Certain infectious agents are associated with lymphomas, but the strength of the association varies geographically, suggesting that local environmental factors make important contributions to lymphomagenesis. Endemic Burkitt’s Lymphoma has well-defined environmental requirements making it particularly suitable for research into local environmental factors. The Epstein-Barr virus and holoendemic Malaria are recognized as important cofactors in endemic Burkitt’s Lymphoma and their contributions are discussed. Additionally, infection with Chikungunya Fever, a potentially oncogenic arbovirus, was associated with the onset of endemic Burkitt’s Lymphoma in one study and also with space-time case clusters of the lymphoma. Chikungunya Virus has several characteristics typical of oncogenic viruses. The Flavivirus, Hepatitis C, a Class 1 Human Carcinogen, closely related to the arboviruses, Yellow Fever, and Dengue, is also more distantly related to Chikungunya Virus. The mechanisms of oncogenesis believed to operate in Hepatitis C lymphomagenesis are discussed, as is their potential applicability to Chikungunya Virus. 1. Introduction It has been estimated that approximately 20% of all cancers, worldwide, are attributable to infectious agents [1]. This is likely to be an underestimate because of under-reporting and under-ascertainment, particularly in resource-poor countries, where the burden of infection-related cancers is almost four times that of the more prosperous countries [1]. A number of infectious agents, comprised of a variety of different types of organisms, have been shown to be associated with lymphomas. It is highly probable that this number will continue to expand as diagnostic methods improve, new organisms emerge and general advances in knowledge are made. Some of the organisms which have been linked with different types of lymphomas have already been designated Class 1 Human Carcinogens by the World Health Organisation. They are the DNA Herpes viruses, the Epstein-Barr virus [2] and Kaposi Sarcoma Herpesvirus [2, 3], the retroviruses Human Immunodeficiency Virus type 1 and Human T Cell Lymphotropic Virus Type 1 [4], the Hepatitis viruses, Hepatitis B, a DNA virus, and Hepatitis C, an RNA virus [5], and the bacterium, Helicobacter pylori [6]. In addition, the bacteria Campylobacter jejuni [7], Chlamydia psittaci and pneumoniae [8, 9], Borrelia burgdorferi [10, 11] and the RNA Alphavirus Chikungunya virus [12], an arbovirus, have been found to be associated with various different forms of lymphoma. The Epstein-Barr virus (EBV) [2], the protozoon,
References
[1]
D. M. Parkin, “The global health burden of infection-associated cancers in the year 2002,” International Journal of Cancer, vol. 118, no. 12, pp. 3030–3044, 2006.
[2]
IARC monographs on the evaluation of carcinogenic risks to humans, Infections with Epstein-Barr virus and human herpes viruses, vol. 70, IARC, Lyon, France, 1997.
[3]
IARC monographs on the evaluation of carcinogenic risks to humans, Review of Human Carcinogens; Kaposi Sarcoma Herpesvirus, vol. 100, IARC Monograph, 2008.
[4]
IARC monographs on the evaluation of carcinogenic risks to humans, Human immunodeficiency viruses and human T-cell lymphotropic viruses, vol. 67, IARC, Lyon, France, 1996.
[5]
IARC monographs on the evaluation of carcinogenic risks to humans, Hepatitis Viruses, vol. 59, IARC, Lyon, France, 1994.
[6]
IARC monographs on the evaluation of carcinogenic risks to humans, Schistosomes, liver flukes and helicobacter pylori, vol. 61, IARC, Lyon, France, 1994.
[7]
M. Lecuit, E. Abachin, A. Martin et al., “Immunoproliferative small intestinal disease associated with Campylobacter jejuni,” New England Journal of Medicine, vol. 350, no. 3, pp. 239–248, 2004.
[8]
A. J. M. Ferreri, M. Guidoboni, M. Ponzoni et al., “Evidence for an association between Chlamydia psittaci and ocular adnexal lymphomas,” Journal of the National Cancer Institute, vol. 96, no. 8, pp. 586–594, 2004.
[9]
E. Chanudet, Y. Zhou, C. M. Bacon et al., “Chlamydia psittaci is variably associated with ocular adnexal MALT lymphoma in different geographical regions,” Journal of Pathology, vol. 209, no. 3, pp. 344–351, 2006.
[10]
L. Cerroni, N. Z？chling, B. Pütz, and H. Kerl, “Infection by Borrelia burgdorferi and cutaneous B-cell lymphoma,” Journal of Cutaneous Pathology, vol. 24, no. 8, pp. 457–461, 1997.
[11]
C. Sch？llkopf, M. Melbye, L. Munksgaard et al., “Borrelia infection and risk of non-Hodgkin lymphoma,” Blood, vol. 111, no. 12, pp. 5524–5529, 2008.
[12]
C. van den Bosch and G. Lloyd, “Chikungunya fever as a risk factor for endemic Burkitt's lymphoma in Malawi,” Transactions of the Royal Society of Tropical Medicine and Hygiene, vol. 94, no. 6, pp. 704–705, 2000.
[13]
R. H. Morrow, “Epidemiological evidence for the role of Falciparum malaria in the pathogenesis of Burkitt’s Lymphoma,” in A Human Cancer Model, Burkitt’s Lymphoma, G. Lenoir, G. O’Conor, and C. L. M. Olweny, Eds., pp. 177–184, IARC, Lyon, France, 1985.
[14]
G. M. Lenoir, T. Philip, and R. Sohier, “Burkitt-type lymphoma: EBV association and cytogenetic markers in cases from various geographic locations,” in Pathogenesis of Leukaemias and Lymphomas: Environmental Influences, Progress in Cancer Research and Therapy, I. T. Magrath, G. T. O’Conor, and B. Ramot, Eds., vol. 27, pp. 283–296, Raven Press, New York, NY, USA, 1984.
[15]
I. Magrath, V. Jain, and K. Bhatia, “Epstein-Barr virus and Burkitt's lymphoma,” Seminars in Cancer Biology, vol. 3, no. 5, pp. 285–295, 1992.
[16]
R. Dolcetti and M. Boiocchi, “Cellular and molecular bases of B-cell clonal expansions,” Clinical and Experimental Rheumatology, vol. 14, no. 14, pp. S3–S13, 1996.
[17]
T. F. E. Barth, M. Bentz, F. Leithuser et al., “Molecular-cytogenetic comparison of mucosa-associated marginal zone B-cell lymphoma and large B-cell lymphoma arising in the gastro-intestinal tract,” Genes Chromosomes and Cancer, vol. 31, no. 4, pp. 316–325, 2001.
[18]
A. Carbone and A. Gloghini, “AIDS-related lymphomas: from pathogenesis to pathology,” British Journal of Haematology, vol. 130, no. 5, pp. 662–670, 2005.
[19]
M. Libra, D. Gasparotto, A. Gloghini, P. M. Navolanic, V. De Re, and A. Carbone, “Hepatitis C virus (HCV) infection and lymphoproliferative disorders,” Frontiers in Bioscience, vol. 10, no. 2, pp. 2460–2471, 2005.
