and J. A. Turpin, “Differential infection of CD34+ cell-derived dendritic cells and monocytes with lymphocyte-tropic and monocyte-tropic HIV-1 strains,” The Journal of Immunology, vol. 158, no. 10, pp. 5035–5042, 1997.
[121]  Y. Tsunetsugu-Yokota, K. Akagawa, H. Kimoto et al., “Monocyte-derived cultured dendritic cells are susceptible to human immunodeficiency virus infection and transmit virus to resting T cells in the process of nominal antigen presentation,” Journal of Virology, vol. 69, no. 7, pp. 4544–4547, 1995.
[122]  Y. Tsunetsugu-Yokota, S. Yasuda, A. Sugimoto et al., “Efficient virus transmission from dendritic cells to CD4+ T cells in response to antigen depends on close contact through adhesion molecules,” Virology, vol. 239, no. 2, pp. 259–268, 1997.
[123]  A. Rubbert, C. Combadiere, M. Ostrowski et al., “Dendritic cells express multiple chemokine receptors used as coreceptors for HIV entry,” The Journal of Immunology, vol. 160, no. 8, pp. 3933–3941, 1998.
[124]  N. Izquierdo-Useros, O. Esteban, M. T. Rodriguez-Plata et al., “Dynamic imaging of cell-free and cell-associated viral capture in mature dendritic cells,” Traffic, vol. 12, no. 12, pp. 1702–1713, 2011.
[125]  Z. Bajtay, C. Speth, A. Erdei, and M. P. Dierich, “Cutting edge: productive HIV-1 infection of dendritic cells via complement receptor type 3 (CR3, CD11b/CD18),” The Journal of Immunology, vol. 173, no. 8, pp. 4775–4778, 2004.
[126]  M. Pruenster, D. Wilflingseder, Z. Bánki et al., “C-type lectin-independent interaction of complement opsonized HIV with monocyte-derived dendritic cells,” European Journal of Immunology, vol. 35, no. 9, pp. 2691–2698, 2005.
[127]  V. Holl, M. Peressin, S. Schmidt et al., “Efficient inhibition of HIV-1 replication in human immature monocyte-derived dendritic cells by purified anti-HIV-1 IgG without induction of maturation,” Blood, vol. 107, no. 11, pp. 4466–4474, 2006.
[128]  D. Wilflingseder, Z. Banki, E. Garcia et al., “IgG opsonization of HIV impedes provirus formation in and infection of dendritic cells and subsequent long-term transfer to T cells,” The Journal of Immunology, vol. 178, no. 12, pp. 7840–7848, 2007.
[129]  A. Soederholm, Z. Bánki, D. Wilflingseder et al., “HIV-1 induced generation of C5a attracts immature dendritic cells and promotes infection of autologous T cells,” European Journal of Immunology, vol. 37, no. 8, pp. 2156–2163, 2007.
[130]  R. M. Steinman, “Decisions about dendritic cells: past, present, and future,” Annual Review of Immunology, vol. 30, pp. 1–22, 2012.
[131]  A. Granelli-Piperno, E. Delgado, V. Finkel, W. Paxton, and R. M. Steinman, “Immature dendritic cells selectively replicate macrophagetropic (M- tropic) human immunodeficiency virus type 1, while mature cells efficiently transmit both M- and T-tropic virus to T cells,” Journal of Virology, vol. 72, no. 4, pp. 2733–2737, 1998.
[132]  J. F. McDyer, M. Dybul, T. J. Goletz et al., “Differential effects of CD40 ligand/trimer stimulation on the ability of dendritic cells to replicate and transmit HIV infection: evidence for CC- chemokine-dependent and -independent mechanisms,” The Journal of Immunology, vol. 162, no. 6, pp. 3711–3717, 1999.
[133]  N. Izquierdo-Useros, J. Blanco, I. Erkizia et al., “Maturation of blood-derived dendritic cells enhances human immunodeficiency virus type 1 capture and transmission,” Journal of Virology, vol. 81, no. 14, pp. 7559–7570, 2007.
[134]  C. Dong, A. M. Janas, J. H. Wang, W. J. Olson, and L. Wu, “Characterization of human immunodeficiency virus type 1 replication in immature and mature dendritic cells reveals dissociable cis- and trans-infection,” Journal of Virology, vol. 81, no. 20, pp. 11352–11362, 2007.
[135]  R. B. Mailliard, A. Wankowicz-Kalinska, Q. Cai et al., “α-type-1 polarized dendritic cells: a novel immunization tool with optimized CTL-inducing activity,” Cancer Research, vol. 64, no. 17, pp. 5934–5937, 2004.
[136]  H. Jonuleit, U. Kühn, G. Müller et al., “Pro-inflammatory cytokines and prostaglandins induce maturation of potent immunostimulatory dendritic cells under fetal calf serum-free conditions,” European Journal of Immunology, vol. 27, no. 12, pp. 3135–3142, 1997.
[137]  R. W. Sanders, E. C. de Jong, C. E. Baldwin, J. H. N. Schuitemaker, M. L. Kapsenberg, and B. Berkhout, “Differential transmission of human immunodeficiency virus type 1 by distinct subsets of effector dendritic cells,” Journal of Virology, vol. 76, no. 15, pp. 7812–7821, 2002.
[138]  I. Frank, L. Kacani, H. Stoiber et al., “Human immunodeficiency virus type 1 derived from cocultures of immature dendritic cells with autologous T cells carries T-cell-specific molecules on its surface and is highly infectious,” Journal of Virology, vol. 73, no. 4, pp. 3449–3454, 1999.
[139]  T. H. J. Macdougall, R. J. Shattock, C. Madsen, B. M. Chain, and D. R. Katz, “Regulation of primary HIV-1 isolate replication in dendritic cells,” Clinical and Experimental Immunology, vol. 127, no. 1, pp. 66–71, 2002.
[140]  M. Cavrois, J. Neidleman, J. F. Kreisberg, D. Fenard, C. Callebaut, and W. C. Greene, “Human immunodeficiency virus fusion to dendritic cells declines as cells mature,” Journal of Virology, vol. 80, no. 4, pp. 1992–1999, 2006.
[141]  M. Pion, J. F. Arrighi, J. Jiang et al., “Analysis of HIV-1-X4 fusion with immature dendritic cells identifies a specific restriction that is independent of CXCR4 levels,” Journal of Investigative Dermatology, vol. 127, no. 2, pp. 319–323, 2007.
[142]  C. Gilbert, C. Barat, R. Cantin, and M. J. Tremblay, “Involvement of Src and Syk tyrosine kinases in HIV-1 transfer from dendritic cells to CD4+ T lymphocytes,” The Journal of Immunology, vol. 178, no. 5, pp. 2862–2871, 2007.
[143]  C. Gilbert, R. Cantin, C. Barat, and M. J. Tremblay, “Human immunodeficiency virus type 1 replication in dendritic cell-T-cell cocultures is increased upon incorporation of host LFA-1 due to higher levels of virus production in immature dendritic cells,” Journal of Virology, vol. 81, no. 14, pp. 7672–7682, 2007.
[144]  N. González, M. Bermejo, E. Calonge et al., “SDF-1/CXCL12 production by mature dendritic cells inhibits the propagation of X4-tropic HIV-1 isolates at the dendritic cell-T-cell infectious synapse,” Journal of Virology, vol. 84, no. 9, pp. 4341–4351, 2010.
[145]  P. Fairman and J. B. Angel, “The effect of human immunodeficiency virus-1 on monocyte-derived dendritic cell maturation and function,” Clinical & Experimental Immunology, vol. 170, no. 1, pp. 101–113, 2012.
[146]  J. H. Wang, A. M. Janas, W. J. Olson, V. N. KewalRamani, and L. Wu, “CD4 coexpression regulates DC-SIGN-mediated transmission of human immunodeficiency virus type 1,” Journal of Virology, vol. 81, no. 5, pp. 2497–2507, 2007.
[147]  J. H. Wang, A. M. Janas, W. J. Olson, and L. Wu, “Functionally distinct transmission of human immunodeficiency virus type 1 mediated by immature and mature dendritic cells,” Journal of Virology, vol. 81, no. 17, pp. 8933–8943, 2007.
[148]  C. Luo, K. Wang, D. Liu, Y. Li, and Q. S. Zhao, “The functional roles of lipid rafts in T cell activation, immune diseases and HIV infection and prevention,” Cellular and Molecular Immunology, vol. 5, no. 1, pp. 1–7, 2008.
[149]  A. Cambi, F. de Lange, N. M. van Maarseveen et al., “Microdomains of the C-type lectin DC-SIGN are portals for virus entry into dendritic cells,” Journal of Cell Biology, vol. 164, no. 1, pp. 145–155, 2004.
[150]  E. Caparrós, P. Munoz, E. Sierra-Filardi et al., “DC-SIGN ligation on dendritic cells results in ERK and PI3K activation and modulates cytokine production,” Blood, vol. 107, no. 10, pp. 3950–3958, 2006.
[151]  S. Gummuluru, M. Rogel, L. Stamatatos, and M. Emerman, “Binding of human immunodeficiency virus type 1 to immature dendritic cells can occur independently of DC-SIGN and mannose binding C-type lectin receptors via a cholesterol-dependent pathway,” Journal of Virology, vol. 77, no. 23, pp. 12865–12874, 2003.
[152]  S. C. Hatch, J. Archer, and S. Gummuluru, “Glycosphingolipid composition of Human Immunodeficiency Virus type 1 (HIV-1) particles is a crucial determinant for dendritic cell-mediated HIV-1 trans-infection,” Journal of Virology, vol. 83, no. 8, pp. 3496–3506, 2009.
[153]  J. H. Wang, C. Wells, and L. Wu, “Macropinocytosis and cytoskeleton contribute to dendritic cell-mediated HIV-1 transmission to CD4+ T cells,” Virology, vol. 381, no. 1, pp. 143–154, 2008.
[154]  T. M. Hanley, W. B. Puryear, S. Gummuluru, and G. A. Viglianti, “PPARγ and LXR signaling inhibit dendritic cell-mediated HIV-1 capture and trans-infection,” PLoS Pathogens, vol. 6, no. 7, Article ID e1000981, 2010.
