HIV-1 group N: travelling beyond Cameroon

Delaugerre, Constance; Oliveira, Fabienne De; Lascoux-Combe, Caroline; Plantier, Jean‐Christophe; Simon, François

doi:10.1016/s0140-6736(11)61457-8

Cited by 32 publications

(32 citation statements)

References 5 publications

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“…However, in 2011, a primary infection was diagnosed in a Togolese patient living in France after returning from Togo, where he probably became infected. This report indicates that HIV-N is circulating outside Cameroon (28).…”

Section: Situation Outside Western Central Africamentioning

confidence: 62%

“…Patients develop clinical manifestations similar to those seen in HIV-M infection, even during the acute phase of the primary infection, and progress to AIDS (9,28,35,46,47). The identification of HIV-N in a 7-year-old orphan suggests that mother-to-child transmission can occur (35,46), and phylogenetic studies have shown the capacity for human-tohuman HIV-N transmission (47,48).…”

Section: Hiv-nmentioning

confidence: 97%

“…To date, nine near-complete genomic sequences and five partial sequences have been determined in 14 cases of HIV-N infection confirmed by molecular biology (28,34). These genomes all have the same profile, including an env gene derived from an SIVcpz variant and gag and pol genes closely related to those of HIV-M.…”

Section: Genetic Diversification In Humansmentioning

confidence: 99%

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Non-M Variants of Human Immunodeficiency Virus Type 1

2013

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SUMMARY The AIDS pandemic that started in the early 1980s is due to human immunodeficiency virus type 1 (HIV-1) group M (HIV-M), but apart from this major group, many divergent variants have been described (HIV-1 groups N, O, and P and HIV-2). The four HIV-1 groups arose from independent cross-species transmission of the simian immunodeficiency viruses (SIVs) SIVcpz, infecting chimpanzees, and SIVgor, infecting gorillas. This, together with human adaptation, accounts for their genomic, phylogenetic, and virological specificities. Nevertheless, the natural course of non-M HIV infection seems similar to that of HIV-M. The virological monitoring of infected patients is now possible with commercial kits, but their therapeutic management remains complex. All non-M variants were principally described for patients linked to Cameroon, where HIV-O accounts for 1% of all HIV infections; only 15 cases of HIV-N infection and 2 HIV-P infections have been reported. Despite improvements in our knowledge, many fascinating questions remain concerning the origin, genetic evolution, and slow spread of these variants. Other variants may already exist or may arise in the future, calling for close surveillance. This review provides a comprehensive, up-to-date summary of the current knowledge on these pathogens, including the historical background of their discovery; the latest advances in the comprehension of their origin and spread; and clinical, therapeutic, and laboratory aspects that may be useful for the management and the treatment of patients infected with these divergent viruses.

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Section: Situation Outside Western Central Africamentioning

confidence: 62%

Section: Hiv-nmentioning

confidence: 97%

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Non-M Variants of Human Immunodeficiency Virus Type 1

2013

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“…Whereas HIV-1 group M, the main HIV-1 group responsible for the global AIDS pandemic, and HIV-1 group N, which has so far been found in fewer than 20 individuals (19), are the result of the cross-species transmission of SIV cpz from chimpanzees to humans (20), HIV-1 groups O and P appear to have originated from gorillas as a result of the zoonotic transmission of SIV gor (21). Although most SIVs, including SIV cpz and SIV gor , use Nef to counteract the tetherin proteins of their hosts, HIV-1 group M evolved to use Vpu as a tetherin antagonist because of an ancestral deletion of 5 amino acids from the N terminus of human tetherin required for susceptibility to Nef (22)(23)(24).…”

mentioning

confidence: 99%

Tetherin Antagonism by HIV-1 Group M Nef Proteins

Arias

Colomer-Lluch

Bredow

et al. 2016

J Virol

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Although Nef is the viral gene product used by most simian immunodeficiency viruses to overcome restriction by tetherin, this activity was acquired by the Vpu protein of HIV-1 group M due to the absence of sequences in human tetherin that confer susceptibility to Nef. Thus, it is widely accepted that HIV-1 group M uses Vpu instead of Nef to counteract tetherin. Challenging this paradigm, we identified Nef alleles of HIV-1 group M isolates with significant activity against human tetherin. These Nef proteins promoted virus release and tetherin downmodulation from the cell surface and, in the context of vpu-deleted HIV-1 recombinants, enhanced virus replication and resistance to antibody-dependent cell-mediated cytotoxicity (ADCC). Further analysis revealed that the Vpu proteins from several of these viruses lack antitetherin activity, suggesting that under certain circumstances, HIV-1 group M Nef may acquire the ability to counteract tetherin to compensate for the loss of this function by Vpu. These observations illustrate the remarkable plasticity of HIV-1 in overcoming restriction by tetherin and challenge the prevailing view that all HIV-1 group M isolates use Vpu to counteract tetherin. IMPORTANCEMost viruses of HIV-1 group M, the main group of HIV-1 responsible for the global AIDS pandemic, use their Vpu proteins to overcome restriction by tetherin (BST-2 or CD317), which is a transmembrane protein that inhibits virus release from infected cells. Here we show that the Nef proteins of certain HIV-1 group M isolates can acquire the ability to counteract tetherin. These results challenge the current paradigm that HIV-1 group M exclusively uses Vpu to counteract tetherin and underscore the importance of tetherin antagonism for efficient viral replication.

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“…Group O accounts for less than 1% of AIDS cases and is largely restricted to Cameroon, Gabon, and neighboring countries (7,8). Groups N and P are much rarer still and have been found in only 17 and 2 individuals, all but 1 from Cameroon, respectively (4,5,9,10). The reasons underlying this extreme variation in distribution of the 4 groups are poorly understood, but most likely involve differences in the degree of adaptation to the new human host (11).…”

mentioning

confidence: 99%