[20]
A. M. Levine, R. Nelson, E. Zuckerman et al., “Lack of association between hepatitis C infection and development of AIDS-related lymphoma,” Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology, vol. 20, no. 3, pp. 255–258, 1999.
[21]
M. Rowe, G. L. Kelly, A. I. Bell, and A. B. Rickinson, “Burkitt's lymphoma: the Rosetta Stone deciphering Epstein-Barr virus biology,” Seminars in Cancer Biology, vol. 19, no. 6, pp. 377–388, 2009.
[22]
C. A. van den Bosch, “Is endemic Burkitt's lymphoma an alliance between three infections and a tumour promoter?” Lancet Oncology, vol. 5, no. 12, pp. 738–746, 2004.
[23]
U. Iversen, O. H. Iversen, A. Z. Bluming, J. L. Ziegler, and S. Kyalwasi, “Cell kinetics of African cases of Burkitt Lymphoma. A preliminary report,” European Journal of Cancer, vol. 8, no. 3, pp. 305–308, 1972.
[24]
N. E. Day, P. G. Smith, and B. Lachet, “The latent period of Burkitt's lymphoma: the evidence from epidemiological clustering,” IARC scientific publications, no. 60, pp. 187–195, 1985.
[25]
D. H. Crawford, “Biology and disease associations of Epstein-Barr virus,” Philosophical Transactions of the Royal Society B, vol. 356, no. 1408, pp. 461–473, 2001.
[26]
D. M. Burns and D. H. Crawford, “Epstein-Barr virus-specific cytotoxic T-lymphocytes for adoptive immunotherapy of post-transplant lymphoproliferative disease,” Blood Reviews, vol. 18, no. 3, pp. 193–209, 2004.
[27]
R. Taub, I. Kirsch, C. Morton, et al., “Translocation of the c-myc gene into the immunoglobulin heavy chain locus in human Burkitt lymphoma and murine plasmacytoma cells,” Proceedings of the National Academy of Sciences of the United States of America, vol. 79, no. 24 I, pp. 7837–7841, 1982.
[28]
A. C. Hayday, S. D. Gillies, and H. Saito, “Activation of a translocated human c-myc gene by an enhancer in the immunoglobulin heavy-chain locus,” Nature, vol. 307, no. 5949, pp. 334–340, 1984.
[29]
I. Magrath, “The pathogenesis of Burkitt's lymphoma,” Advances in Cancer Research, vol. 55, pp. 133–270, 1990.
[30]
G. Klein, “EBV-B cell interactions: immortalization, rescue from apoptosis, tumorigenicity (A short review),” Acta Microbiologica et Immunologica Hungarica, vol. 43, no. 2-3, pp. 97–105, 1996.
[31]
K. Klapproth and T. Wirth, “Advances in the understanding of MYC-induced lymphomagenesis,” British Journal of Haematology, vol. 149, no. 4, pp. 484–497, 2010.
[32]
M. E. Drotar, S. Silva, E. Barone et al., “Epstein-Barr virus nuclear antigen-1 and myc cooperate in lymphomagenesis,” International Journal of Cancer, vol. 106, no. 3, pp. 388–395, 2003.
[33]
N. A. Hotchin, M. J. Allday, and D. H. Crawford, “Deregulated c-myc expression in Epstein-Barr-virus-immortalized B-cells induces altered growth properties and surface phenotype but not tumorigenicity,” International Journal of Cancer, vol. 45, no. 3, pp. 566–571, 1990.
[34]
P. J. Farrell, G. J. Allan, F. Shanahan, K. H. Vousden, and T. Crook, “P53 is frequently mutated in Burkitt's lymphoma cell lines,” EMBO Journal, vol. 10, no. 10, pp. 2879–2888, 1991.
[35]
T. Goossens, U. Klein, and R. Küppers, “Frequent occurrence of deletions and duplications during somatic hypermutation: implications for oncogene translocations and heavy chain disease,” Proceedings of the National Academy of Sciences of the United States of America, vol. 95, no. 5, pp. 2463–2468, 1998.
[36]
G. Klein, “The role of gene dosage and genetic transpositions in carcinogenesis,” Nature, vol. 294, no. 5839, pp. 313–318, 1981.
[37]
F. G. Haluska, S. Finver, Y. Tsujimoto, and C. M. Croce, “The t(8;14) chromosomal translocation occurring in B-cell malignancies results from mistakes in V-D-J joining,” Nature, vol. 324, no. 6093, pp. 158–161, 1986.
[38]
G. J. Vanasse, P. Concannon, and D. M. Willerford, “Regulated genomic instability and neoplasia in the lymphoid lineage,” Blood, vol. 94, no. 12, pp. 3997–4010, 1999.
[39]
P. Riboldi, W. Ikematsu, B. Brambilla, C. Caprani, M. Gerosa, and P. Casali, “Diversity and somatic hypermutation of the Ig VHDJH, VκJκ, and VλJλ gene segments in lymphoma B cells: relevance to the origin of the neoplastic B cell clone,” Human Immunology, vol. 64, no. 1, pp. 69–81, 2003.
[40]
G. Klein, “Lymphoma development in mice and humans: delivery of initiation is followed by convergent cytogenetic evolution,” Proceedings of the National Academy of Sciences of the United States of America, vol. 76, no. 5, pp. 2442–2446, 1979.
[41]
G. W. Bornkamm, “Epstein-Barr virus and its role in the pathogenesis of Burkitt's lymphoma: an unresolved issue,” Seminars in Cancer Biology, vol. 19, no. 6, pp. 351–365, 2009.
[42]
D. T. Purtilo, Y. Manolov, S. Manolova, H. Harada, H. Lipscomb, and E. Tatsumi, “Role of Epstein-Barr virus in the etiology of Burkitt’s lymphoma,” in A Human Cancer Model, Burkitt's Lymphoma, G. Lenoir, G. O’Conor, and C. L. M. Olweny, Eds., pp. 231–247, IARC, 1985.
[43]
K. Hirai, T. Yamamoto, T. Hironaka, et al., “Epstein-Barr virus genome in infected cells and cancer,” in Epstein-Barr virus and Human Cancer, Gann Monograph on Cancer Research no. 45, pp. 29–39, Japanese Cancer Association. Japan Scientific Societies Press, Tokyo, Japan, 1998.
[44]
K. Yamamoto, F. Mizuno, and T. Matsuo, “Epstein-Barr virus and human chromosomes: close association of the resident viral genome and the expression of the virus-determined nuclear antigen (EBNA) with the presence of chromosome 14 in human-mouse hybrid cells,” Proceedings of the National Academy of Sciences of the United States of America, vol. 75, no. 10, pp. 5155–5159, 1978.
[45]
G. De The, A. Geser, and N. E. Day, “Epidemiological evidence for causal relationship between Epstein-Barr virus and Burkitt's lymphoma from Ugandan prospective study,” Nature, vol. 274, no. 5673, pp. 756–761, 1978.
[46]
A. S. Evans and R. A. Kaslow, “Surveillance and Sero-epidemiology,” in Viral Infections of Humans: Epidemiology and Control, chapter 3, pp. 107–108, Springer, New York, NY, USA, 4th edition, 1997.