[155]  W. B. Puryear, X. Yu, N. P. Ramirez, B. M. Reinhard, and S. Gummuluru, “HIV-1 incorporation of host-cell-derived glycosphingolipid GM3 allows for capture by mature dendritic cells,” Proceedings of the National Academy of Sciences of the United States of America, vol. 109, no. 19, pp. 7475–7480, 2012.
[156]  N. Izquierdo-Useros, M. Lorizate, F. X. Contreras et al., “Sialyllactose in viral membrane gangliosides is a novel molecular recognition pattern for mature dendritic cell capture of HIV-1,” PLOS Biologyogy, vol. 10, no. 4, Article ID e1001315, 2012.
[157]  N. Izquierdo-Useros, M. Lorizate, M. C. Puertas et al., “Siglec-1 is a novel dendritic cell receptor that mediates HIV-1 trans-infection through recognition of viral membrane gangliosides,” PLOS Biology, vol. 10, no. 12, Article ID e1001448, 2012.
[158]  M. Blanc, W. Y. Hsieh, K. A. Robertson et al., “Host defense against viral infection involves interferon mediated down-regulation of sterol biosynthesis,” PLOS Biology, vol. 9, no. 3, Article ID e1000598, 2011.
[159]  M. Blanc, W. Y. Hsieh, K. A. Robertson et al., “The transcription factor STAT-1 couples macrophage synthesis of 25-hydroxycholesterol to the interferon antiviral response,” Immunity, vol. 38, no. 1, pp. 106–118, 2013.
[160]  S. Y. Liu, R. Aliyari, K. Chikere et al., “Interferon-Inducible Cholesterol-25-Hydroxylase Broadly Inhibits Viral Entry by Production of 25-Hydroxycholesterol,” Immunity, vol. 38, no. 1, pp. 92–105, 2013.
[161]  E. Garcia, D. S. Nikolic, and V. Piguet, “HIV-1 replication in dendritic cells occurs through a tetraspanin-containing compartment enriched in AP-3,” Traffic, vol. 9, no. 2, pp. 200–214, 2008.
[162]  S. G. Turville, M. Aravantinou, H. St？ssel, N. Romani, and M. Robbiani, “Resolution of de novo HIV production and trafficking in immature dendritic cells,” Nature Methods, vol. 5, no. 1, pp. 75–85, 2008.
[163]  S. Nydegger, S. Khurana, D. N. Krementsov, M. Foti, and M. Thali, “Mapping of tetraspanin-enriched microdomains that can function as gateways for HIV-1,” Journal of Cell Biology, vol. 173, no. 5, pp. 795–807, 2006.
[164]  A. Ono, “Relationships between plasma membrane microdomains and HIV-1 assembly,” Biology of the Cell, vol. 102, no. 6, pp. 335–350, 2010.
[165]  G. T. Spear, M. R. Zariffard, J. Xin, and M. Saifuddin, “Inhibition of DC-SIGN-mediated trans infection of T cells by mannose-binding lectin,” Immunology, vol. 110, no. 1, pp. 80–85, 2003.
[166]  J. F. Arrighi, M. Pion, E. Garcia et al., “DC-SIGN-mediated infectious synapse formation enhances X4 HIV-1 transmission from dendritic cells to T cells,” Journal of Experimental Medicine, vol. 200, no. 10, pp. 1279–1288, 2004.
[167]  J. F. Arrighi, M. Pion, M. Wiznerowicz et al., “Lentivirus-mediated RNA interference of DC-SIGN expression inhibits human immunodeficiency virus transmission from dendritic cells to T cells,” Journal of Virology, vol. 78, no. 20, pp. 10848–10855, 2004.
[168]  L. Wu, T. D. Martin, Y. C. Han, S. K. J. Breun, and V. N. KewalRamani, “Trans-dominant cellular inhibition of DC-SIGN-mediated HIV-1 transmission,” Retrovirology, vol. 1, article 14, 2004.
[169]  C. L. Lin, A. K. Sewell, G. F. Gao, K. T. Whelan, R. E. Phillips, and J. M. Austyn, “Macrophage-tropic HIV induces and exploits dendritic cell chemotaxis,” Journal of Experimental Medicine, vol. 192, no. 4, pp. 587–593, 2000.
[170]  D. S. Kwon, G. Gregorio, N. Bitton, W. A. Hendrickson, and D. R. Littman, “DC-SIGN-mediated internalization of HIV is required for trans-enhancement of T cell infection,” Immunity, vol. 16, no. 1, pp. 135–144, 2002.
[171]  O. K. Bernhard, J. Lai, J. Wilkinson, M. M. Sheil, and A. L. Cunningham, “Proteomic analysis of DC-SIGN on dendritic cells detects tetramers required for ligand binding but no association with CD4,” Journal of Biological Chemistry, vol. 279, no. 50, pp. 51828–51835, 2004.
[172]  P. W. P. Hong, S. Nguyen, S. Young, S. V. Su, and B. Lee, “Identification of the optimal DC-SIGN binding site on human immunodeficiency virus type 1 gp120,” Journal of Virology, vol. 81, no. 15, pp. 8325–8336, 2007.
[173]  T. van Montfort, D. Eggink, M. Boot et al., “HIV-1 N-glycan composition governs a balance between dendritic cell-mediated viral transmission and antigen presentation,” The Journal of Immunology, vol. 187, no. 9, pp. 4676–4685, 2011.
[174]  S. Sato, C. St-Pierre, P. Bhaumik, and J. Nieminen, “Galectins in innate immunity: dual functions of host soluble β-galactoside-binding lectins as damage-associated molecular patterns (DAMPs) and as receptors for pathogen-associated molecular patterns (PAMPs),” Immunological Reviews, vol. 230, no. 1, pp. 172–187, 2009.
[175]  R. L. Sabado, E. Babcock, D. G. Kavanagh et al., “Pathways utilized by dendritic cells for binding, uptake, processing and presentation of antigens derived from HIV-1,” European Journal of Immunology, vol. 37, no. 7, pp. 1752–1763, 2007.
[176]  A. L. Smith, L. Ganesh, K. Leung, J. Jongstra-Bilen, J. Jongstra, and G. J. Nabel, “Leukocyte-specific protein 1 interacts with DC-SIGN and mediates transport of HIV to the proteasome in dendritic cells,” Journal of Experimental Medicine, vol. 204, no. 2, pp. 421–430, 2007.
[177]  R. T. Martinez-Nunez, F. Louafi, P. S. Friedmann, and T. Sanchez-Eisner, “MicroRNA-155 modulates the pathogen binding ability of dendritic cells (DCs) by down-regulation of DC-specific intercellular adhesion molecule-3 grabbing non-integrin (DC-SIGN),” Journal of Biological Chemistry, vol. 284, no. 24, pp. 16334–16342, 2009.
[178]  A. A. Nabatov, T. van Montfort, T. B. H. Geijtenbeek, G. Pollakis, and W. A. Paxton, “Interaction of HIV-1 with dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin-expressing cells is influenced by gp120 envelope modifications associated with disease progression,” FEBS Journal, vol. 273, no. 21, pp. 4944–4958, 2006.
[179]  M. Borggren, J. Repits, C. Kuylenstierna et al., “Evolution of DC-SIGN use revealed by fitness studies of R5 HIV-1 variants emerging during AIDS progression,” Retrovirology, vol. 5, article 28, 2008.
[180]  J. C. Reece, N. J. Vardaxis, J. A. Marshall, S. M. Crowe, and P. U. Cameron, “Uptake of HIV and latex particles by fresh and cultured dendritic cells and monocytes,” Immunology and Cell Biology, vol. 79, no. 3, pp. 255–263, 2001.
[181]  A. Engering, T. B. H. Geijtenbeek, S. J. van Vliet et al., “The dendritic cell-specific adhesion receptor DC-SIGN internalizes antigen for presentation to T cells,” The Journal of Immunology, vol. 168, no. 5, pp. 2118–2126, 2002.
[182]  S. Popov, A. L. Chenine, A. Gruber, P. L. Li, and R. M. Ruprecht, “Long-term productive human immunodeficiency virus infection of CD1a-sorted myeloid dendritic cells,” Journal of Virology, vol. 79, no. 1, pp. 602–608, 2005.
[183]  C. Nobile, C. Petit, A. Moris et al., “Covert human immunodeficiency virus replication in dendritic cells and in DC-SIGN-expressing cells promotes long-term transmission to lymphocytes,” Journal of Virology, vol. 79, no. 9, pp. 5386–5399, 2005.
[184]  S. I. Gringhuis, M. van der Vlist, L. M. van den Berg, J. Den Dunnen, M. Litjens, and T. B. H. Geijtenbeek, “HIV-1 exploits innate signaling by TLR8 and DC-SIGN for productive infection of dendritic cells,” Nature Immunology, vol. 11, no. 5, pp. 419–426, 2010.
[185]  S. A. David, M. S. Smith, G. J. Lopez et al., “Selective transmission of R5-tropic HIV type 1 from dendritic cells to resting CD4+ T cells,” AIDS Research and Human Retroviruses, vol. 17, no. 1, pp. 59–68, 2001.
[186]  L. Ganesh, K. Leung, K. Loré et al., “Infection of specific dendritic cells by CCR5-tropic human immunodeficiency virus type 1 promotes cell-mediated transmission of virus resistant to broadly neutralizing antibodies,” Journal of Virology, vol. 78, no. 21, pp. 11980–11987, 2004.
[187]  T. van Montfort, A. A. Nabatov, T. B. H. Geijtenbeek, G. Pollakis, and W. A. Paxton, “Efficient capture of antibody neutralized HIV-1 by cells expressing DC-SIGN and transfer to CD4+ T lymphocytes,” The Journal of Immunology, vol. 178, no. 5, pp. 3177–3185, 2007.
[188]  D. Scales, H. Ni, F. Shaheen, J. Capodici, G. Cannon, and D. Weissman, “Nonproliferating bystander CD4+ T cells lacking activation markers support HIV replication during immune activation,” The Journal of Immunology, vol. 166, no. 10, pp. 6437–6443, 2001.
[189]  A. Moris, A. Pajot, F. Blanchet, F. Guivel-Benhassine, M. Salcedo, and O. Schwartz, “Dendritic cells and HIV-specific CD4+ T cells: HIV antigen presentation, T-cell activation, and viral transfer,” Blood, vol. 108, no. 5, pp. 1643–1651, 2006.
