Type I interferon (IFN-I) play a critical role in the innate immune response against viral infections. They actively participate in antiviral immunity by inducing molecular mechanisms of viral restriction and by limiting the spread of the infection, but they also orchestrate the initial phases of the adaptive immune response and influence the quality of T cell immunity. During infection with the human immunodeficiency virus type 1 (HIV-1), the production of and response to IFN-I may be severely altered by the lymphotropic nature of the virus. In this review I consider the different aspects of virus sensing, IFN-I production, signalling, and effects on target cells, with a particular focus on the alterations observed following HIV-1 infection. 1. Introduction Interferons (IFN) are a heterogeneous class of soluble immune mediators which were originally defined by their ability to interfere with the replication of diverse types of viruses in vitro and in vivo. Human type I IFN (IFN-I) include IFN-α (14 genes, resulting in more than 22 products) and IFN-β, both encoded by genes clustered on chromosome 9, probably generated as a result of gene duplication events, as epitomized by the presence of multiple pseudogenes [1]. IFN-ε, IFN-κ, IFN-τ, and IFN-ω have also been described in mammals as members of the IFN-I family. This review is focused on the literature covering the regulation and the function of IFN-α and IFN-β. IFN-I are produced in large quantities in response to viral infections and are generally regarded as a key bridging mechanism between innate and adaptive immune responses, exerting both antiviral activity, and immunostimulatory functions, such as promoting antigen-presenting cell maturation and molding T helper cell responses [2–8]. However, the notion that IFN-I serve only as effector immune mechanisms may need to be revised based on accumulating evidence which highlights the potent immunoregulatory ability of these molecules. During chronic viral infections, the beneficial antiviral and immunostimulatory effects of IFN-I may be overruled by the prolonged stimulation of IFN-I-induced cytostatic and proapoptotic mechanisms. Infection by the human immunodeficiency virus type 1 (HIV-1) may represent an extreme example of how chronic IFN-I production progressively undermines the development of efficient long-term antiviral immunity [9, 10]. Different cells have the potential to produce IFN-I and the mechanism by which viral insults are sensed varies depending on the cell type, as does the potency of the IFN-I-producing response. In the case of
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