[47]
G. Henle, W. Henle, G. Klein et al., “Antibodies to early Epstein-Barr virus-induced antigens in Burkitt's lymphoma,” Journal of the National Cancer Institute, vol. 46, no. 4, pp. 861–871, 1971.
[48]
G. R. Pearson, L. F. Qualtiere, and G. Klein, “Epstein-Barr virus-specific antibody-dependent cellular cytotoxicity in patients with Burkitt's lymphoma,” International Journal of Cancer, vol. 24, no. 4, pp. 402–406, 1979.
[49]
P. H. Levine, J. F. Fraumeni, J. I. Reisher, and D. E. Waggoner, “Antibodies to Epstein Barr virus associated antigens in relatives of cancer patients,” Journal of the National Cancer Institute, vol. 52, no. 4, pp. 1037–1040, 1974.
[50]
C. A. Facer and J. H. L. Playfair, “Malaria, Epstein-Barr Virus, and the genesis of lymphomas,” Advances in Cancer Research, vol. 53, pp. 33–72, 1989.
[51]
A. M. Moormann, K. Chelimo, O. P. Sumba et al., “Exposure to holoendemic malaria results in elevated Epstein-Barr virus loads in children,” Journal of Infectious Diseases, vol. 191, no. 8, pp. 1233–1238, 2005.
[52]
A. Hildesheim, S. West, E. DeVeyra et al., “Herbal medicine use, Epstein-Barr virus, and risk of nasopharyngeal carcinoma,” Cancer Research, vol. 52, no. 11, pp. 3048–3051, 1992.
[53]
T. Osato, S. Imai, and S. Koizumi, “African Burkitt's lymphoma and an Epstein-Barr virus-enhancing plant Euphorbia triucalli,” Lancet, vol. 1, no. 8544, pp. 1257–1258, 1987.
[54]
C. Van den Bosch, B. E. Griffin, P. Kazembe, C. Dziweni, and L. Kadzamira, “Are plant factors a missing link in the evolution of endemic Burkitt's Lymphoma?” British Journal of Cancer, vol. 68, no. 6, pp. 1232–1235, 1993.
[55]
F. Mizuno, T. Osato, S. Imai et al., “Epstein-Barr virus-enhancing plant promoters in east Africa,” AIDS research, vol. 2, pp. S151–S155, 1986.
[56]
C. van den Bosch, “The pathogenesis of Burkitt’s lymphoma-an alternative hypothesis: The arbovirus theory revisited,” in New Developments in Lymphoma and Hodgkin's Disease Research, S. D. Tules, Ed., chapter 9, pp. 149–194, Nova Publishers, New York, NY, USA, 2006.
[57]
J. Rastelli, C. H？mig-H？lzel, J. Seagal et al., “LMP1 signaling can replace CD40 signaling in B cells in vivo and has unique features of inducing class-switch recombination to IgG1,” Blood, vol. 111, no. 3, pp. 1448–1455, 2008.
[58]
H. H. Niller, D. Salamon, K. Ilg et al., “The in vivo binding site for oncoprotein c-Myc in the promoter for Epstein-Barr virus (EBV) encoding RNA (EBER) 1 suggests a specific role for EBV in lymphomagenesis,” Medical Science Monitor, vol. 9, no. 1, pp. HY1–HY9, 2003.
[59]
M. Takacs, J. Segesdi, F. Banati, et al., “The importance of epigenetic alterations in the development of Epstein-Barr virus-related lymphomas,” Mediterranean Journal of Hematology and Infectious Diseases, vol. 1, no. 2, Article ID e2009012, 2009.
[60]
H. H. Niller, H. Wolf, E. Ay, and J. Minarovits, “Epigenetic dysregulation of epstein-barr virus latency and development of autoimmune disease,” Advances in Experimental Medicine and Biology, vol. 711, pp. 82–102, 2011.
[61]
C. Mancao and W. Hammerschmidt, “Epstein-Barr virus latent membrane protein 2A is a B-cell receptor mimic and essential for B-cell survival,” Blood, vol. 110, no. 10, pp. 3715–3721, 2007.
[62]
C. Mancao, M. Altmann, B. Jungnickel, and W. Hammerschmidt, “Rescue of "crippled" germinal center B cells from apoptosis by Epstein-Barr virus,” Blood, vol. 106, no. 13, pp. 4339–4344, 2005.
[63]
G. L. Kelly, H. M. Long, J. Stylianou et al., “An epstein-barr virus anti-apoptotic protein constitutively expressed in transformed cells and implicated in burkitt lymphomagenesis: the Wp/BHRF1 link,” PLoS Pathogens, vol. 5, no. 3, Article ID e1000341, 2009.
[64]
G. L. Kelly, A. E. Milner, G. S. Baldwin, A. I. Bell, and A. B. Rickinson, “Three restricted forms of Epstein-Barr virus latency counteracting apoptosis in c-myc-expressing Burkitt lymphoma cells,” Proceedings of the National Academy of Sciences of the United States of America, vol. 103, no. 40, pp. 14935–14940, 2006.
[65]
D. A. Thorley-Lawson and A. Gross, “Persistence of the Epstein-Barr virus and the origins of associated lymphomas,” New England Journal of Medicine, vol. 350, no. 13, pp. 1328–1337, 2004.
[66]
W. Heise, “GI-lymphomas in immunosuppressed patients (organ transplantation; HIV),” Best Practice and Research: Clinical Gastroenterology, vol. 24, no. 1, pp. 57–69, 2010.
[67]
D. M. Knowles, “Immunodeficiency-associated lymphoproliferative disorders,” Modern Pathology, vol. 12, no. 2, pp. 200–217, 1999.
[68]
J. I. Cohen, “The biology of Epstein-Barr virus: lessons learned from the virus and the host,” Current Opinion in Immunology, vol. 11, no. 4, pp. 365–370, 1999.
[69]
D. A. Thorley-Lawson, “EBV persistence and latent infections in vivo,” in Epstein-Barr Virus, E. S. Robinson, Ed., chapter 17, pp. 309–357, Caister Academic Press, Norfolk, UK, 2005.
[70]
Lawrence S. Young, John R. Arrand, and Paul G. Murray, “EBV gene expression and regulation,” in Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis, A. Arvin, G. Campadelli-Fiume, E. Mocarski, et al., Eds., chapter 27, Cambridge University Press, Cambridge, UK, 2007.
[71]
S. A. Xue, L. G. Labrecque, Q. L. Lu et al., “Promiscuous expression of Epstein-Barr virus genes in Burkitt's lymphoma from the central African country Malawi,” International Journal of Cancer, vol. 99, no. 5, pp. 635–643, 2002.
[72]
G. Kelly, A. Bell, and A. Rickinson, “Epstein-Barr virus-associated Burkitt lymphomagenesis selects for downregulation of the nuclear antigen EBNA2,” Nature Medicine, vol. 8, no. 10, pp. 1098–1104, 2002.