[190]  H. Bouhlal, N. Chomont, M. Réquena et al., “Opsonization of HIV with complement enhances infection of dendritic cells and viral transfer to CD4 T cells in a CR3 and DC-SIGN-dependent manner,” The Journal of Immunology, vol. 178, no. 2, pp. 1086–1095, 2007.
[191]  V. Tjomsland, R. Ellegard, K. Che, J. Hinkula, J. D. Lifson, and M. Larsson, “Complement opsonization of HIV-1 enhances the uptake by dendritic cells and involves the endocytic lectin and integrin receptor families,” PLoS One, vol. 6, no. 8, Article ID e23542, 2011.
[192]  S. G. Turville, J. J. Santos, I. Frank et al., “Immunodeficiency virus uptake, turnover, and 2-phase transfer in human dendritic cells,” Blood, vol. 103, no. 6, pp. 2170–2179, 2004.
[193]  C. Muratori, R. Bona, E. Ruggiero et al., “DC contact with HIV-1-infected cells leads to high levels of Env-mediated virion endocytosis coupled with enhanced HIV-1 Ag presentation,” European Journal of Immunology, vol. 39, no. 2, pp. 404–416, 2009.
[194]  N. J. Venkatachari, S. Alber, S. C. Watkins, and V. Ayyavoo, “HIV-1 infection of DC: evidence for the acquisition of virus particles from infected T cells by antigen uptake mechanism,” PLoS ONE, vol. 4, no. 10, Article ID e7470, 2009.
[195]  E. Ruggiero, E. Toschi, and M. Federico, “The activity of matrix metalloproteinase-9 is part of the mechanism of cell-to-cell HIV-1 endocytosis in dendritic cells,” Current Drug Discovery Technologies, vol. 8, no. 2, pp. 112–118, 2011.
[196]  I. Clotet-Codina, B. Bosch, J. Senserrich et al., “HIV endocytosis after dendritic cell to T cell viral transfer leads to productive virus infection,” Antiviral Research, vol. 83, no. 1, pp. 94–98, 2009.
[197]  C. Muratori, E. Ruggiero, A. Sistigu, R. Bona, and M. Federico, “Human immunodeficiency virus type 1 (HIV-1) protease inhibitors block cell-to-cell HIV-1 endocytosis in dendritic cells,” Journal of General Virology, vol. 90, part 11, pp. 2777–2787, 2009.
[198]  E. Garcia, M. Pion, A. Pelchen-Matthews et al., “HIV-1 trafficking to the dendritic cell-T-cell infectious synapse uses a pathway of tetraspanin sorting to the immunological synapse,” Traffic, vol. 6, no. 6, pp. 488–501, 2005.
[199]  A. K. Neumann, N. L. Thompson, and K. Jacobson, “Distribution and lateral mobility of DC-SIGN on immature dendritic cells—implications for pathogen uptake,” Journal of Cell Science, vol. 121, part 5, pp. 634–643, 2008.
[200]  A. M. Janas, C. Dong, J. H. Wang, and L. Wu, “Productive infection of human immunodeficiency virus type 1 in dendritic cells requires fusion-mediated viral entry,” Virology, vol. 375, no. 2, pp. 442–451, 2008.
[201]  K. Hijazi, Y. Wang, C. Scala et al., “DC-SIGN increases the affinity of HIV-1 envelope glycoprotein interaction with CD4,” PLoS One, vol. 6, no. 12, Article ID e28307, 2011.
[202]  F. Baribaud, S. P？hlmann, G. Leslie, F. Mortari, and R. W. Doms, “Quantitative expression and virus transmission analysis of DC-SIGN on monocyte-derived dendritic cells,” Journal of Virology, vol. 76, no. 18, pp. 9135–9142, 2002.
[203]  A. N. Harman, M. Kraus, C. R. Bye et al., “HIV-1-infected dendritic cells show 2 phases of gene expression changes, with lysosomal enzyme activity decreased during the second phase,” Blood, vol. 114, no. 1, pp. 85–94, 2009.
[204]  M. Cavrois, J. Neidleman, and W. C. Greene, “The Achilles Heel of the Trojan horse model of HIV-1 trans-infection,” PLoS Pathogens, vol. 4, no. 6, Article ID e1000051, 2008.
[205]  L. Burleigh, P. Y. Lozach, C. Schiffer et al., “Infection of dendritic cells (DCs), not DC-SIGN-mediated internalization of human immunodeficiency virus, is required for long-term transfer of virus to T cells,” Journal of Virology, vol. 80, no. 6, pp. 2949–2957, 2006.
[206]  H. J. Yu, M. A. Reuter, and D. McDonald, “HIV traffics through a specialized, surface-accessible intracellular compartment during trans-infection of T cells by mature dendritic cells,” PLoS Pathogens, vol. 4, no. 8, Article ID e1000134, 2008.
[207]  M. Cavrois, J. Neidleman, J. F. Kreisberg, and W. C. Greene, “In vitro derived dendritic cells trans-infect CD4 T cells primarily with surface-bound HIV-1 virions,” PLoS pathogens, vol. 3, no. 1, p. e4, 2007.
[208]  R. D. Wiley and S. Gummuluru, “Immature dendritic cell-derived exosomes can mediate HIV-1 trans infection,” Proceedings of the National Academy of Sciences of the United States of America, vol. 103, no. 3, pp. 738–743, 2006.
[209]  R. Sealy, B. G. Jones, S. L. Surman, and J. L. Hurwitz, “Short communication: the dead cell: a potent escort for HIV type 1 transinfection,” AIDS Research and Human Retroviruses, vol. 25, no. 11, pp. 1123–1128, 2009.
[210]  N. Izquierdo-Useros, M. Naranjo-Gómez, J. Archer et al., “Capture and transfer of HIV-1 particles by mature dendritic cells converges with the exosome-dissemination pathway,” Blood, vol. 113, no. 12, pp. 2732–2741, 2009.
[211]  V. Mohanram, U. Johansson, A. E. Sk？ld et al., “Exposure to apoptotic activated CD4+ T cells induces maturation and APOBEC3G- mediated inhibition of HIV-1 infection in dendritic cells,” PLoS One, vol. 6, no. 6, Article ID e21171, 2011.
[212]  C. Boggiano, N. Manel, and D. R. Littman, “Dendritic cell-mediated trans-enhancement of human immunodeficiency virus type 1 infectivity is independent of DC-SIGN,” Journal of Virology, vol. 81, no. 5, pp. 2519–2523, 2007.
[213]  S. Gummuluru, V. N. KewalRamani, and M. Emerman, “Dendritic cell-mediated viral transfer to T cells is required for human immunodeficiency virus type 1 persistence in the face of rapid cell turnove,” Journal of Virology, vol. 76, no. 21, pp. 10692–10701, 2002.
[214]  L. Wu, T. D. Martin, R. Vazeux, D. Unutmaz, and V. N. KewalRamani, “Functional evaluation of DC-SIGN monoclonal antibodies reveals DC-SIGN interactions with ICAM-3 do not promote human immunodeficiency virus type 1 transmission,” Journal of Virology, vol. 76, no. 12, pp. 5905–5914, 2002.
[215]  S. Bounou, J. F. Giguère, R. Cantin et al., “The importance of virus-associated host ICAM-1 in human immunodeficiency virus type 1 dissemination depends on the cellular context,” FASEB Journal, vol. 18, no. 11, pp. 1294–1296, 2004.
[216]  A. Moris, C. Nobile, F. Buseyne, F. Porrot, J. P. Abastado, and O. Schwartz, “DC-SIGN promotes exogenous MHC-I-restricted HIV-1 antigen presentation,” Blood, vol. 103, no. 7, pp. 2648–2654, 2004.
[217]  A. A. Lambert, C. Gilbert, M. Richard, A. D. Beaulieu, and M. J. Tremblay, “The C-type lectin surface receptor DCIR acts as a new attachment factor for HIV-1 in dendritic cells and contributes to trans- and cis-infection pathways,” Blood, vol. 112, no. 4, pp. 1299–1307, 2008.
[218]  E. Klechevsky, A. L. Flamar, Y. Cao et al., “Cross-priming CD8+ T cells by targeting antigens to human dendritic cells through DCIR,” Blood, vol. 116, no. 10, pp. 1685–1697, 2010.
[219]  A. A. Lambert, M. L. Imbeault, C. Gilbert, and M. J. Tremblay, “HIV-1 induces DCIR expression in CD4+ T cells,” PLoS Pathogens, vol. 6, no. 11, Article ID e1001188, 2010.
[220]  A. A. Lambert, F. Barabé, C. Gilbert, and M. J. Tremblay, “DCIR-mediated enhancement of HIV-1 infection requires the ITIM-associated signal transduction pathway,” Blood, vol. 117, no. 24, pp. 6589–6599, 2011.
[221]  L. de Witte, M. Bobardt, U. Chatterji et al., “Syndecan-3 is a dendritic cell-specific attachment receptor for HIV-1,” Proceedings of the National Academy of Sciences of the United States of America, vol. 104, no. 49, pp. 19464–19469, 2007.
[222]  G. D. Gaiha, T. Dong, N. Palaniyar, D. A. Mitchell, K. B. M. Reid, and H. W. Clark, “Surfactant protein a binds to HIV and inhibits direct infection of cd4+ cells, but enhances dendritic cell-mediated viral transfer,” The Journal of Immunology, vol. 181, no. 1, pp. 601–609, 2008.
[223]  A. Magérus-Chatinet, H. Yu, S. Garcia, E. Ducloux, B. Terris, and M. Bomsel, “Galactosyl ceramide expressed on dendritic cells can mediate HIV-1 transfer from monocyte derived dendritic cells to autologous T cells,” Virology, vol. 362, no. 1, pp. 67–74, 2007.
[224]  J. A. Bluestone, C. R. MacKay, J. J. O'Shea, and B. Stockinger, “The functional plasticity of T cell subsets,” Nature Reviews Immunology, vol. 9, no. 11, pp. 811–816, 2009.
