We searched PubMed for publications in English from Jan 1, 2008, to Oct 31, 2013, but did not exclude commonly referenced and highly regarded older publications. We used the search terms “HIV” or “AIDS” in combinations with “epidemiology”, “prevention”, “pathogenesis”, “antiretroviral therapy”, “resistance”, and “latency”. We also searched the reference lists of articles identified by this search strategy and selected those we judged relevant. Review articles are cited to provide readers with
SeminarHIV infection: epidemiology, pathogenesis, treatment, and prevention
Section snippets
Epidemiology
The HIV epidemic arose after zoonotic infections with simian immunodeficiency viruses from African primates; bushmeat hunters were probably the first group to be infected with HIV.1 HIV-1 was transmitted from apes and HIV-2 from sooty mangabey monkeys.1 Four groups of HIV-1 exist and represent three separate transmission events from chimpanzees (M, N, and O), and one from gorillas (P). Groups N, O, and P are restricted to west Africa. Group M, which is the cause of the global HIV pandemic,
HIV-1 transmission
The most important factor that increases the risk of sexual transmission of HIV-1 is the number of copies per mL of plasma HIV-1 RNA (viral load), with a 2·4 times increased risk of sexual transmission for every 1 log10 increase.19 Acute HIV infection, which causes very high plasma viral loads in the first few months, is an important driver of HIV epidemics.20 A reduction in plasma viral load of 0·7 log10 is estimated to reduce HIV-1 transmission by 50%.21 Seminal and endocervical viral load
HIV life cycle and host immune responses
Figure 2 shows the virus life cycle. The main target of HIV is activated CD4 T lymphocytes; entry is via interactions with CD4 and the chemokine coreceptors, CCR5 or CXCR4. Other cells bearing CD4 and chemokine receptors are also infected, including resting CD4 T cells, monocytes and macrophages, and dendritic cells. CD4-independent HIV infection of cells can happen, notably in astrocytes37 and renal epithelial cells,38 and subsequent HIV gene expression has an important role in the
Mother-to-child HIV-1 transmission
During the past two decades, remarkable progress has been made in the risk reduction of perinatal HIV-1 transmission. Knowledge about the timing of HIV-1 transmission to infants has allowed the development of appropriate interventions. The risk of HIV-1 transmission to the infant is about 25% at delivery in the absence of interventions, with most of the risk arising after 36 weeks and especially intrapartum.127 HIV-1 transmission happens at a rate of 8·9 per 100 child-years of breastfeeding
Conclusions
HIV continues to be a major contributor to the global burden of disease, especially in sub-Saharan Africa. Antiretroviral therapy is changing the global epidemiology of HIV by increasing prevalence because of reductions in AIDS deaths, and is contributing to decreasing HIV incidence by reduction of the risk of transmission. HIV incidence in men who have sex with men is not decreasing despite high antiretroviral therapy coverage. The drivers of the HIV epidemic in men who have sex with men
Search strategy and selection criteria
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AIDS
HIV transmission risk through anal intercourse: systematic review, meta-analysis and implications for HIV prevention
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Male circumcision and risk of HIV infection in sub-Saharan Africa: a systematic review and meta-analysis
AIDS
Modelling the global competing risks of a potential interaction between injectable hormonal contraception and HIV risk
AIDS
Concurrent partnerships and HIV: an inconvenient truth
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J Infect Dis
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The antiretroviral enzyme APOBEC3G is degraded by the proteasome in response to HIV-1 Vif
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The cytoplasmic body component TRIM5alpha restricts HIV-1 infection in Old World monkeys
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Tetherin inhibits retrovirus release and is antagonized by HIV-1 Vpu
Nature
Vpx relieves inhibition of HIV-1 infection of macrophages mediated by the SAMHD1 protein
Nature
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