[73]
B. E. Griffin and R. Rochford, “Endemic Burkitt's lymphoma,” in Epstein-Barr Virus, E. S. Robinson, Ed., chapter 9, pp. 113–137, Caister Academic Press, Norfolk, UK, 2005.
[74]
J. Yates, N. Warren, D. Reisman, and B. Sugden, “A cis-acting element from the Epstein-Barr viral genome that permits stable replication of recombinant plasmids in latently infected cells,” Proceedings of the National Academy of Sciences of the United States of America, vol. 81, no. 12 I, pp. 3806–3810, 1984.
[75]
D. K. Snudden, J. Hearing, P. R. Smith, F. A. Grasser, and B. E. Griffin, “EBNA-1, the major nuclear antigen of Epstein-Barr virus, resembles 'RGG' RNA binding proteins,” EMBO Journal, vol. 13, no. 20, pp. 4840–4847, 1994.
[76]
S. K. Srinivas and J. W. Sixbey, “Epstein-Barr virus induction of recombinase-activating genes RAG1 and RAG2,” Journal of Virology, vol. 69, no. 12, pp. 8155–8158, 1995.
[77]
S. Humme, G. Reisbach, R. Feederle et al., “The EBV nuclear antigen 1 (EBNA1) enhances B cell immortalization several thousandfold,” Proceedings of the National Academy of Sciences of the United States of America, vol. 100, no. 19, pp. 10989–10994, 2003.
[78]
J. B. Wilson, J. L. Bell, and A. J. Levine, “Expression of Epstein-Barr virus nuclear antigen-1 induces B cell neoplasia in transgenic mice,” EMBO Journal, vol. 15, no. 12, pp. 3117–3126, 1996.
[79]
J. Komano, S. Maruo, K. Kurozumi, T. Oda, and K. Takada, “Oncogenic role of Epstein-Barr virus-encoded RNAs in Burkitt's lymphoma cell line Akata,” Journal of Virology, vol. 73, no. 12, pp. 9827–9831, 1999.
[80]
K. Takada, “Role of Epstein-Barr virus in Burkitt's lymphoma,” Current Topics in Microbiology and Immunology, vol. 258, pp. 141–151, 2001.
[81]
W. E. Miller, H. S. Earp, and N. Raab-Traub, “The Epstein-Barr virus latent membrane protein 1 induces expression of the epidermal growth factor receptor,” Journal of Virology, vol. 69, no. 7, pp. 4390–4398, 1995.
[82]
A. Nanbo and K. Takada, “The role of Epstein-Barr virus-encoded small RNAs (EBERs) in oncogenesis,” Reviews in Medical Virology, vol. 12, no. 5, pp. 321–326, 2002.
[83]
A. K. F. Lo, K. F. To, K. W. Lo et al., “Modulation of LMP1 protein expression by EBV-encoded microRNAs,” Proceedings of the National Academy of Sciences of the United States of America, vol. 104, no. 41, pp. 16164–16169, 2007.
[84]
D. Wang, D. Liebowitz, and E. Kieff, “An EBV membrane protein expressed in immortalized lymphocytes transforms established rodent cells,” Cell, vol. 43, no. 3, pp. 831–840, 1985.
[85]
S. Henderson, M. Rowe, C. Gregory et al., “Induction of bcl-2 expression by Epstein-Barr virus latent membrane protein 1 protects infected B cells from programmed cell death,” Cell, vol. 65, no. 7, pp. 1107–1115, 1991.
[86]
G. De Thé, “Epstein-Barr virus and Burkitt's lymphoma worldwide: the casual relationship revisited,” in A Human Cancer Model, Burkitt’s Lymphoma, G. Lenoir, G. O'Conor, and C. L. M. Olweny, Eds., IARC Scientific Publication No. 60, pp. 165–175, IARC, 1985.
[87]
B. M. Greenwood, “Possible role of a B cell mitogen in hypergammaglobulinaemia in malaria and trypanosomiasis,” Lancet, vol. 1, no. 7855, pp. 435–436, 1974.
[88]
K. M. C. Lam, N. Syed, H. Whittle, and D. H. Crawford, “Circulating Epstein-Barr virus-carrying B cells in acute malaria,” Lancet, vol. 337, no. 8746, pp. 876–878, 1991.
[89]
H. C. Whittle, J. Brown, K. Marsh, M. Blackman, O. Jobe, and F. Shenton, “The effects of Plasmodium falciparum malaria on immune control of B lymphocytes in Gambian children,” Clinical and Experimental Immunology, vol. 80, no. 2, pp. 213–218, 1990.
[90]
A. J. Haddow, “An improved map for the study of Burkitt’s lymphoma syndrome in Africa,” East African Medical Journal, vol. 40, pp. 429–432, 1963.
[91]
A. J. Haddow, “Epidemiological evidence suggesting an infective element in the aetiology of Burkitt’s lymphoma,” in Burkitt’s Lymphoma, D. P. Burkitt and D. H. Wright, Eds., chapter 18, pp. 198–209, Churchill Livingstone, Edinburgh, UK, 1970.
[92]
L. K. Goma, “The environmental background to cases of Burkitt's lymphoma syndrome in Uganda,” East African Medical Journal, vol. 42, pp. 62–66, 1965.
[93]
G. Pialoux, B.-A. Gaüzère, S. Jauréguiberry, and M. Strobel, “Chikungunya, an epidemic arbovirosis,” The Lancet Infectious Diseases, vol. 7, no. 5, pp. 319–327, 2007.
[94]
J. P. Chapin, “Ecological aspects of bird distribution in Tropical Africa,” The American Naturalist, vol. 62, no. 649, pp. 106–125, 1923.
[95]
E. H. Williams, N. E. Day, and A. G. Geser, “Seasonal variation in onset of Burkitt's lymphoma in the West Nile District of Uganda,” Lancet, vol. 2, no. 7871, pp. 19–22, 1974.
[96]
R. H. Morrow, A. Kisuule, M. C. Pike, and P. G. Smith, “Burkitt's lymphoma in the Mengo districts of Uganda: epidemiologic features and their relationship to malaria,” Journal of the National Cancer Institute, vol. 56, no. 3, pp. 479–483, 1976.
[97]
E. H. Williams, P. Spit, and M. C. Pike, “Further evidence of space-time clustering of Burkitt's lymphoma patients in the West Nile District of Uganda,” British Journal of Cancer, vol. 23, no. 2, pp. 235–246, 1969.
[98]
E. H. Williams, P. G. Smith, and N. E. Day, “Space-time clustering of Burkitt's lymphoma in the West Nile district of Uganda: 1961–1975,” British Journal of Cancer, vol. 37, no. 1, pp. 109–122, 1978.
[99]
J. J. Rainey, W. O. Mwanda, P. Wairiumu, A. M. Moormann, M. L. Wilson, and R. Rochford, “Spatial distribution of Burkitt's lymphoma in Kenya and association with malaria risk,” Tropical Medicine and International Health, vol. 12, no. 8, pp. 936–943, 2007.
