The early spread and epidemic ignition of HIV-1 in human populations

Faria, Nuno Rodrigues; Rambaut, Andrew; Suchard, Marc A.; Baele, Guy; Bedford, Trevor; Ward, Melissa J.; Tatem, Andrew J.; Sousa, Joao; Arinaminpathy, Nimalan; Pépin, Jacques; Posada, David; Peeters, Martine; Pybus, Oliver G.; Lemey, Philippe

doi:10.1126/science.1256739

Cited by 574 publications

(538 citation statements)

References 84 publications

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“…The striking correlation between the presence of asp in nonpandemic groups and M subtypes and CRFs, and their prevalence, strongly supports the idea that ASP could play a role in spreading. This contradicts a common argument that the difference among HIV-1 groups in terms of prevalence and impact in human populations has no molecular basis, but is mostly due to social changes in ∼1960 in central Africa, where the group M was already well established (35).…”

Section: Resultscontrasting

confidence: 48%

Concomitant emergence of the antisense protein gene of HIV-1 and of the pandemic

Cassan

Arigon-Chifolleau

Mesnard

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

114

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Recent experiments provide sound arguments in favor of the in vivo expression of the AntiSense Protein (ASP) of HIV-1. This putative protein is encoded on the antisense strand of the provirus genome and entirely overlapped by the env gene with reading frame −2. The existence of ASP was suggested in 1988, but is still controversial, and its function has yet to be determined. We used a large dataset of ∼23,000 HIV-1 and SIV sequences to study the origin, evolution, and conservation of the asp gene. We found that the ASP ORF is specific to group M of HIV-1, which is responsible for the human pandemic. Moreover, the correlation between the presence of asp and the prevalence of HIV-1 groups and M subtypes appeared to be statistically significant. We then looked for evidence of selection pressure acting on asp. Using computer simulations, we showed that the conservation of the ASP ORF in the group M could not be due to chance. Standard methods were ineffective in disentangling the two selection pressures imposed by both the Env and ASP proteins-an expected outcome with overlaps in frame −2. We thus developed a method based on careful evolutionary analysis of the presence/absence of stop codons, revealing that ASP does impose significant selection pressure. All of these results support the idea that asp is the 10th gene of HIV-1 group M and indicate a correlation with the spread of the pandemic.HIV-1 | asp and env genes | overlapping genes | phylogenetic analyses | selection pressure

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Section: Resultscontrasting

confidence: 48%

Concomitant emergence of the antisense protein gene of HIV-1 and of the pandemic

Cassan

Arigon-Chifolleau

Mesnard

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

114

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“…The most recent common ancestors of HIV-1 groups M and O are both estimated to have existed around 1920 (46,47), whereas the lower levels of diversity seen in group N, and especially in group P, indicate that they emerged more recently. Coalescent studies suggest that groups O and M underwent similar rates of exponential growth until about 1960, and only since then has the spread of group M far outstripped the spread of group O (47).…”

Section: Sivgor Resulted From a Single Introduction Of Sivcpz From Symentioning

confidence: 95%

Origin of the HIV-1 group O epidemic in western lowland gorillas

D’arc

Ayouba

Esteban

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

136

149

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HIV-1, the cause of AIDS, is composed of four phylogenetic lineages, groups M, N, O, and P, each of which resulted from an independent cross-species transmission event of simian immunodeficiency viruses (SIVs) infecting African apes. Although groups M and N have been traced to geographically distinct chimpanzee communities in southern Cameroon, the reservoirs of groups O and P remain unknown. Here, we screened fecal samples from western lowland (n = 2,611), eastern lowland (n = 103), and mountain (n = 218) gorillas for gorilla SIV (SIVgor) antibodies and nucleic acids. Despite testing wild troops throughout southern Cameroon (n = 14), northern Gabon (n = 16), the Democratic Republic of Congo (n = 2), and Uganda (n = 1), SIVgor was identified at only four sites in southern Cameroon, with prevalences ranging from 0.8–22%. Amplification of partial and full-length SIVgor sequences revealed extensive genetic diversity, but all SIVgor strains were derived from a single lineage within the chimpanzee SIV (SIVcpz) radiation. Two fully sequenced gorilla viruses from southwestern Cameroon were very closely related to, and likely represent the source population of, HIV-1 group P. Most of the genome of a third SIVgor strain, from central Cameroon, was very closely related to HIV-1 group O, again pointing to gorillas as the immediate source. Functional analyses identified the cytidine deaminase APOBEC3G as a barrier for chimpanzee-to-gorilla, but not gorilla-to-human, virus transmission. These data indicate that HIV-1 group O, which spreads epidemically in west central Africa and is estimated to have infected around 100,000 people, originated by cross-species transmission from western lowland gorillas.

