Abstract
The expression of intrinsic antiviral factors by myeloid cells is a recently recognized mechanism of restricting lentiviral replication. Viruses that enter these cells must develop strategies to evade cellular antiviral factors to establish a productive infection. By studying the cellular targets of virally encoded proteins that are necessary to infect myeloid cells, a better understanding of cellular intrinsic antiviral strategies has now been achieved. Recent findings have provided insight into how the lentiviral accessory proteins, Vpx, Vpr and Vif counteract antiviral factors found in myeloid cells including SAMHD1, APOBEC3G, APOBEC3A, UNG2 and uracil. Here we review our current understanding of the molecular basis of how cellular antiviral factors function and the viral countermeasures that antagonize them to promote viral transmission and spread.
Highlights
IntroductionMyeloid cells, including dendritic cells and macrophages, play an important role in the innate and adaptive immune response against viral pathogens like HIV
Intrinsic Anti-Viral Factors Limit Infection of Myeloid Cells by HIV and SIVMyeloid cells, including dendritic cells and macrophages, play an important role in the innate and adaptive immune response against viral pathogens like HIV
Based on in situ hybridization, 98% of infected cells found in secondary lymphoid tissue were lymphocytes, whereas infected myeloid cells were rare [33]
Summary
Myeloid cells, including dendritic cells and macrophages, play an important role in the innate and adaptive immune response against viral pathogens like HIV. Macrophages and dendritic cells (DCs) express the necessary receptors (CD4 and chemokine co-receptor(s)) required for HIV-1 entry and, like CD4+ T cells [3,4], are amongst the earliest targets for HIV-1 and SIV in vivo [5,6], (reviewed in [7]). It is possible that the main role of DCs in HIV disease is to transmit internalized viral particles to CD4+ T cells rather than to directly support productive infection [14,23] (reviewed in [24,25]). Current data indicates that myeloid cells play an important role in the pathogenesis of HIV-1 infection as a relatively long-lived target of HIV and as a viral conduit to CD4+ T cells.
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