[100]
N. J. Wright, P. B. Hesseling, P. McCormick, and F. Tchintseme, “The incidence, clustering and characteristics of Burkitt lymphoma in the Northwest province of Cameroon,” Tropical Doctor, vol. 39, no. 4, pp. 228–230, 2009.
[101]
M. C. Pike, E. H. Williams, and B. Wright, “Burkitt's tumour in the West Nile District Uganda, 1961-5,” British Medical Journal, vol. 2, no. 549, pp. 395–399, 1967.
[102]
R. H. Morrow, M. C. Pike, P. G. Smith, J. L. Ziegler, and A. Kisuule, “Burkitt's lymphoma: a time-space cluster of cases in Bwamba County of Uganda,” British Medical Journal, vol. 2, no. 760, pp. 491–492, 1971.
[103]
J. Siemiatycki, G. Brubaker, and A. Geser, “Space-time clustering of Burkitt's lymphoma in East Africa: analysis of recent data and a new look at old data,” International Journal of Cancer, vol. 25, no. 2, pp. 197–203, 1980.
[104]
C. Van den Bosch, M. Hills, P. Kazembe, C. Dziweni, and L. Kadzamira, “Time-space case clusters of Burkitt's lymphoma in Malawi,” Leukemia, vol. 7, no. 11, pp. 1875–1878, 1993.
[105]
R. H. Morrow, M. C. Pike, and P. G. Smith, “Further studies of space time clustering of Burkitt's lymphoma in Uganda,” British Journal of Cancer, vol. 35, no. 5, pp. 668–673, 1977.
[106]
J. Lubega, “T-helper I versus T-helper 2 lymphocyte immunodysregulation is the central factor in genesis of Burkitt lymphoma: hypothesis,” Infectious Agents and Cancer, vol. 2, no. 1, article no. 10, 2007.
[107]
I. Araujo, H. D. Foss, A. Bittencourt et al., “Expression of Epstein-Barr virus gene products in Burkitt's lymphoma in Northeast Brazil,” Blood, vol. 87, no. 12, pp. 5279–5286, 1996.
[108]
A. J. Haddow, “Age incidence in Burkitt’s lymphoma syndrome,” East African Medical Journal, vol. 41, pp. 1–6, 1964.
[109]
D. I. H. Simpson, L. K. H. Goma, and E. H. Williams, “The West Nile survey,” East African Virus Research Institute Report, vol. 13, pp. 36–39, 1964.
[110]
A. G. Dean, E. H. Williams, and G. Attobua, “Clinical events suggesting Herpes simplex infection before onset of Burkitt's lymphoma: a case control study in West Nile, Uganda,” Lancet, vol. 2, no. 7840, pp. 1225–1228, 1973.
[111]
M. C. Williams, D. I. H. Simpson, and J. P. Woodhall, “Work on Burkitt’s lymphoma syndrome-antibody studies using BUN,” East African Virus Research Institute Report, vol. 13, p. 40, 1964.
[112]
A. M. Powers, A. C. Brault, R. B. Tesh, and S. C. Weaver, “Re-emergence of chikungunya and o'nyong-nyong viruses: Evidence for distinct geographical lineages and distant evolutionary relationships,” Journal of General Virology, vol. 81, no. 2, pp. 471–479, 2000.
[113]
E. B. Rwaguma, J. J. Lutwama, S. D. Sempala et al., “Emergence of epidemic O'nyong-nyong fever in southwestern Uganda, after an absence of 35 years,” Emerging Infectious Diseases, vol. 3, no. 1, p. 77, 1997.
[114]
A. M. Powers and C. H. Logue, “Changing patterns of chikungunya virus: re-emergence of a zoonotic arbovirus,” Journal of General Virology, vol. 88, no. 9, pp. 2363–2377, 2007.
[115]
S. C. Weaver and W. K. Reisen, “Present and future arboviral threats,” Antiviral Research, vol. 85, no. 2, pp. 328–345, 2010.
[116]
N. Senn, D. Luang-Suarkia, D. Manong, P. M. Siba, and W. J. H. McBride, “Contribution of dengue fever to the burden of acute febrile illnesses in Papua New Guinea: an age-specific prospective study,” American Journal of Tropical Medicine and Hygiene, vol. 85, no. 1, pp. 132–137, 2011.
[117]
A. R. Filipe and M. R. Pinto, “Arbovirus studies in Luanda, Angola. 2. Virological and serological studies during an outbreak of dengue like disease caused by the Chikungunya virus,” Bulletin of the World Health Organization, vol. 49, no. 1, pp. 37–40, 1973.
[118]
U. Raheel, M. Faheem, M. N. Riaz et al., “Dengue fever in the Indian subcontinent: an overview,” Journal of Infection in Developing Countries, vol. 5, no. 4, pp. 239–247, 2011.
[119]
P. Jeandel, R. Josse, and J. P. Durand, “Exotic viralarthritis: Role of alphavirus,” Medecine Tropicale, vol. 64, no. 1, pp. 81–88, 2004.
[120]
D. E. Griffin, A. P. Byrnes, and S. B. Cook, “Emergence and virulence of encephalitogenic arboviruses,” in Emergence and Control of Zoonotic Viral Encephalitides, C. H. Calisher and D. E. Griffin, Eds., Springer, New York, NY, USA, 2004.
[121]
C. Arpino, P. Curatolo, and G. Rezza, “Chikungunya and the nervous system: what we do and do not know,” Reviews in Medical Virology, vol. 19, no. 3, pp. 121–129, 2009.
[122]
J. J. Hoarau, M. C. J. Bandjee, P. K. Trotot et al., “Persistent chronic inflammation and infection by Chikungunya arthritogenic alphavirus in spite of a robust host immune response,” Journal of Immunology, vol. 184, no. 10, pp. 5914–5927, 2010.
[123]
P. Gérardin, A. Fianu, D. Malvy et al., “Perceived morbidity and community burden after a Chikungunya outbreak: the TELECHIK survey, a population-based cohort study,” BMC Medicine, vol. 9, article 5, 2011.
[124]
M. Al-Hazmi, E. A. Ayoola, M. Abdurahman et al., “Epidemic Rift Valley fever in Saudi Arabia: a clinical study of severe illness in humans,” Clinical Infectious Diseases, vol. 36, no. 3, pp. 245–252, 2003.
[125]
A. D. LaBeaud, F. Bashir, and C. H. King, “Measuring the burden of arboviral diseases: the spectrum of morbidity and mortality from four prevalent infections,” Population Health Metrics, vol. 9, article 1, 2011.
[126]
D. E. Griffin, “Arboviruses and the central nervous system,” Springer Seminars in Immunopathology, vol. 17, no. 2-3, pp. 121–132, 1995.
[127]
G. Kuno, “Persistence of arboviruses and antiviral antibodies in vertebrate hosts: its occurrence and impacts,” Reviews in Medical Virology, vol. 11, no. 3, pp. 165–190, 2001.
[128]
M. Padnos, N. Molomut, and R. Hofer, “Antibody formation in mice with viral lymphopaenia,” Federation Proceedings, vol. 28, p. 430, 1969.