[225]  L. M. Coussens, L. Zitvogel, and A. K. Palucka, “Neutralizing tumor-promoting chronic inflammation: a magic bullet?” Science, vol. 339, no. 6117, pp. 286–291, 2013.
[226]  M. Perreau, A. L. Savoye, E. de Crignis et al., “Follicular helper T cells serve as the major CD4 T cell compartment for HIV-1 infection, replication, and production,” The Journal of Experimental Medicine, vol. 210, no. 1, pp. 143–156, 2013.
[227]  C. S. Ma, E. K. Deenick, M. Batten, and S. G. Tangye, “The origins, function, and regulation of T follicular helper cells,” The Journal of Experimental Medicine, vol. 209, no. 7, pp. 1241–1253, 2012.
[228]  S. Pallikkuth, A. Parmigiani, and S. Pahwa, “The role of interleukin-21 in HIV infection,” Cytokine & Growth Factor Reviews, vol. 23, no. 4-5, pp. 173–180, 2012.
[229]  L. Shan, K. Deng, N. S. Shroff et al., “Stimulation of HIV-1-specific cytolytic T lymphocytes facilitates elimination of latent viral reservoir after virus reactivation,” Immunity, vol. 36, no. 3, pp. 491–501, 2012.
[230]  M. Massanella, J. Martinez-Picado, and J. Blanco, “Attacking the HIV reservoir from the immune and viral perspective,” Current HIV/AIDS Reports, vol. 10, no. 1, pp. 33–41, 2013.
[231]  S. G. Deeks, B. Autran, B. Berkhout et al., “Towards an HIV cure: a global scientific strategy,” Nature Reviews Immunology, vol. 12, no. 8, pp. 607–614, 2012.
[232]  N. Chomont, M. El-Far, P. Ancuta et al., “HIV reservoir size and persistence are driven by T cell survival and homeostatic proliferation,” Nature Medicine, vol. 15, no. 8, pp. 893–900, 2009.
[233]  O. T. Fackler, A. Alcover, and O. Schwartz, “Modulation of the immunological synapse: a key to HIV-1 pathogenesis?” Nature Reviews Immunology, vol. 7, no. 4, pp. 310–317, 2007.
[234]  M. Lehmann, D. S. Nikolic, and V. Piguet, “How HIV-1 takes advantage of the cytoskeleton during replication and cell-to-cell transmission,” Viruses, vol. 3, no. 9, pp. 1757–1776, 2011.
[235]  D. S. Nikolic, M. Lehmann, R. Felts et al., “HIV-1 activates Cdc42 and induces membrane extensions in immature dendritic cells to facilitate cell-to-cell virus propagation,” Blood, vol. 118, no. 18, pp. 4841–4852, 2011.
[236]  A. Aggarwal, T. L. Iemma, I. Shih et al., “Mobilization of HIV spread by diaphanous 2 dependent filopodia in infected dendritic cells,” PLOS Pathogens, vol. 8, no. 6, Article ID e1002762, 2012.
[237]  R. L. Felts, K. Narayan, J. D. Estes et al., “3D visualization of HIV transfer at the virological synapse between dendritic cells and T cells,” Proceedings of the National Academy of Sciences of the United States of America, vol. 107, no. 30, pp. 13336–13341, 2010.
[238]  I. B. Hogue, S. H. Bajaria, B. A. Fallert, S. Qin, T. A. Reinhart, and D. E. Kirschner, “The dual role of dendritic cells in the immune response to human immunodeficiency virus type 1 infection,” Journal of General Virology, vol. 89, part 9, pp. 2228–2239, 2008.
[239]  C. Barat, C. Gilbert, and M. J. Tremblay, “Efficient replication of human immunodeficiency virus type 1 in resting CD4+ T lymphocytes is induced by coculture with autologous dendritic cells in the absence of foreign antigens,” Journal of Virology, vol. 83, no. 6, pp. 2778–2782, 2009.
[240]  J. Dai, L. M. Agosto, C. Baytop et al., “Human immunodeficiency virus integrates directly into na？ve resting CD4+ T cells but enters na？ve cells less efficiently than memory cells,” Journal of Virology, vol. 83, no. 9, pp. 4528–4537, 2009.
[241]  M. Lichtner, C. Mara？ón, P. O. Vidalain et al., “HIV type 1-infected dendritic cells induce apoptotic death in infected and uninfected primary CD4+ T lymphocytes,” AIDS Research and Human Retroviruses, vol. 20, no. 2, pp. 175–182, 2004.
[242]  K. F. Che, E. M. Shankar, S. Muthu et al., “P38MAPK/STAT3 pathway signaling regulates expression of inhibitory molecules in T-cells activated by HIV-1 exposed dendritic cells,” Molecular Medicine, vol. 18, pp. 1169–1182, 2012.
[243]  J. H. Wang, C. Kwas, and L. Wu, “Intercellular adhesion molecule 1 (ICAM-1), but not ICAM-2 and -3, is important for dendritic cell-mediated human immunodeficiency virus type 1 transmission,” Journal of Virology, vol. 83, no. 9, pp. 4195–4204, 2009.
[244]  F. Groot, T. W. Kuijpers, B. Berkhout, and E. C. de Jong, “Dendritic cell-mediated HIV-1 transmission to T cells of LAD-1 patients is impaired due to the defect in LFA-1,” Retrovirology, vol. 3, article 75, 2006.
[245]  J. E. Biggins, T. Biesinger, M. T. Yu Kimata, R. Arora, and J. T. Kimata, “ICAM-3 influences human immunodeficiency virus type 1 replication in CD4+ T cells independent of DC-SIGN-mediated transmission,” Virology, vol. 364, no. 2, pp. 383–394, 2007.
[246]  T. J. Ketas, P. J. Klasse, C. Spenlehauer et al., “Entry inhibitors SCH-C, RANTES, and T-20 block HIV type 1 replication in multiple cell types,” AIDS Research and Human Retroviruses, vol. 19, no. 3, pp. 177–186, 2003.
[247]  T. J. Ketas, I. Frank, P. J. Klasse et al., “Human immunodeficiency virus type 1 attachment, coreceptor, and fusion inhibitors are active against both direct and trans infection of primary cells,” Journal of Virology, vol. 77, no. 4, pp. 2762–2767, 2003.
[248]  A. Hodges, K. Sharrocks, M. Edelmann et al., “Activation of the lectin DC-SIGN induces an immature dendritic cell phenotype triggering Rho-GTPase activity required for HIV-1 replication,” Nature Immunology, vol. 8, no. 6, pp. 569–577, 2007.
[249]  T. Yamamoto, Y. Tsunetsugu-Yokota, Y. Y. Mitsuki et al., “Selective transmission of R5 HIV-1 over X4 HIV-1 at the dendritic cell-T cell infectious synapse is determined by the T cell activation state,” PLoS Pathogens, vol. 5, no. 1, Article ID e1000279, 2009.
[250]  F. Groot, T. M. M. van Capel, J. H. N. Schuitemaker, B. Berkhout, and E. C. de Jong, “Differential susceptibility of na？ve, central memory and effector memory T cells to dendritic cell-mediated HIV-1 transmission,” Retrovirology, vol. 3, article 52, 2006.
[251]  C. Petit, F. Buseyne, C. Boccaccio, J. P. Abastado, J. M. Heard, and O. Schwartz, “Nef is required for efficient HIV-1 replication in cocultures of dendritic cells and lymphocytes,” Virology, vol. 286, no. 1, pp. 225–236, 2001.
[252]  D. Messmer, J. M. Jacqué, C. Santisteban et al., “Endogenously expressed nef uncouples cytokine and chemokine production from membrane phenotypic maturation in dendritic cells,” The Journal of Immunology, vol. 169, no. 8, pp. 4172–4182, 2002.
[253]  C. St Gelais, C. M. Coleman, J. H. Wang, and L. Wu, “HIV-1 Nef enhances dendritic cell-mediated viral transmission to CD4+ T cells and promotes T-cell activation,” PLoS One, vol. 7, no. 3, Article ID e34521, 2012.
[254]  C. M. Coleman, P. Spearman, and L. Wu, “Tetherin does not significantly restrict dendritic cell-mediated HIV-1 transmission and its expression is upregulated by newly synthesized HIV-1 Nef,” Retrovirology, vol. 8, article 26, 2011.
[255]  S. S. Frankel, R. M. Steinman, N. L. Michael et al., “Neutralizing monoclonal antibodies block human immunodeficiency virus type 1 infection of dendritic cells and transmission to T cells,” Journal of Virology, vol. 72, no. 12, pp. 9788–9794, 1998.
[256]  T. van Montfort, A. A. M. Thomas, G. Pollakis, and W. A. Paxton, “Dendritic cells preferentially transfer CXCR4-using human immunodeficiency virus type 1 variants to CD4+ T lymphocytes in trans,” Journal of Virology, vol. 82, no. 16, pp. 7886–7896, 2008.
[257]  M. Sagar, H. Akiyama, B. Etemad, N. Ramirez, I. Freitas, and S. Gummuluru, “Transmembrane domain membrane proximal external region but not surface unit-directed broadly neutralizing HIV-1 antibodies can restrict dendritic cell-mediated HIV-1 trans-infection,” The Journal of Infectious Diseases, vol. 205, no. 8, pp. 1248–1257, 2012.
[258]  R. B. Mailliard, S. M. Alber, H. Shen et al., “IL-18-induced CD83+CCR7+ NK helper cells,” Journal of Experimental Medicine, vol. 202, no. 7, pp. 941–953, 2005.
[259]  R. B. Mailliard, Y. I. Son, R. Redlinger et al., “Dendritic cells mediate NK cell help for Th1 and CTL responses: two-signal requirement for the induction of NK cell helper function,” The Journal of Immunology, vol. 171, no. 5, pp. 2366–2373, 2003.
[260]  A. Valentin-Torres, C. M. Ramirez Kitchen, H. S. Haller, and H. B. Bernstein, “Bidirectional NK/DC interactions promote CD4 expression on NK cells, DC maturation, and HIV infection,” Virology, vol. 433, no. 1, pp. 203–215, 2012.
[261]  J. Funke, R. Durr, U. Dietrich, and J. Koch, “Natural killer cells in HIV-1 infection: a double-edged sword,” AIDS Review, vol. 13, no. 2, pp. 67–76, 2011.
