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“The importance of Fc-mediated effector function in protective selleck products immunity to HIV-1 (hereafter referred to simply as HIV) is becoming increasingly apparent. A large of number of studies in natural infection cohorts, spanning the last 26 years, have associated

Fc-mediated effector function, particularly antibody-dependent cellular cytotoxicity, with a favourable clinical course. These studies strongly suggest a role for Fc-mediated effector function in the post-infection control of viraemia. More recently, studies in both humans and non-human primates (NHPs) also implicate Fc-mediated effector function in blocking HIV acquisition. Accordingly, this review will discuss the results supporting a role of Fc-mediated effector FDA approved Drug Library function in both blocking acquisition and post-infection control of viraemia. Parallel studies in NHPs and humans will be compared for common themes. Context for this discussion will be provided by summarizing the temporal emergence of key host and virological events over the course of an untreated HIV infection framing where, when and how Fc-mediated effector function might be protective. A hypothesis that Fc-mediated effector function

protects primarily in the early stages of both acquisition

and post-infection control of viraemia will be developed. The course of HIV infection is shown in Fig. 1, which depicts the classical pattern seen in untreated individuals. The advent of potent anti-retroviral therapy dramatically changed this course and deaths from uncontrolled infections are increasingly rare. The course is marked by two major phases leading to AIDS. The first phase is acquisition that occurs during eclipse, which is the time from exposure to HIV to the time of first detectable viraemia (T0). The eclipse phase is approximately 10 days in HIV-infected individuals.[1] The precise time it takes HIV to Gefitinib clinical trial establish an irreversible foothold is unknown but the outer bound is probably the point at which the latent viral reservoir is established in resting memory CD4+ T cells.[2, 3] This is known to occur as early as 10 days after acute retroviral symptoms appear in humans.[4] However, studies using anti-retroviral post-exposure prophylaxis to block infection of non-human primates (NHPs) with simian immunodeficiency virus indicate that the reservoir is established much earlier, between 24 and 72 hr post-exposure,[5] which places it significantly before T0.[1] Hence, for Fc-mediated effector function to block acquisition it must do so in this ‘window of opportunity’. The second phase is post-infection control of viraemia, which begins at T0 and continues until control is lost.