[129]
S. Thangamani, S. Higgs, S. Ziegler, D. Vanlandingham, R. Tesh, and S. Wikel, “Host immune response to mosquito-transmitted chikungunya virus differs from that elicited by needle inoculated virus,” PLoS One, vol. 5, no. 8, Article ID e12137, 2010.
[130]
T. P. Monath, “Viral febrile illnesses: Chikungunya Fever,” in Hunter’s Tropical Medicine, G. T. Strickland, Ed., chapter 18.3, pp. 149–151, W.B.Saunders, Philadelphia, Pa, USA, 6th edition, 1984.
[131]
M. N. M. Mangada and A. Igarashi, “Molecular and in vitro analysis of eight dengue type 2 viruses isolated from patients exhibiting different disease severities,” Virology, vol. 244, no. 2, pp. 458–466, 1998.
[132]
T. Dong, E. Moran, N. V. Chau et al., “High pro-inflammatory cytokine secretion and loss of high avidity cross-reactive cytotoxic T-cells during the course of secondary dengue virus infection,” PLoS One, vol. 2, no. 12, Article ID e1192, 2007.
[133]
D. W. Vaughn, S. Green, S. Kalayanarooj et al., “Dengue viremia titer, antibody response pattern, and virus serotype correlate with disease severity,” Journal of Infectious Diseases, vol. 181, no. 1, pp. 2–9, 2000.
[134]
E. V. Agapov, I. Frolov, B. D. Lindenbach, B. M. Prágai, S. Schlesinger, and C. M. Rice, “Noncytopathic sindbis virus RNA vectors for heterologous gene expression,” Proceedings of the National Academy of Sciences of the United States of America, vol. 95, no. 22, pp. 12989–12994, 1998.
[135]
S. S. Talsma, J. E. Babensee, N. Murthy, and I. R. Williams, “Development and in vitro validation of a targeted delivery vehicle for DNA vaccines,” Journal of Controlled Release, vol. 112, no. 2, pp. 271–279, 2006.
[136]
D. Louz, H. E. Bergmans, B. P. Loos, and R. C. Hoeben, “Cross-species transfer of viruses: implications for the use of viral vectors in biomedical research, gene therapy and as live-virus vaccines,” Journal of Gene Medicine, vol. 7, no. 10, pp. 1263–1274, 2005.
[137]
S. W. Precious, H. E. Webb, and E. T. W. Bowen, “Isolation and persistence of Chikungunya virus in cultures of mouse brain cells,” Journal of General Virology, vol. 23, no. 3, pp. 271–279, 1974.
[138]
P. S. Vernon and D. E. Griffin, “Characterization of an in vitro model of alphavirus infection of immature and mature neurons,” Journal of Virology, vol. 79, no. 6, pp. 3438–3447, 2005.
[139]
B. Williams, “Tumor induction by viruses isolated from Mansonia africana,” African Journal of Medicine and Medical Sciences, vol. 10, no. 1-2, pp. 19–27, 1981.
[140]
T. M. Bell, A. Massie, M. G. R. Ross, and M. C. Williams, “Isolation of a reovirus from a case of Burkitt's lymphoma,” British Medical Journal, vol. 1, pp. 1212–1213, 1964.
[141]
T. M. Bell, A. Massie, M. G. Ross, D. I. Simpson, and E. Griffin, “Further isolations of reovirus type 3 from cases of Burkitt's lymphoma,” British Medical Journal, vol. 5502, pp. 1514–1517, 1966.
[142]
T. M. Bell, “Viruses associated with Burkitt's tumor,” Progress in Medical Virology, vol. 9, pp. 1–34, 1967.
[143]
G. M. Munube, T. M. Bell, P. M. Tukei, and P. G. Smith, “Sero-epidemiology of reovirus type 3 infections in four areas of Uganda with varying incidence of Burkitt's tumour,” East African Medical Journal, vol. 49, no. 5, pp. 369–375, 1972.
[144]
T. M. Bell, G. M. Munube, and D. H. Wright, “Malignant lymphoma in a rabbit inoculated with reovirus,” Lancet, vol. 1, no. 7549, pp. 955–957, 1968.
[145]
T. M. Bell, G. M. Munube, and D. H. Wright, “Malignant lymphoma in a rabbit inoculated with reovirus,” Lancet, vol. 1, no. 7549, pp. 955–957, 1968.
[146]
N. F. Stanley, M. N. Walters, P. J. Leak, and D. Keast, “The association of murine lymphoma with reovirus type 3 infection,” Proceedings of the Society for Experimental Biology and Medicine, vol. 121, no. 1, pp. 90–93, 1966.
[147]
D. Keast and N. F. Stanley, “Studies on a murine lymphoma induced by reovirus type 3: some general aspects of the lymphoma 2731/L,” Proceedings of the Society for Experimental Biology and Medicine, vol. 122, no. 4, pp. 1091–1098, 1966.
[148]
R. A. Joske, P. J. Leak, J. M. Papadimitriou, N. F. Stanley, and M. N. Walters, “Murine infection with reovirus. IV. Late chronic disease and the induction of lymphoma after reovirus type 3 infection,” British Journal of Experimental Pathology, vol. 47, no. 4, pp. 337–346, 1966.
[149]
J. A. Levy and R. J. Huebner, “Association of murine leukaemia virus from a Mouse lymphoma (2731/L) with reovirus Type 3 infection,” Nature, vol. 225, no. 5236, pp. 949–950, 1970.
[150]
S. Tanaka and C. M. Southam, “Joint action of West Nile virus and chemical carcinogens in production of papillomas in mice,” Journal of the National Cancer Institute, vol. 29, pp. 711–722, 1962.
[151]
A. MacNeil, O. P. Sumba, M. L. Lutzke, A. Moormann, and R. Rochford, “Activation of the Epstein-Barr virus lytic cycle by the latex of the plant Euphorbia tirucalli,” British Journal of Cancer, vol. 88, no. 10, pp. 1566–1569, 2003.
[152]
Y. Ito, “Vegetable activators of the viral genome and the Causations of Burkitt's lymphoma and Nasopharyngeal carcinoma,” in The Epstein-Barr Virus: Recent Advances, M. A. Epstein and B. G. Achong, Eds., Chapter 8, pp. 207–237, William Heinemann, London, UK, 1986.
[153]
AL Schmaljohn and D. McClain, “Alphaviruses (Togaviridae) and Flaviviruses (Flaviviridae),” in Medical Microbiology, S. Baron, Ed., Chapter 54, University of Texas Medical Branch at Galveston, Galveston, Tex, USA, 4th edition, 1996.
[154]
G. M. Lauer and B. D. Walker, “Hepatitis C virus infection,” New England Journal of Medicine, vol. 345, no. 1, pp. 41–52, 2001.
[155]
B. Robertson, G. Myers, C. Howard et al., “Classification, nomenclature, and database development for hepatitis C virus (HCV) and related viruses: proposals for standardization,” Archives of Virology, vol. 143, no. 12, pp. 2493–2503, 1998.
[156]
P. Simmonds, “The origin and evolution of hepatitis viruses in humans,” Journal of General Virology, vol. 82, no. 4, pp. 693–712, 2001.