[262]  M. T. Melki, H. Sa？di, A. Dufour, J. C. Olivo-Marin, and M. L. Gougeon, “Escape of HIV-1-infected dendritic cells from TRAIL-mediated NK cell cytotoxicity during NK-DC cross-talk—a pivotal role of HMGB1,” PLoS Pathogens, vol. 6, no. 4, Article ID e1000862, 2010.
[263]  D. N. Fredricks, T. L. Fiedler, and J. M. Marrazzo, “Molecular identification of bacteria associated with bacterial vaginosis,” The New England Journal of Medicine, vol. 353, no. 18, pp. 1899–1911, 2005.
[264]  L. Myer, L. Denny, R. Telerant, M. de Souza, T. C. Wright Jr., and L. Kuhn, “Bacterial vaginosis and susceptibility to HIV infection in South African women: a nested case-control study,” Journal of Infectious Diseases, vol. 192, no. 8, pp. 1372–1380, 2005.
[265]  E. P. St John, J. Martinson, J. A. Simoes, A. L. Landay, and G. T. Spear, “Dendritic cell activation and maturation induced by mucosal fluid from women with bacterial vaginosis,” Clinical Immunology, vol. 125, no. 1, pp. 95–102, 2007.
[266]  E. P. St John, M. R. Zariffard, J. A. Martinson, J. A. Simoes, A. L. Landay, and G. T. Spear, “Effect of mucosal fluid from women with bacterial vaginosis on HIV trans-infection mediated by dendritic cells,” Virology, vol. 385, no. 1, pp. 22–27, 2009.
[267]  D. McDonald, L. Wu, S. M. Bohks, V. N. KewalRamani, D. Unutmaz, and T. J. Hope, “Recruitment of HIV and its receptors to dendritic cell-T cell junctions,” Science, vol. 300, no. 5623, pp. 1295–1297, 2003.
[268]  M. F. Tsan and B. Gao, “Endogenous ligands of Toll-like receptors,” Journal of Leukocyte Biology, vol. 76, no. 3, pp. 514–519, 2004.
[269]  S. Thibault, R. Fromentin, M. R. Tardif, and M. J. Tremblay, “TLR2 and TLR4 triggering exerts contrasting effects with regard to HIV-1 infection of human dendritic cells and subsequent virus transfer to CD4+ T cells,” Retrovirology, vol. 6, article 42, 2009.
[270]  C. B. Huang, Y. V. Alimova, S. Strange, and J. L. Ebersole, “Polybacterial challenge enhances HIV reactivation in latently infected macrophages and dendritic cells,” Immunology, vol. 132, no. 3, pp. 401–409, 2011.
[271]  N. G. Sandler and D. C. Douek, “Microbial translocation in HIV infection: causes, consequences and treatment opportunities,” Nature Reviews Microbiology, vol. 10, no. 9, pp. 655–666, 2012.
[272]  P. W. Hunt, “Th17, gut, and HIV: therapeutic implications,” Current Opinion in HIV and AIDS, vol. 5, no. 2, pp. 189–193, 2010.
[273]  S. M. Dillon, L. M. Rogers, R. Howe et al., “Human intestinal lamina propria CD1c+ dendritic cells display an activated phenotype at steady state and produce IL-23 in response to TLR7/8 stimulation,” The Journal of Immunology, vol. 184, no. 12, pp. 6612–6621, 2010.
[274]  S. M. Dillon, J. A. Manuzak, A. K. Leone et al., “HIV-1 infection of human intestinal lamina propria CD4+ T cells in vitro is enhanced by exposure to commensal escherichia coli,” The Journal of Immunology, vol. 189, no. 2, pp. 885–896, 2012.
[275]  A. D. Harries, S. D. Lawn, H. Getahun, R. Zachariah, and D. V. Havlir, “HIV and tuberculosis—science and implementation to turn the tide and reduce deaths,” Journal of the International AIDS Society, vol. 15, no. 2, p. 17396, 2012.
[276]  J. Zuniga, D. Torres-Garcia, T. Santos-Mendoza, T. S. Rodriguez-Reyna, J. Granados, and E. J. Yunis, “Cellular and humoral mechanisms involved in the control of tuberculosis,” Clinical and Developmental Immunology, vol. 2012, Article ID 193923, 18 pages, 2012.
[277]  S. Ehlers, “DC-SIGN and mannosylated surface structures of Mycobacterium tuberculosis: a deceptive liaison,” European Journal of Cell Biology, vol. 89, no. 1, pp. 95–101, 2010.
[278]  J. Mazurek, L. Ignatowicz, G. Kallenius, M. Jansson, and A. Pawlowski, “Mycobacteria-infected bystander macrophages trigger maturation of dendritic cells and enhance their ability to mediate HIV transinfection,” European Journal of Immunology, vol. 42, no. 5, pp. 1192–1202, 2012.
[279]  M. A. Reuter, N. D. Pecora, C. V. Harding, D. H. Canaday, and D. McDonald, “Mycobacterium tuberculosis promotes HIV trans-infection and suppresses major histocompatibility complex class II antigen processing by dendritic cells,” Journal of Virology, vol. 84, no. 17, pp. 8549–8560, 2010.
[280]  L. Vachot, V. G. Williams, J. W. Bess Jr., J. D. Lifson, and M. Robbiani, “Candida albicans-induced DC activation partially restricts HIV amplification in DCs and increases DC to T-cell spread of HIV,” Journal of Acquired Immune Deficiency Syndromes, vol. 48, no. 4, pp. 398–407, 2008.
[281]  Y. Qin, Y. Li, W. Liu et al., “Penicillium marneffei-stimulated dendritic cells enhance HIV-1 trans-infection and promote viral infection by activating primary CD4+ T cells,” PLoS One, vol. 6, no. 11, Article ID e27609, 2011.
[282]  Y. Qin, Y. Y. Li, A. P. Jiang, J. F. Jiang, and J. H. Wang, “Stimulation of Cryptococcus neoformans isolated from skin lesion of AIDS patient matures dendritic cells and promotes HIV-1 trans-infection,” Biochemical and Biophysical Research Communications, vol. 423, no. 4, pp. 709–714, 2012.
[283]  R. Gonzalez, R. Ataide, D. Naniche, C. Menendez, and A. Mayor, “HIV and malaria interactions: where do we stand?” Expert Review of Anti-Infective Therapy, vol. 10, no. 2, pp. 153–165, 2012.
[284]  G. Andreani, R. Lodge, D. Richard, and M. J. Tremblay, “Mechanisms of interaction between protozoan parasites and HIV,” Current Opinion in HIV and AIDS, vol. 7, no. 3, pp. 276–282, 2012.
[285]  J. Diou, M. R. Tardif, C. Barat, and M. J. Tremblay, “Dendritic cells derived from hemozoin-loaded monocytes display a partial maturation phenotype that promotes HIV-1 trans-infection of CD4+ T cells and virus replication,” The Journal of Immunology, vol. 184, no. 6, pp. 2899–2907, 2010.
[286]  J. Diou, M. R. Tardif, C. Barat, and M. J. Tremblay, “Malaria hemozoin modulates susceptibility of immature monocyte-derived dendritic cells to HIV-1 infection by inducing a mature-like phenotype,” Cellular Microbiology, vol. 12, no. 5, pp. 615–625, 2010.
[287]  C. Zhao, R. Cantin, M. Breton, B. Papadopoulou, and M. J. Tremblay, “DC-SIGN-mediated transfer of HIV-1 is compromised by the ability of Leishmania infantum to exploit DC-SIGN as a ligand,” Journal of Infectious Diseases, vol. 191, no. 10, pp. 1665–1669, 2005.
[288]  A. T. Haase, “Targeting early infection to prevent HIV-1 mucosal transmission,” Nature, vol. 464, no. 7286, pp. 217–223, 2010.
[289]  M. J. Ploquin, B. Jacquelin, S. P. Jochems, F. Barre-Sinoussi, and M. C. Muller-Trutwin, “Innate immunity in the control of HIV/AIDS: recent advances and open questions,” AIDS, vol. 26, no. 10, pp. 1269–1279, 2012.
[290]  R. C. da Silva, L. Segat, and S. Crovella, “Role of DC-SIGN and L-SIGN receptors in HIV-1 vertical transmission,” Human Immunology, vol. 72, no. 4, pp. 305–311, 2011.
[291]  A. Ceballos, F. R. Lenicov, J. Sabatté et al., “Spermatozoa capture HIV-1 through heparan sulfate and efficiently transmit the virus to dendritic cells,” Journal of Experimental Medicine, vol. 206, no. 12, pp. 2717–2733, 2009.
[292]  R. Shen, H. E. Richter, and P. D. Smith, “Early HIV-1 target cells in human vaginal and ectocervical mucosa,” American Journal of Reproductive Immunology, vol. 65, no. 3, pp. 261–267, 2011.
[293]  J. Sabatté, A. Ceballos, S. Raiden et al., “Human seminal plasma abrogates the capture and transmission of human immunodeficiency virus type 1 to CD4+ T cells mediated by DC-SIGN,” Journal of Virology, vol. 81, no. 24, pp. 13723–13734, 2007.
[294]  D. O. Ochiel, C. Ochsenbauer, J. C. Kappes, M. Ghosh, J. V. Fahey, and C. R. Wira, “Uterine epithelial cell regulation of DC-SIGN expression inhibits transmitted/founder HIV-1 trans infection by immature dendritic cells,” PLoS One, vol. 5, no. 12, Article ID e14306, 2010.
[295]  D. Fontenot, H. He, S. Hanabuchi et al., “TSLP production by epithelial cells exposed to immunodeficiency virus triggers DC-mediated mucosal infection of CD4+ T cells,” Proceedings of the National Academy of Sciences of the United States of America, vol. 106, no. 39, pp. 16776–16781, 2009.
[296]  T. T. Murooka, M. Deruaz, F. Marangoni et al., “HIV-infected T cells are migratory vehicles for viral dissemination,” Nature, vol. 490, no. 7419, pp. 283–287, 2012.
[297]  H. F. Njai, P. J. Lewi, C. G. M. Janssen et al., “Pre-incubation of cell-free HIV-1 group M isolates with non-nucleoside reverse transcriptase inhibitors blocks subsequent viral replication in co-cultures of dendritic cells and T cells,” Antiviral Therapy, vol. 10, no. 2, pp. 255–262, 2005.
