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Review
. 2019 Nov 28;11(12):1104.
doi: 10.3390/v11121104.

HIV-1 Latency and Latency Reversal: Does Subtype Matter?

Indra Sarabia  1 , Alberto Bosque  1
Affiliations
Review

HIV-1 Latency and Latency Reversal: Does Subtype Matter?

Indra Sarabia et al. Viruses. .

Abstract

Cells that are latently infected with HIV-1 preclude an HIV-1 cure, as antiretroviral therapy does not target this latent population. HIV-1 is highly genetically diverse, with over 10 subtypes and numerous recombinant forms circulating worldwide. In spite of this vast diversity, much of our understanding of latency and latency reversal is largely based on subtype B viruses. As such, most of the development of cure strategies targeting HIV-1 are solely based on subtype B. It is currently assumed that subtype does not influence the establishment or reactivation of latent viruses. However, this has not been conclusively proven one way or the other. A better understanding of the factors that influence HIV-1 latency in all viral subtypes will help develop therapeutic strategies that can be applied worldwide. Here, we review the latest literature on subtype-specific factors that affect viral replication, pathogenesis, and, most importantly, latency and its reversal.

Keywords: HIV-1; HIV-1 latency; clade; shock and kill; subtype.

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Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.

Figures

Figure 1
Figure 1
Global distribution of HIV-1 subtypes. The major subtype that circulates in distinct geographical locations are listed first and are in bold, followed by other reported subtypes in the region of interest. This depiction is based on estimates of circulating subtypes from 2004 to 2007 [18,21,22,23]. CRF: circulating recombinant form; this describes other CRFs which are not AE, AB, or AG. URFs: unique recombinant forms.
Figure 2
Figure 2
Long terminal repeat (LTR) from diverse subtypes. Main transcription factor binding sites in each LTR. Activated protein-1 (AP-1); specificity protein-1 (Sp1); nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB); GA-binding protein (GABP); TATA box promoter sequence for transcription initiation. Several other transcription factor binding sites have been identified and are not denoted in the graph for simplicity. This schematic is based on binding sites reported elsewhere [66,69,71].
See this image and copyright information in PMC

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