Tracking a century of global expansion and evolution of HIV to drive understanding and to combat disease

Tebit, Denis M.; Arts, Eric J.

doi:10.1016/s1473-3099(10)70186-9

Cited by 224 publications

(247 citation statements)

References 125 publications

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“…Probably, transmission of SIV from monkeys to humans is very recent. The use of molecular clocks has allowed the dating of the first event of cross-species transmission between monkey hosts to humans to the early 20th century in regions of central Africa where socioeconomical changes catalyzed the initial spread of the pandemic (reviewed in [78]). Transmission must have occurred on several occasions, followed by rapid diversification, to give rise to all the clades, subtypes and recombinant forms of viruses now infecting humans [78].…”

Section: Box 1 About the Origins Of Hiv-1-associated Pathogenicitymentioning

confidence: 99%

How Samhd1 changes our view of viral restriction

Laguette¹,

Benkirane²

2012

Trends in Immunology

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Recent studies have uncovered sterile alpha motif and HD domain 1 (SAMHD1) as the restriction factor that blocks HIV-1 replication in myeloid cells. In contrast to previously identified HIV-1 restriction factors, SAMHD1 does not meet a countermeasure developed by HIV-1. However, HIV-2 and certain simian immunodeficiency virus (SIV) strains express the auxiliary protein Vpx that potently blocks SAMHD1. It is therefore perplexing why this function has been lost or not acquired during the course of lentiviral evolution. This article summarizes the similarities and differences between SAMHD1 and other HIV-1 restriction factors, while highlighting the new questions that are emerging about the crosstalk between restriction factors and innate immune responses. Intrinsic cellular defenses and the viral arsenalHIV was identified as a human pathogen 28 years ago [1]. As a result of the inability of the human host to mount a coordinated immune response to the virus, infection by HIV usually results in chronic activation of the immune system that paradoxically allows for poorly controlled viral replication and immune exhaustion: the hallmark of AIDS. HIV-1 has evolved from SIVcpz, which causes AIDS in its natural chimpanzee host, whereas HIV-2 has evolved from SIVsm, which replicates to high levels in its natural simian host without causing disease [2] (Box 1). Hence, it is possible to speculate that lentiviruses and their host immune systems undergo an evolutionary co-adaptation to establish an equilibrium that will permit efficient spread without killing the host. However, tolerance to the infection is a multifactorial process that requires a fertile ground in the host as much as specific features of the virus. Here, we review the recent advances related to how host restriction factors may influence immune sensing and response against HIV. In particular, we examine the recent identification that the immune modulator SAMHD1 is the HIV restriction factor operating in myeloid cells, which are key players in the immune response during viral infection. A not so fertile ground?Upon entry into the human host, viruses are confronted with numerous blocks that oppose their replication (Figure 1). The first line of defense to be triggered is the so-called 'intrinsic' immune system. The intrinsic immune system includes proteins that detect the presence of the assailant pattern recognition receptors (PRRs), [Box 2] and which initiate a subsequent immune response, as well as proteins referred to as restriction factors that are directly devoted to arresting the replication cycle of the virus. To date, four restriction factors have been identified that specifically block HIV-1 replication: tripartite motif (TRIM)5α, apolipoprotein B mRNA-editing, enzyme-catalytic, polypeptide-like 3G Europe PMC Funders Author ManuscriptsEurope PMC Funders Author Manuscripts (APOBEC3G) (A3G), bone marrow stromal cell antigen 2 (BST-2) (also known as tetherin) and SAMHD1 [3][4][5][6][7]. Host restriction factor characteristicsTRIM5α interacts with...

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Section: Box 1 About the Origins Of Hiv-1-associated Pathogenicitymentioning

confidence: 99%

How Samhd1 changes our view of viral restriction

Laguette¹,

Benkirane²

2012

Trends in Immunology

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“…Additionally, since the time of its origin, subtype C has expanded at a faster rate as compared to any other viral subtype. 16 For instance, the incidence of the subtype C strains in China increased from 5.1% in 1992 to nearly 90% in 2002. 15 Additionally, the apparent genetic stability of the subtype C strains in India appears to be quite unusual.…”

mentioning

confidence: 99%

Sequence Insertions in the HIV Type 1 Subtype C Viral Promoter Predominantly Generate an Additional NF-κB Binding Site

Bachu

Mukthey²,

Murali³

et al. 2012

AIDS Research and Human Retroviruses

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After screening a large number of clinical samples of HIV-1 subtype C in India, a subset of viral strains containing sequence insertions upstream of the viral enhancer has been identified. The sequence insertions contained binding sites for at least two different transcription factors NF-jB and RBEIII, importantly, in a mutually exclusive fashion. Furthermore, while some of the viral strains contained insertions of jB-like sites, a few others contained dual insertions of the RBEIII and jB sites together but only one of the two was intact. NFjB acquisition appears to be the most common phenotype unique for subtype C with nearly half of the variant strains containing such insertions. Given that subtype C already contains three functional NF-jB sites in the viral enhancer, acquisition of a fourth NF-jB motif in some variant viral strains is intriguing. Further investigation is warranted to examine the significance of the sequence insertions for the replicative fitness of the variant viral strains.

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“…1,2 At present, HIV-1 is classified into four Groups (M, N, O, and P) with Group M further subdivided into nine major subtypes (A-D, F-H, J, and K), over 49 circulating recombinant forms (CRF), and numerous unique recombinant forms (URF). [3][4][5] The extensive diversity and rapid evolution of HIV pose serious challenges for maintaining reliable serologic and nucleic acid tests 6 for blood screening, epidemiological surveillance, diagnosis, and clinical management of infected persons. 7 Different test manufacturers target different HIV genes in their nucleic acid tests (NAT) for screening and quantitative HIV RNA determinations, with varying degrees of success in correctly identifying or quantifying emerging isolates.…”

mentioning

confidence: 99%

Pilot Studies for Development of an HIV Subtype Panel for Surveillance of Global Diversity

Manak

Sina²,

Anekella³

et al. 2012

AIDS Research and Human Retroviruses

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The continued global spread and evolution of HIV diversity pose significant challenges to diagnostics and vaccine strategies. NIAID partnered with the FDA, WRAIR, academia, and industry to form a Viral Panel Working Group to design and prepare a panel of well-characterized current and diverse HIV isolates. Plasma samples that had screened positive for HIV infection and had evidence of recently acquired infection were donated by blood centers in North and South America, Europe, and Africa. A total of 80 plasma samples were tested by quantitative nucleic acid tests, p24 antigen, EIA, and Western blot to assign a Fiebig stage indicative of approximate time from initial infection. Evaluation of viral load using FDA-cleared assays showed excellent concordance when subtype B virus was tested, but lower correlations for subtype C. Plasma samples were cocultivated with phytohemagglutinin (PHA)-stimulated peripheral blood mononuclear cells (PBMCs) from normal donors to generate 30 viral isolates (50-80% success rate for samples with viral load > 10,000 copies/ml), which were then expanded to 10 7

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Tracking a century of global expansion and evolution of HIV to drive understanding and to combat disease

Cited by 224 publications

References 125 publications

How Samhd1 changes our view of viral restriction

How Samhd1 changes our view of viral restriction

Sequence Insertions in the HIV Type 1 Subtype C Viral Promoter Predominantly Generate an Additional NF-κB Binding Site

Pilot Studies for Development of an HIV Subtype Panel for Surveillance of Global Diversity

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