[157]
E. Giannoulis, T. Economopoulos, K. Mandraveli et al., “The prevalence of hepatitis C and hepatitis G virus infection in patients with B cell non-Hodgkin lymphomas in Greece: a Hellenic Cooperative Oncology Group study,” Acta Haematologica, vol. 112, no. 4, pp. 189–193, 2004.
[158]
V. Wiwanitkit, “Individuals with HGV-RNA are at high risk of B cell non-Hodgkin's lymphoma development,” Asian Pacific Journal of Cancer Prevention, vol. 6, no. 2, pp. 215–216, 2005.
[159]
E. Zuckerman, T. Zuckerman, A. M. Levine et al., “Hepatitis C virus infection in patients with B-cell non-Hodgkin lymphoma,” Annals of Internal Medicine, vol. 127, no. 6, pp. 423–428, 1997.
[160]
M. D. Mccoll, I. O. Singer, R. C. Tait, I. R. R. McNeil, R. L. C. Cumming, and R. B. Hogg, “The role of hepatitis C virus in the aetiology of non-Hodgkins lymphoma—a regional association?” Leukemia and Lymphoma, vol. 26, no. 1-2, pp. 127–130, 1997.
[161]
C. Mazzaro, V. Zagonel, S. Monfardini et al., “Hepatitis C virus and non-Hodgkin's lymphomas,” British Journal of Haematology, vol. 94, no. 3, pp. 544–550, 1996.
[162]
A. L. Zignego, C. Giannini, and C. Ferri, “Hepatitis C virus-related lymphoproliferative disorders: an overview,” World Journal of Gastroenterology, vol. 13, no. 17, pp. 2467–2478, 2007.
[163]
P. D. King, J. D. Wilkes, and A. A. Diaz-Arias, “Hepatitis C virus infection in non-Hodgkin's lymphoma,” Clinical and Laboratory Haematology, vol. 20, no. 2, pp. 107–110, 1998.
[164]
J. Kuroda, A. Omoto, H. Fujiki et al., “Primary hepatic Burkitt's lymphoma with chronic hepatitis C,” Acta Haematologica, vol. 105, no. 4, pp. 237–240, 2001.
[165]
J. Kuroda, S. Kimura, T. Akaogi et al., “Primary cardiac lymphoma with variant Burkitt-type translocation, t(8;22)(q24;q11),” American Journal of Hematology, vol. 65, no. 4, pp. 327–328, 2000.
[166]
A. Unholzer, H. Starz, O. Hirschsteiner, and B.-R. Balda, “Gingival Burkitt lymphoma in a hepatitis C-positive renal transplant patient,” Journal of the German Society of Dermatology, vol. 3, no. 1, pp. 46–51, 2005.
[167]
K. Machida, K. T. H. Cheng, V. M. H. Sung, A. M. Levine, S. Foung, and M. M. C. Lai, “Hepatitis C virus induces toll-like receptor 4 expression, leading to enhanced production of beta interferon and interleukin-6,” Journal of Virology, vol. 80, no. 2, pp. 866–874, 2006.
[168]
D. Sansonno, A. Carbone, V. De Re, and F. Dammacco, “Hepatitis C virus infection, cryoglobulinaemia, and beyond,” Rheumatology, vol. 46, no. 4, pp. 572–578, 2007.
[169]
A. Nieters, B. Kallinowski, P. Brennan et al., “Hepatitis C and risk of lymphoma: results of the European Multicenter Case-Control Study EPILYMPH,” Gastroenterology, vol. 131, no. 6, pp. 1879–1886, 2006.
[170]
K. Machida, K. T.-H. Cheng, V. M.-H. Sung, K. J. Lee, A. M. Levine, and M. M. C. Lai, “Hepatitis C virus infection activates the immunologic (type II) isoform of nitric oxide synthase and thereby enhances DNA damage and mutations of cellular genes,” Journal of Virology, vol. 78, no. 16, pp. 8835–8843, 2004.
[171]
K. Machida, K. T. N. Cheng, V. M. H. Sung et al., “Hepatitis C virus induces a mutator phenotype: enhanced mutations of immunoglobulin and protooncogenes,” Proceedings of the National Academy of Sciences of the United States of America, vol. 101, no. 12, pp. 4262–4267, 2004.
[172]
K. Machida, G. McNamara, K. T. H. Cheng et al., “Hepatitis C virus inhibits DNA damage repair through reactive oxygen and nitrogen species and by interfering with the ATM-NBS1/Mre11/Rad50 DNA repair pathway in monocytes and hepatocytes,” Journal of Immunology, vol. 185, no. 11, pp. 6985–6998, 2010.
[173]
K. Machida, J. C. Liu, G. McNamara, A. Levine, L. Duan, and M. M. C. Lai, “Hepatitis C virus causes uncoupling of mitotic checkpoint and chromosomal polyploidy through the Rb pathway,” Journal of Virology, vol. 83, no. 23, pp. 12590–12600, 2009.
[174]
D. Sakamuro, T. Furukawa, and T. Takegami, “Hepatitis C virus nonstructural protein NS3 transforms NIH 3T3 cells,” Journal of Virology, vol. 69, no. 6, pp. 3893–3896, 1995.
[175]
C. G. Wu, A. Budhu, S. Chen et al., “Effect of hepatitis C virus core protein on the molecular profiling of human B lymphocytes,” Molecular Medicine, vol. 12, no. 1–3, pp. 47–53, 2006.
[176]
A. Kasprzak and A. Adamek, “Role of hepatitis C virus proteins (C, NS3, NS5A) in hepatic oncogenesis,” Hepatology Research, vol. 38, no. 1, pp. 1–26, 2008.
[177]
Y. L. Chung, M. L. Sheu, and S. H. Yen, “Hepatitis C virus NS5A as a potential viral Bcl-2 homologue interacts with Bax and inhibits apoptosis in hepatocellular carcinoma,” International Journal of Cancer, vol. 107, no. 1, pp. 65–73, 2003.
[178]
K. H. Lan, M. L. Sheu, S. J. Hwang et al., “HCV NS5A interacts with p53 and inhibits p53-mediated apoptosis,” Oncogene, vol. 21, no. 31, pp. 4801–4811, 2002.
[179]
J. M. Sugalski, B. Rodriguez, S. Moir, and D. D. Anthony, “Peripheral blood B cell subset skewing is associated with altered cell cycling and intrinsic resistance to apoptosis and reflects a state of immune activation in chronic hepatitis C Virus infection,” Journal of Immunology, vol. 185, no. 5, pp. 3019–3027, 2010.
[180]
Z. Chen, Y. Zhu, Y. Ren et al., “Hepatitis C virus protects human B lymphocytes from fas-mediated apoptosis via E2-CD81 engagement,” PLoS One, vol. 6, no. 4, Article ID e18933, 2011.
[181]
J. P. Horcajada, M. García-Bengoechea, G. Cilla, P. Etxaniz, E. Cuadrado, and J. I. Arenas, “Mixed cryoglobulinaemia in patients with chronic hepatitis C infection: prevalence, significance and relationship with different viral genotypes,” Annals of Medicine, vol. 31, no. 5, pp. 352–358, 1999.