[298]  M. Stefanidou, C. Herrera, N. Armanasco, and R. J. Shattock, “Saquinavir inhibits early events associated with establishment of HIV-1 infection: potential role for protease inhibitors in prevention,” Antimicrob Agents Chemother, vol. 56, no. 8, pp. 4381–4390, 2012.
[299]  I. Frank and M. Robbiani, “Attachment and fusion inhibitors potently prevent dendritic cell-driven HIV infection,” Journal of Acquired Immune Deficiency Syndromes, vol. 56, no. 3, pp. 204–212, 2011.
[300]  S. E. VanCompernolle, R. J. Taylor, K. Oswald-Richter et al., “Antimicrobial peptides from amphibian skin potently inhibit human immunodeficiency virus infection and transfer of virus from dendritic cells to T cells,” Journal of Virology, vol. 79, no. 18, pp. 11598–11606, 2005.
[301]  K. Terrazas-Aranda, Y. van Herrewege, D. Hazuda et al., “Human immunodeficiency virus type 1 (HIV-1) integration: a potential target for microbicides to prevent cell-free or cell-associated HIV-1 infection,” Antimicrobial Agents and Chemotherapy, vol. 52, no. 7, pp. 2544–2554, 2008.
[302]  R. Garg and M. J. Tremblay, “Miltefosine represses HIV-1 replication in human dendritic cell/T-cell cocultures partially by inducing secretion of type-I interferon,” Virology, vol. 432, no. 2, pp. 271–276, 2012.
[303]  T. L. Chang, N. Teleshova, A. Rapista et al., “SAMMA, a mandelic acid condensation polymer, inhibits dendritic cell-mediated HIV transmission,” FEBS Letters, vol. 581, no. 24, pp. 4596–4602, 2007.
[304]  I. Frank, H. St？ssel, A. Gettie et al., “A fusion inhibitor prevents spread of immunodeficiency viruses, but not activation of virus-specific T cells, by dendritic cells,” Journal of Virology, vol. 82, no. 11, pp. 5329–5339, 2008.
[305]  A. A. Nabatov, M. A. W. P. de Jong, L. de Witte, S. Bulgheresi, and T. B. H. Geijtenbeek, “C-type lectin Mermaid inhibits dendritic cell mediated HIV-1 transmission to CD4+ T cells,” Virology, vol. 378, no. 2, pp. 323–328, 2008.
[306]  N. Teleshova, T. Chang, A. Profy, and M. E. Klotman, “Inhibitory effect of PRO 2000, a candidate microbicide, on dendritic cell-mediated human immunodeficiency virus transfer,” Antimicrobial Agents and Chemotherapy, vol. 52, no. 5, pp. 1751–1758, 2008.
[307]  T. Du, K. Hu, J. Yang et al., “Bifunctional CD4-DC-SIGN fusion proteins demonstrate enhanced avidity to gp120 and inhibit HIV-1 infection and dissemination,” Antimicrob Agents Chemother, vol. 56, no. 9, pp. 4640–4649, 2012.
[308]  A. Berzi, J. J. Reina, R. Ottria et al., “A glycomimetic compound inhibits DC-SIGN-mediated HIV infection in cellular and cervical explant models,” AIDS, vol. 26, no. 2, pp. 127–137, 2012.
[309]  D. Serrano-Gómez, R. T. Martínez-Nunez, E. Sierra-Filardi et al., “AM3 modulates dendritic cell pathogen recognition capabilities by targeting DC-SIGN,” Antimicrobial Agents and Chemotherapy, vol. 51, no. 7, pp. 2313–2323, 2007.
[310]  S. G. Turville, K. Vermeire, J. Balzarini, and D. Schols, “Sugar-binding proteins potently inhibit dendritic cell human immunodeficiency virus type 1 (HIV-1) infection and dendritic-cell-directed HIV-1 transfer,” Journal of Virology, vol. 79, no. 21, pp. 13519–13527, 2005.
[311]  J. Balzarini, Y. van Herrewege, K. Vermeire, G. Vanham, and D. Schols, “Carbohydrate-binding agents efficiently prevent dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN)-directed HIV-1 transmission to T lymphocytes,” Molecular Pharmacology, vol. 71, no. 1, pp. 3–11, 2007.
[312]  S. K. Wang, P. H. Liang, R. D. Astronomo et al., “Targeting the carbohydrates on HIV-1: interaction of oligomannose dendrons with human monoclonal antibody 2G12 and DC-SIGN,” Proceedings of the National Academy of Sciences of the United States of America, vol. 105, no. 10, pp. 3690–3695, 2008.
[313]  S. Sattin, A. Daghett, M. Thépaut et al., “Inhibition of DC-SIGN-mediated HIV infection by a linear trimannoside mimic in a tetravalent presentation,” ACS Chemical Biology, vol. 5, no. 3, pp. 301–312, 2010.
[314]  L. Dehuyser, E. Schaeffer, O. Chaloin, C. G. Mueller, R. Baati, and A. Wagner, “Synthesis of novel mannoside glycolipid conjugates for inhibition of HIV-1 trans-infection,” Bioconjug Chem, vol. 23, no. 9, pp. 1731–1739, 2012.
[315]  N. Nasreddine, C. Borde, J. Gozlan, L. Bélec, V. Maréchal, and H. Hocini, “Advanced glycation end products inhibit both infection and transmission in trans of HIV-1 from monocyte-derived dendritic cells to autologous T cells,” The Journal of Immunology, vol. 186, no. 10, pp. 5687–5695, 2011.
[316]  F. P. Siegal, N. Kadowaki, M. Shodell et al., “The nature of the principal Type 1 interferon-producing cells in human blood,” Science, vol. 284, no. 5421, pp. 1835–1837, 1999.
[317]  J. J. Ferbas, J. F. Toso, A. J. Logar, J. S. Navratil, and C. R. Rinaldo, “CD4+ blood dendritic cells are potent producers of IFN-α in response to in vitro HIV-1 infection,” The Journal of Immunology, vol. 152, no. 9, pp. 4649–4662, 1994.
[318]  P. Fitzgerald-Bocarsly, J. Dai, and S. Singh, “Plasmacytoid dendritic cells and type I IFN: 50 years of convergent history,” Cytokine and Growth Factor Reviews, vol. 19, no. 1, pp. 3–19, 2008.
[319]  P. Fitzgerald-Bocarsly and E. S. Jacobs, “Plasmacytoid dendritic cells in HIV infection: striking a delicate balance,” Journal of Leukocyte Biology, vol. 87, no. 4, pp. 609–620, 2010.
[320]  J. Tel, A. M. van der Leun, C. G. Figdor, R. Torensma, and I. J. de Vries, “Harnessing human plasmacytoid dendritic cells as professional APCs,” Cancer Immunol Immunother, vol. 61, no. 8, pp. 1279–1288, 2012.
[321]  S. Patterson, A. Rae, N. Hockey, J. Gilmour, and F. Gotch, “Plasmacytoid dendritic cells are highly susceptible to human immunodeficiency virus type 1 infection and release infectious virus,” Journal of Virology, vol. 75, no. 14, pp. 6710–6713, 2001.
[322]  N. Schmitt, M. T. Nugeyre, D. Scott-Algara et al., “Differential susceptibility of human thymic dendritic cell subsets to X4 and R5 HIV-1 infection,” AIDS, vol. 20, no. 4, pp. 533–542, 2006.
[323]  V. A. Evans, L. Lal, R. Akkina et al., “Thymic plasmacytoid dendritic cells are susceptible to productive HIV-1 infection and efficiently transfer R5 HIV-1 to thymocytes in vitro,” Retrovirology, vol. 8, article 43, 2011.
[324]  L. Fong, M. Mengozzi, N. W. Abbey, B. G. Herndier, and E. G. Engleman, “Productive infection of plasmacytoid dendritic cells with human immunodeficiency virus type 1 is triggered by CD40 ligation,” Journal of Virology, vol. 76, no. 21, pp. 11033–11041, 2002.
[325]  K. Loré, A. Smed-S？rensen, J. Vasudevan, J. R. Mascola, and R. A. Koup, “Myeloid and plasmacytoid dendritic cells transfer HIV-1 preferentially to antigen-specific CD4+ T cells,” Journal of Experimental Medicine, vol. 201, no. 12, pp. 2023–2033, 2005.
[326]  F. Groot, T. M. M. van Capel, M. L. Kapsenberg, B. Berkhout, and E. C. de Jong, “Opposing roles of blood myeloid and plasmacytoid dendritic cells in HIV-1 infection of T cells: transmission facilitation versus replication inhibition,” Blood, vol. 108, no. 6, pp. 1957–1964, 2006.
[327]  D. L. Mann, S. Gartner, F. Le Sane, H. Buchow, and M. Popovic, “HIV-1 transmission and function of virus-infected monocytes/macrophages,” The Journal of Immunology, vol. 144, no. 6, pp. 2152–2158, 1990.
[328]  J. M. Carr, H. Hocking, P. Li, and C. J. Burrell, “Rapid and efficient cell-to-cell transmission of human immunodeficiency virus infection from monocyte-derived macrophages to peripheral blood lymphocytes,” Virology, vol. 265, no. 2, pp. 319–329, 1999.
[329]  C. J. Duncan and Q. J. Sattentau, “Viral determinants of HIV-1 macrophage tropism,” Viruses, vol. 3, no. 11, pp. 2255–2279, 2011.
[330]  M. M. Goodenow and R. G. Collman, “HIV-1 coreceptor preference is distinct from target cell tropism: a dual-parameter nomenclature to define viral phenotypes,” Journal of Leukocyte Biology, vol. 80, no. 5, pp. 965–972, 2006.
[331]  E. J. Soilleux and N. Coleman, “Expression of DC-SIGN in human foreskin may facilitate sexual transmission of HIV,” Journal of Clinical Pathology, vol. 57, no. 1, pp. 77–78, 2004.
[332]  C. McClure, C. Bowman, I. Geary, C. Ryan, J. Ball, and A. Eley, “HIV-1 co-receptor expression and epithelial immune cells of the cervix in asymptomatic women attending a genitourinary medicine clinic,” HIV Medicine, vol. 14, no. 2, pp. 108–114, 2013.