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“…2b), one could speculate that wildlife or bats might be one of the sources from where human and porcine bufaviruses have emerged. However, current limited knowledge of bufaviruses is unable to reveal the emergence, speciation and spread among different hosts, which is in sharp contrast to the well-studied human immunodeficiency virus (HIV) where rich data have enabled scientists to reconstruct the very early spread and epidemic ignition in human populations (Faria et al, 2014). Finally, a high evolutionary rate of bufaviruses (1.6Â10 -3 substitutions per site per year) was determined, which is similar to that of the single-stranded DNA virus porcine circovirus 2 (Firth et al, 2009).…”

mentioning

confidence: 94%

Identification of a novel bufavirus in domestic pigs by a viral metagenomic approach

Schwarz

Ullman

Ahola

et al. 2016

Journal of General Virology

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Bufavirus is a single-stranded DNA virus belonging to the genus Protoparvovirus. This study reports the identification and characterization of a porcine bufavirus by a metagenomic approach, and a limited epidemiology investigation of bufavirus in six swine farms. A comparative genome analysis showed a similarity of 93 % to a Hungarian porcine bufavirus. Bayesian and maximumlikelihood analyses of genome sequences showed a close relationship of porcine bufaviruses to human and monkey bufaviruses. Molecular dating of the most recent common ancestors supported a recent introduction of bufaviruses into human and pig populations, respectively. A real-time PCR method was developed to screen 60 faecal samples for the porcine bufavirus DNA, and eight positive samples were found in two neighbouring farms, suggesting a relatively low prevalence (13.3 %). No direct transmission of porcine bufaviruses between two neighbouring farms was found, suggesting that bufaviruses may have spread widely in different geographical regions.Bufavirus belongs to the genus Protoparvovirus in the subfamily Parvovirinae (Cotmore et al., 2014). The virus has a single-stranded DNA genome, encoding non-structural protein 1 (NS1), a putative structural protein 1 (VP1), a small hypothetical protein of 130 aa residues and a structural protein 2 (VP2), as demonstrated in a reference genome (GenBank accession number: NC_024888). Genome comparison and phylogenetic analysis have grouped human bufaviruses into three genotypes (Yahiro et al., 2014). Bufavirus has first been identified in faeces of children with acute diarrhoea in Burkina Faso, a landlocked country in West Africa, and found in one Tunisian child (Phan et al., 2012). Subsequently, the virus has been discovered sporadically in cases of diarrhoea in Bhutan (Yahiro et al., 2014), Finland (V€ ais€ anen et al., 2014, the Netherlands (Smits et al., 2014), Turkey (Altay et al., 2015), Thailand (Chieochansin et al., 2015) and China (Huang et al., 2015). The role of bufaviruses as an etiologic agent of human gastroenteritis has not been firmly established yet. Further metagenomic investigations show distinct lineages of bufavirus in wild shrews and non-human primates from Zambia (Sasaki et al., 2015), in Hungarian bats (Kemenesi et al., 2015) and pigs (Hargitai et al., 2016) and in Chinese rats (Yang et al., 2016). This report describes the identification and characterization of bufavirus in faeces of domestic pigs by a metagenomic approach.A total of 60 samples were collected from 6-10-week-old pigs, on five Austrian farms and one Hungarian farm (Fig. 1). The samples consisted of five diarrhoeic (semiliquid or liquid form) and five normal faeces per farm. One diarrhoeic and one normal sample from each farm were used for the metagenomic studies and all samples were used for subsequent epidemiological investigation. About 200 mg of faeces were diluted to 1 ml of water, vortexed vigorously for 1 min and centrifuged at 14 000 g for 10 min. Supernatant (400 µl) was treated with 400 U ml À1 DNase I (Ro...

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The early spread and epidemic ignition of HIV-1 in human populations

Cited by 574 publications

References 84 publications

Concomitant emergence of the antisense protein gene of HIV-1 and of the pandemic

Concomitant emergence of the antisense protein gene of HIV-1 and of the pandemic

Origin of the HIV-1 group O epidemic in western lowland gorillas

Identification of a novel bufavirus in domestic pigs by a viral metagenomic approach

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