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Viruses 2013, 5(1), 1-14; doi:10.3390/v5010001

Molecular Mechanisms of HIV Immune Evasion of the Innate Immune Response in Myeloid Cells

Received: 7 November 2012 / Revised: 19 December 2012 / Accepted: 19 December 2012 / Published: 21 December 2012
(This article belongs to the Special Issue Immune Evasion)
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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.
Keywords: HIV; immune evasion; Vpr; Ung2; myeloid HIV; immune evasion; Vpr; Ung2; myeloid
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Mashiba, M.; Collins, K.L. Molecular Mechanisms of HIV Immune Evasion of the Innate Immune Response in Myeloid Cells. Viruses 2013, 5, 1-14.

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