[333]  Y. Xu, H. Zhu, C. K. Wilcox et al., “Blood monocytes harbor HIV type 1 strains with diversified phenotypes including macrophage-specific CCR5 virus,” Journal of Infectious Diseases, vol. 197, no. 2, pp. 309–318, 2008.
[334]  J. Münch, E. Rücker, L. St？ndker et al., “Semen-derived amyloid fibrils drastically enhance HIV infection,” Cell, vol. 131, no. 6, pp. 1059–1071, 2007.
[335]  H. Koppensteiner, R. Brack-Werner, and M. Schindler, “Macrophages and their relevance in human immunodeficiency virus type I infection,” Retrovirology, vol. 9, article 82, 2012.
[336]  H. Chu, J. J. Wang, M. Qi et al., “The intracellular virus-containing compartments in primary human macrophages are largely inaccessible to antibodies and small molecules,” PLoS One, vol. 7, no. 5, Article ID e35297, 2012.
[337]  D. Schneberger, K. Aharonson-Raz, and B. Singh, “Monocyte and macrophage heterogeneity and Toll-like receptors in the lung,” Cell and Tissue Research, vol. 343, no. 1, pp. 97–106, 2011.
[338]  T. M. Hanley and G. A. Viglianti, “Nuclear receptor signaling inhibits HIV-1 replication in macrophages through multiple trans-repression mechanisms,” Journal of Virology, vol. 85, no. 20, pp. 10834–10850, 2011.
[339]  G. Peng, T. Greenwell-Wild, S. Nares et al., “Myeloid differentiation and susceptibility to HIV-1 are linked to APOBEC3 expression,” Blood, vol. 110, no. 1, pp. 393–400, 2007.
[340]  B. K. Thielen, J. P. McNevin, M. J. McElrath, B. V. S. Hunt, K. C. Klein, and J. R. Lingappa, “Innate immune signaling induces high levels of TC-specific deaminase activity in primary monocyte-derived cells through expression of APOBEC3A isoforms,” Journal of Biological Chemistry, vol. 285, no. 36, pp. 27753–27766, 2010.
[341]  S. M. Bol, P. D. Moerland, S. Limou et al., “Genome-wide association study identifies single nucleotide polymorphism in DYRK1A associated with replication of HIV-1 in monocyte-derived macrophages,” PLoS One, vol. 6, no. 2, Article ID e17190, 2011.
[342]  A. Sica and A. Mantovani, “Macrophage plasticity and polarization: in vivo veritas,” The Journal of Clinical Investigation, vol. 122, no. 3, pp. 787–795, 2012.
[343]  E. Cassol, L. Cassetta, C. Rizzi, M. Alfano, and G. Poli, “M1 and M2a polarization of human monocyte-derived macrophages inhibits HIV-1 replication by distinct mechanisms,” The Journal of Immunology, vol. 182, no. 10, pp. 6237–6246, 2009.
[344]  H. Sa？di, G. Magri, C. Carbonneil, N. Nasreddine, M. Réquena, and L. Bélec, “IFN-γ-activated monocytes weakly produce HIV-1 but induce the recruitment of HIV-sensitive T cells and enhance the viral production by these recruited T cells,” Journal of Leukocyte Biology, vol. 81, no. 3, pp. 642–653, 2007.
[345]  V. Cobos-Jimenez, T. Booiman, J. Hamann, and N. A. Kootstra, “Macrophages and HIV-1,” Current Opinion in HIV and AIDS, vol. 6, no. 5, pp. 385–390, 2011.
[346]  N. Laguette, B. Sobhian, N. Casartelli et al., “SAMHD1 is the dendritic- and myeloid-cell-specific HIV-1 restriction factor counteracted by Vpx,” Nature, vol. 474, no. 7353, pp. 654–657, 2011.
[347]  K. Hrecka, C. Hao, M. Gierszewska et al., “Vpx relieves inhibition of HIV-1 infection of macrophages mediated by the SAMHD1 protein,” Nature, vol. 474, no. 7353, pp. 658–661, 2011.
[348]  J. Y. Seo, R. Yaneva, and P. Cresswell, “Viperin: a multifunctional, interferon-inducible protein that regulates virus replication,” Cell Host Microbe, vol. 10, no. 6, pp. 534–539, 2011.
[349]  N. Nasr, S. Maddocks, S. G. Turville et al., “HIV-1 infection of human macrophages directly induces viperin which inhibits viral production,” Blood, vol. 120, no. 4, pp. 778–788, 2012.
[350]  B. Levine, N. Mizushima, and H. W. Virgin, “Autophagy in immunity and inflammation,” Nature, vol. 469, no. 7330, pp. 323–335, 2011.
[351]  S. Borel, L. Espert, and M. Biard-Piechaczyk, “Macroautophagy regulation during HIV-1 infection of CD4+ T cells and macrophages,” Frontiers in Immunology, vol. 3, p. 97, 2012.
[352]  L. Espert, M. Varbanov, V. Robert-Hebmann et al., “Differential role of autophagy in CD4 T cells and macrophages during X4 and R5 HIV-1 infection,” PLoS One, vol. 4, no. 6, Article ID e5787, 2009.
[353]  G. B. Kyei, C. Dinkins, A. S. Davis et al., “Autophagy pathway intersects with HIV-1 biosynthesis and regulates viral yields in macrophages,” Journal of Cell Biology, vol. 186, no. 2, pp. 255–268, 2009.
[354]  J. Chehimi, Q. Luo, L. Azzoni et al., “HIV-1 transmission and cytokine-induced expression of DC-SIGN in human monocyte-derived macrophages,” Journal of Leukocyte Biology, vol. 74, no. 5, pp. 757–763, 2003.
[355]  G. Rappocciolo, F. J. Jenkins, H. R. Hensler et al., “DC-SIGN is a receptor for human herpesvirus 8 on dendritic cells and macrophages,” The Journal of Immunology, vol. 176, no. 3, pp. 1741–1749, 2006.
[356]  F. O. Martinez, L. Helming, and S. Gordon, “Alternative activation of macrophages: an immunologic functional perspective,” Annual Review of Immunology, vol. 27, pp. 451–483, 2009.
[357]  E. Cassol, L. Cassetta, M. Alfano, and G. Poli, “Macrophage polarization and HIV-1 infection,” Journal of Leukocyte Biology, vol. 87, no. 4, pp. 599–608, 2010.
[358]  E. Cassol, L. Cassetta, C. Rizzi, D. Gabuzda, M. Alfano, and G. Poli, “Dendritic cell-specific ICAM-3 grabbing nonintegrin mediates HIV-1 infection of and transmission by M2a-polarized macrophages in vitro,” AIDS, vol. 27, no. 5, pp. 707–716, 2013.
[359]  D. G. Nguyen and J. E. K. Hildreth, “Involvement of macrophage mannose receptor in the binding and transmission of HIV by macrophage,” European Journal of Immunology, vol. 33, no. 2, pp. 483–493, 2003.
[360]  M. Pollicita, D. Schols, S. Aquaro et al., “Carbohydrate-binding agents (CBAs) inhibit HIV-1 infection in human primary monocyte-derived macrophages (MDMs) and efficiently prevent MDM-directed viral capture and subsequent transmission to CD4+ T lymphocytes,” Virology, vol. 370, no. 2, pp. 382–391, 2008.
[361]  A. Granelli-Piperno, A. Pritsker, M. Pack et al., “Dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin/CD209 is abundant on macrophages in the normal human lymph node and is not required for dendritic cell stimulation of the mixed leukocyte reaction,” The Journal of Immunology, vol. 175, no. 7, pp. 4265–4273, 2005.
[362]  G. Boily-Larouche, M. P. Milev, L. S. Zijenah et al., “Naturally-occurring genetic variants in human DC-SIGN increase HIV-1 capture, cell-transfer and risk of mother-to-child transmission,” PLoS One, vol. 7, no. 7, Article ID e40706, 2012.
[363]  D. Creery, W. Weiss, G. Graziani-Bowering et al., “Differential regulation of CXCR4 and CCR5 expression by interleukin (IL)-4 and IL-13 is associated with inhibition of chemotaxis and human immunodeficiency virus (HIV) type 1 replication but not HIV entry into human monocytes,” Viral Immunology, vol. 19, no. 3, pp. 409–423, 2006.
[364]  J. F. Salazar-Gonzalez, M. G. Salazar, B. F. Keele et al., “Genetic identity, biological phenotype, and evolutionary pathways of transmitted/founder viruses in acute and early HIV-1 infection,” Journal of Experimental Medicine, vol. 206, no. 6, pp. 1273–1289, 2009.
[365]  G. Cannon, Y. Yi, H. Ni et al., “HIV envelope binding by macrophage-expressed gp340 promotes HIV-1 infection,” The Journal of Immunology, vol. 181, no. 3, pp. 2065–2070, 2008.
[366]  N. Sharova, C. Swingler, M. Sharkey, and M. Stevenson, “Macrophages archive HIV-1 virions for dissemination in trans,” EMBO Journal, vol. 24, no. 13, pp. 2481–2489, 2005.
[367]  D. Rudnicka, J. Feldmann, F. Porrot et al., “Simultaneous cell-to-cell transmission of human immunodeficiency virus to multiple targets through polysynapses,” Journal of Virology, vol. 83, no. 12, pp. 6234–6246, 2009.
[368]  H. Rempel, C. Calosing, B. Sun, and L. Pulliam, “Sialoadhesin expressed on IFN-induced monocytes binds HIV-1 and enhances infectivity,” PLoS One, vol. 3, no. 4, Article ID e1967, 2008.
[369]  K. Gousset, S. D. Ablan, L. V. Coren et al., “Real-time visualization of HIV-1 GAG trafficking in infected macrophages,” PLoS Pathogens, vol. 4, no. 3, Article ID e1000015, 2008.
[370]  F. Groot, S. Welsch, and Q. J. Sattentau, “Efficient HIV-1 transmission from macrophages to T cells across transient virological synapses,” Blood, vol. 111, no. 9, pp. 4660–4663, 2008.