[182]
A. L. Zignego, C. Ferri, F. Giannelli et al., “Prevalence of bcl-2 rearrangement in patients with hepatitis C virus-related mixed cryoglobulinemia with or without B-cell lymphomas,” Annals of Internal Medicine, vol. 137, no. 7, pp. 571–580, 2002.
[183]
F. Franzin, D. G. Efremov, G. Pozzato, P. Tulissi, F. Batista, and O. R. Burrone, “Clonal B-cell expansions in peripheral blood of HCV-infected patients,” British Journal of Haematology, vol. 90, no. 3, pp. 548–552, 1995.
[184]
F. Dammacco, P. Gatti, and D. Sansonno, “Hepatitis C virus infection, mixed cryoglobulinemia, and non-Hodgkin's lymphoma: an emerging picture,” Leukemia and Lymphoma, vol. 31, no. 5-6, pp. 463–476, 1998.
[185]
V. De Re, S. De Vita, A. Marzotto et al., “Sequence analysis of the immunoglobulin antigen receptor of hepatitis C virus—associated non-Hodgkin lymphomas suggests that the malignant cells are derived from the rheumatoid factorn—producing cells that occur mainly in type II cryoglobulinemia,” Blood, vol. 96, no. 10, pp. 3578–3584, 2000.
[186]
P. Andreone, A. L. Zignego, C. Cursaro et al., “Prevalence of monoclonal gammopathies in patients with hepatitis C virus infection,” Annals of Internal Medicine, vol. 129, no. 4, pp. 294–298, 1998.
[187]
M. Ivanovski, F. Silvestri, G. Pozzato et al., “Somatic hypermutation, clonal diversity, and preferential expression of the V(H) 51p1/V(L) kv325 immunoglobulin gene combination in hepatitis C virus-associated immunocytomas,” Blood, vol. 91, no. 7, pp. 2433–2442, 1998.
[188]
V. De Re, S. De Vita, A. Marzotto et al., “Pre-malignant and malignant lymphoproliferations in an HCV-infected type II mixed cryoglobulinemic patient are sequential phases of an antigen-driven pathological process,” International Journal of Cancer, vol. 87, no. 2, pp. 211–216, 2000.
[189]
F. Giannelli, S. Moscarella, C. Giannini et al., “Effect of antiviral treatment in patients with chronic HCV infection and t(14;18) translocation,” Blood, vol. 102, no. 4, pp. 1196–1201, 2003.
[190]
E. Zuckerman, T. Zuckerman, D. Sahar et al., “The effect of antiviral therapy on t(14;18) translocation and immunoglobulin gene rearrangement in patients with chronic hepatitis C virus infection,” Blood, vol. 97, no. 6, pp. 1555–1559, 2001.
[191]
O. Hermine, F. Lefrère, J. P. Bronowicki et al., “Regression of splenic lymphoma with villous lymphocytes after treatment of hepatitis C virus infection,” New England Journal of Medicine, vol. 347, no. 2, pp. 89–94, 2002.
[192]
S. Akhter, H. Liu, R. Prabhu et al., “Epstein-Barr virus and human hepatocellular carcinoma,” Cancer Letters, vol. 192, no. 1, pp. 49–57, 2003.
[193]
Y. Sugawara, M. Makuuchi, N. Kato, K. Shimotohno, and K. Takada, “Enhancement of hepatitis C virus replication by Epstein-Barr virus-encoded nuclear antigen 1,” EMBO Journal, vol. 18, no. 20, pp. 5755–5760, 1999.
[194]
T. A. Souza, B. D. Stollar, J. L. Sullivan, K. Luzuriaga, and D. A. Thorley-Lawson, “Influence of EBV on the peripheral blood memory B cell compartment,” Journal of Immunology, vol. 179, no. 5, pp. 3153–3160, 2007.
[195]
M. Oliver, M. Grandadam, C. Marimoutou et al., “Persisting mixed cryoglobulinemia in Chikungunya infection,” PLoS Neglected Tropical Diseases, vol. 3, no. 2, article no. e374, 2009.
[196]
S. Green, D. W. Vaughn, S. Kalayanarooj et al., “Early immune activation in acute dengue illness is related to development of plasma leakage and disease severity,” Journal of Infectious Diseases, vol. 179, no. 4, pp. 755–762, 1999.
[197]
S. Green, D. W. Vaughn, S. Kalayanarooj et al., “Elevated plasma interleukin-10 levels in acute dengue correlate with disease severity,” Journal of Medical Virology, vol. 59, no. 3, pp. 329–334, 1999.
[198]
S. N. Hammond, A. Balmaseda, L. Pérez et al., “Differences in dengue severity in infants, children, and adults in a 3-year hospital-based study in Nicaragua,” American Journal of Tropical Medicine and Hygiene, vol. 73, no. 6, pp. 1063–1070, 2005.
[199]
D. S. Burke, A. Nisalak, D. E. Johnson, and R. M. Scott, “A prospective study of dengue infections in Bangkok,” American Journal of Tropical Medicine and Hygiene, vol. 38, no. 1, pp. 172–180, 1988.
[200]
L. Markoff, “Togaviridae: Alphaviruses,” in Mandell, Douglas and Bennett, Principles and Practice of Infectious Diseases, G. L. Mandell, J. E. Bennett, and R. Dolin, Eds., vol. 2, Chapter 129, pp. 1455–1459, Churchill Livingstone, 4th edition, 1995.
[201]
T. P. Monath, “Flavividae: Flaviviruses (Yellow Fever, Dengue, Dengue Haemorrhagic Fever, Japanese Encephalitis, St Louis Encephalitis, Tick-borne Encephalitis),” in Mandell, Douglas and Bennett, Principles and Practice of Infectious Diseases, G. L. Mandell, J. E. Bennett, and R. Dolin, Eds., vol. 2, Chapter 129, pp. 1465–1474, Churchill Livingstone, 4th edition, 1995.
[202]
J. M. Davies, “Molecular mimicry: can epitope mimicry induce autoimmune disease?” Immunology and Cell Biology, vol. 75, no. 2, pp. 113–126, 1997.
[203]
M. Demanou, C. Antonio-Nkondjio, E. Ngapana et al., “Chikungunya outbreak in a rural area of Western Cameroon in 2006: a retrospective serological and entomological survey,” BMC Research Notes, vol. 3, article no. 128, 2010.
[204]
D. P. Burkitt, “The discovery of Burkitt's lymphoma,” Cancer, vol. 51, no. 10, pp. 1777–1786, 1983.
[205]
G. Rezza, L. Nicoletti, R. Angelini et al., “Infection with chikungunya virus in Italy: an outbreak in a temperate region,” Lancet, vol. 370, no. 9602, pp. 1840–1846, 2007.
[206]
R. Angelini, A. C. Finarelli, P. Angelini et al., “Chikungunya in north-eastern Italy: a summing up of the outbreak,” Euro Surveillance, vol. 12, no. 11, Article ID E071122.2, 2007.
