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• W2317989125 abstract "After HIV-1 transmission, viral replication leads to a peak in blood plasma viral load, and over a short period the virus declines to a stable concentration [1]. The steady state concentration of virus in blood plasma, generally referred to as the viral ‘set point,’ correlates directly with the rate of clinical disease progression and the CD4 cell count depletion [2]. In addition, HIV-1 transmission probability can be correlated with the viral load in blood [3,4] and genital secretions [4]. In 1998, Dyer et al.[5] made a direct comparison of blood and semen HIV RNA in patients with chronic clade C and clade B HIV infections. Patients with clade C infection had five to seven times more HIV in blood and semen than patients with clade B infection regardless of similar CD4 cell count. The results were used to specifically warn against more rapid diseases progression and to help explain the spread of HIV in sub-Saharan Africa where clade C is dominant. In this issue of AIDS, Novitsky et al.[6] provide a longitudinal description of 77 individuals in Botswana and South Africa with newly acquired (primary) HIV-1 infection. These patients were followed for a median of 572 days (range 226–968) and the authors noted that 19% had blood HIV RNA viral load greater than 100 000 copies/ml during 200–400 days of follow-up. Patients with higher viral load had more rapid decline in CD4 cell count, as might be expected [2]. Are the observations presented by Dyer et al. [5] and Novitsky et al. [6] representative of the overall population of individuals infected by clade C HIV? The patients studied by Dyer et al. [5] and Novitsky et al. [6] are ‘convenience samples’ and may not reflect the overall population of patients who have acquired clade C HIV infection. Selection bias may have generated cohorts that are in some way unique. However, using a cross-sectional screening strategy the Center for HIV Vaccine Immunology (CHAVI) has identified 345 patients with acute HIV infection (unpublished observations). Among 125 patients with clade C infection, 31% had more than 100 000 copies of HIV RNA in blood plasma at set point. However, these individuals may not be representative either, as persons with recently acquired HIV who come into a care or research setting may be different (e.g. more symptoms, greater risk, better access to care) than those with recently acquired infection who are not captured. These concerns notwithstanding, the continued replication of clade C HIV-1 in African individuals at a high level deserves attention. Acute HIV infection is operationally defined as the stage of HIV replication before a complete antibody response has developed, when HIV-1 RNA or P24 antigen can be detected to demonstrate infection [7]. More than 80% of people with acute HIV have acquired a single viral variant [8], although tremendous viral diversification occurs over subsequent months. Most people with acute HIV-1 infection are symptomatic, reflecting a demonstrable cytokine storm [9] and massive apoptosis [10]. The continuing, unresolved high replication of HIV-1 observed by Novitsky et al. and in CHAVI participants represents de facto an unfortunate imbalance between the virus and the host. Control of HIV-1 has been extensively studied. First, genome-wide association studies have demonstrated that patients with some unique genetic backgrounds have lower HIV set point [11,12]. Investigators at Harvard and South Africa have reported that CD8 lymphocytes drive viral changes that limit effective replication [13], especially in patients with the protective human leukocyte antigen (HLA) types including HLA B*5701, B*5703, B*5801 and B*81. Goonetilleke et al.[14] have mapped very specific T-cell responses during acute infection that account for a large part of the restraint of viral replication in clade B infections. Studies from Leslie et al.[15] indicate that T-cell responses are likely to be similarly important in clade C infections. The effectiveness of the responses may be explained by the specificity of these protective T-cell responses for regions of the viral capsid protein (Gag p24) that cannot escape from T-cell recognition by mutation without impairing the replicative fitness of the virus. The virus itself must also contribute to exceptional replication. Hollingsworth et al. [16] have argued that concordant HIV-1 ‘transmission pairs’ who share the same virus share the same set point, suggesting some critical viral properties are retained regardless of viral diversification and different genetic host backgrounds; other investigators have made a similar observation [17]. Also, it has long been appreciated that concomitant infections that activate a host inflammatory response (e.g. malaria) can reversibly raise viral burden [18]. Clade C HIV-1 infection dominates the HIV-1 pandemic and some transmission and replication advantages may help to explain this reality. Clade C HIV-1 retains the R5 coreceptor usage even during advanced infection [19] and this may provide some advantage against the ‘transmission bottleneck’ [8]. However, it has been difficult to show increased HIV replication fitness of clade C HIV in vitro[20]. A sustained high HIV viral load increases the efficiency of HIV-1 transmission and is almost certainly important to the spread of the virus. Understanding this phenomenon may help to explain the dynamics of the HIV pandemic and leads to better HIV prevention strategies. Novitsky et al.[21] have argued that patients with the highest viral loads must be targeted for prevention intervention and the current results reinforce concerns about clade C HIV infection, the viral subtype at the center of the HIV pandemic." @default.
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• W2317989125 date "2011-07-31" @default.
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• W2317989125 title "High clade C HIV-1 viremia" @default.
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• W2317989125 doi "https://doi.org/10.1097/qad.0b013e328348a4d2" @default.
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