[371]  H. Koppensteiner, C. Banning, C. Schneider, H. Hohenberg, and M. Schindler, “Macrophage internal HIV-1 is protected from neutralizing antibodies,” Journal of Virology, vol. 86, no. 5, pp. 2826–2836, 2012.
[372]  S. Kimura, K. Hase, and H. Ohno, “The molecular basis of induction and formation of tunneling nanotubes,” Cell and Tissue Research, vol. 352, no. 1, pp. 67–76, 2013.
[373]  N. M. Sherer, M. J. Lehmann, L. F. Jimenez-Soto, C. Horensavitz, M. Pypaert, and W. Mothes, “Retroviruses can establish filopodial bridges for efficient cell-to-cell transmission,” Nature Cell Biology, vol. 9, no. 3, pp. 310–315, 2007.
[374]  E. A. Eugenin, P. J. Gaskill, and J. W. Berman, “Tunneling nanotubes (TNT) are induced by HIV-infection of macrophages: a potential mechanism for intercellular HIV trafficking,” Cellular Immunology, vol. 254, no. 2, pp. 142–148, 2009.
[375]  I. Kadiu and H. E. Gendelman, “Human immunodeficiency virus type 1 endocytic trafficking through macrophage bridging conduits facilitates spread of infection,” Journal of NeuroImmune Pharmacology, vol. 6, no. 4, pp. 658–675, 2011.
[376]  I. Kadiu and H. E. Gendelman, “Macrophage bridging conduit trafficking of HIV-1 through the endoplasmic reticulum and golgi network,” Journal of Proteome Research, vol. 10, no. 7, pp. 3225–3238, 2011.
[377]  W. Xu, P. A. Santini, J. S. Sullivan et al., “HIV-1 evades virus-specific IgG2 and IgA responses by targeting systemic and intestinal B cells via long-range intercellular conduits,” Nature Immunology, vol. 10, no. 9, pp. 1008–1017, 2009.
[378]  J. A. Davis and S. Yawetz, “Management of HIV in the pregnant woman,” Clinical Obstetrics and Gynecology, vol. 55, no. 2, pp. 531–540, 2012.
[379]  P. van de Perre, P. A. Rubbo, J. Viljoen et al., “HIV-1 reservoirs in breast milk and challenges to elimination of breast-feeding transmission of HIV-1,” Science Translational Medicine, vol. 4, no. 143, Article ID 143sr3, 2012.
[380]  M. A. Naarding, I. S. Ludwig, F. Groot et al., “Lewis X component in human milk binds DC-SIGN and inhibits HIV-1 transfer to CD4+ T lymphocytes,” Journal of Clinical Investigation, vol. 115, no. 11, pp. 3256–3264, 2005.
[381]  M. A. Naarding, A. M. Dirac, I. S. Ludwig et al., “Bile salt-stimulated lipase from human milk binds DC-SIGN and inhibits human immunodeficiency virus type 1 transfer to CD4+ T cells,” Antimicrobial Agents and Chemotherapy, vol. 50, no. 10, pp. 3367–3374, 2006.
[382]  M. Requena, H. Bouhlal, N. Nasreddine et al., “Inhibition of HIV-1 transmission in trans from dendritic cells to CD4+ T lymphocytes by natural antibodies to the CRD domain of DC-SIGN purified from breast milk and intravenous immunoglobulins,” Immunology, vol. 123, no. 4, pp. 508–518, 2008.
[383]  Y. Yagi, E. Watanabe, E. Watari et al., “Inhibition of DC-SIGN-mediated transmission of human immunodeficiency virus type 1 by Toll-like receptor 3 signalling in breast milk macrophages,” Immunology, vol. 130, no. 4, pp. 597–607, 2010.
[384]  S. Moir and A. S. Fauci, “B cells in HIV infection and disease,” Nature Reviews Immunology, vol. 9, no. 4, pp. 235–245, 2009.
[385]  P. R. Clapham and A. McKnight, “Cell surface receptors, virus entry and tropism of primate lentiviruses,” Journal of General Virology, vol. 83, part 8, pp. 1809–1829, 2002.
[386]  S. Moir, A. Malaspina, Y. Li et al., “B cells of HIV-1-infected patients bind virions through CD21-complement interactions and transmit infectious virus to activated T cells,” Journal of Experimental Medicine, vol. 192, no. 5, pp. 637–646, 2000.
[387]  A. Malaspina, S. Moir, D. C. Nickle et al., “Human immunodeficiency virus type 1 bound to B cells: relationship to virus replicating in CD4+ T cells and circulating in plasma,” Journal of Virology, vol. 76, no. 17, pp. 8855–8863, 2002.
[388]  J. J. Jakubik, M. Saifuddin, D. M. Takefman, and G. T. Spear, “Immune complexes containing human immunodeficiency virus type 1 primary isolates bind to lymphoid tissue B lymphocytes and are infectious for T lymphocytes,” Journal of Virology, vol. 74, no. 1, pp. 552–555, 2000.
[389]  S. D？pper, D. Wilflingseder, W. M. Prodinger et al., “Mechanism(s) promoting HIV-1 infection of primary unstimulated T lymphocytes in autologous B cell/T cell co-cultures,” European Journal of Immunology, vol. 33, no. 8, pp. 2098–2107, 2003.
[390]  J. J. Jakubik, M. Saifuddin, D. M. Takefman, and G. T. Spear, “B lymphocytes in lymph nodes and peripheral blood are important for binding immune complexes containing HIV-1,” Immunology, vol. 96, no. 4, pp. 612–619, 1999.
[391]  B. A. Smith, S. Gartner, Y. Liu et al., “Persistence of infectious HIV on follicular dendritic cells,” The Journal of Immunology, vol. 166, no. 1, pp. 690–696, 2001.
[392]  B. F. Keele, L. Tazi, S. Gartner et al., “Characterization of the follicular dendritic cell reservoir of human immunodeficiency virus type 1,” Journal of Virology, vol. 82, no. 11, pp. 5548–5561, 2008.
[393]  T. C. Thacker, X. Zhou, J. D. Estes et al., “Follicular dendritic cells and human immunodeficiency virus type 1 transcription in CD4+ T cells,” Journal of Virology, vol. 83, no. 1, pp. 150–158, 2009.
[394]  B. He, X. Qiao, P. J. Klasse et al., “HIV-1 envelope triggers polyclonal Ig class switch recombination through a CD40-independent mechanism involving BAFF and C-type lectin receptors,” The Journal of Immunology, vol. 176, no. 7, pp. 3931–3941, 2006.
[395]  G. Rappocciolo, P. Piazza, C. L. Fuller et al., “DC-SIGN on B lymphocytes is required for transmission of HIV-1 to T lymphocytes,” PLoS Pathogens, vol. 2, no. 7, p. e70, 2006.
[396]  L. Wu, T. D. Martin, M. Carrington, and V. N. KewalRamani, “Raji B cells, misidentified as THP-1 cells, stimulate DC-SIGN-mediated HIV transmission,” Virology, vol. 318, no. 1, pp. 17–23, 2004.
[397]  Z. Stamataki, C. Shannon-Lowe, J. Shaw et al., “Hepatitis C virus association with peripheral blood B lymphocytes potentiates viral infection of liver-derived hepatoma cells,” Blood, vol. 113, no. 3, pp. 585–593, 2009.
[398]  G. Martin, J. Roy, C. Barat, M. Ouellet, C. Gilbert, and M. J. Tremblay, “Human immunodeficiency virus type 1-associated CD40 ligand transactivates B lymphocytes and promotes infection of CD4+ T cells,” Journal of Virology, vol. 81, no. 11, pp. 5872–5881, 2007.
[399]  M. Imbeault, M. Ouellet, K. Giguère et al., “Acquisition of host-derived CD40L by HIV-1 in vivo and its functional consequences in the B-cell compartment,” Journal of Virology, vol. 85, no. 5, pp. 2189–2200, 2011.
[400]  V. Holl, K. Xu, M. Peressin et al., “Stimulation of HIV-1 replication in immature dendritic cells in contact with primary CD4 T or B lymphocytes,” Journal of Virology, vol. 84, no. 9, pp. 4172–4182, 2010.
[401]  R. C. Rickert, J. Jellusova, and A. V. Miletic, “Signaling by the TNFR superfamily in B-cell biology and disease,” Immunological Reviews, vol. 244, no. 1, pp. 115–133, 2011.
[402]  J. Poudrier, J. Chagnon-Choquet, and M. Roger, “Influence of dendritic cells on B-cell responses during HIV infection,” Clinical and Developmental Immunology, vol. 2012, Article ID 592187, 10 pages, 2012.
[403]  E. P. Browne, “Regulation of B-cell responses by Toll-like receptors,” Immunology, vol. 136, no. 4, pp. 370–379, 2012.
[404]  M. B. Uccellini, A. M. Avalos, A. Marshak-Rothstein, and G. A. Viglianti, “Toll-like receptor-dependent immune complex activation of B cells and dendritic cells,” Methods in Molecular Biology, vol. 517, pp. 363–380, 2009.
[405]  S. Swingler, B. Brichacek, J. M. Jacque, C. Ulich, J. Zhou, and M. Stevenson, “HIV-1 Nef intersects the macrophage CD40L signalling pathway to promote resting-cell infection,” Nature, vol. 424, no. 6945, pp. 213–219, 2003.
[406]  B. D. Walker, “Elite control of HIV Infection: implications for vaccines and treatment,” Topics in HIV Medicine, vol. 15, no. 4, pp. 134–136, 2007.
[407]  J. F. Okulicz and O. Lambotte, “Epidemiology and clinical characteristics of elite controllers,” Current Opinion in HIV and AIDS, vol. 6, no. 3, pp. 163–168, 2011.
[408]  B. Autran, B. Descours, V. Avettand-Fenoel, and C. Rouzioux, “Elite controllers as a model of functional cure,” Current Opinion in HIV and AIDS, vol. 6, no. 3, pp. 181–187, 2011.
[409]  J. Huang, P. S. Burke, T. D. H. Cung et al., “Leukocyte immunoglobulin-like receptors maintain unique antigen-presenting properties of circulating myeloid dendritic cells in HIV-1-infected elite controllers,” Journal of Virology, vol. 84, no. 18, pp. 9463–9471, 2010.

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