HIV-1 genomic rna diversification following sexual and parenteral virus transmission

Wolfs, Tom F. W.; Zwart, G.; Bakker, Margreet; Goudsmit, Jaap

doi:10.1016/0042-6822(92)90685-i

Cited by 266 publications

(179 citation statements)

References 10 publications

Supporting

Mentioning

164

Contrasting

Order By: Relevance

“…A phylogenetic analysis of the sequence data has been published (21). A total of 77 sequences of the V3 region, 231 bp long, were obtained; the overall level of variation was similar to that observed in other studies (22,23). Only plasma viral sequences were included to ensure that the sample represented the recently replicated viral population; it has been shown that the proviral population in peripheral blood is heterogeneous, containing both recently replicated and older variants (9).…”

Section: Methodsmentioning

confidence: 71%

Analysis of HIV-1envgene sequences reveals evidence for a low effective number in the viral population

Brown

1997

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

185

102

View full text Add to dashboard Cite

Selection is usually considered to be the dominant force controlling viral variation; the large population sizes suggest that deterministic population genetic models are appropriate. To investigate their validity for HIV, samples of env gene sequences were tested for departure from neutrality because of mutation-selection balance. None of the samples departed significantly when tested as nucleotide sequences. At the amino acid level, significantly elevated diversity was detected in two samples within, but not outside, the V3 loop. The effective population number has been estimated (using a phylogenetic method) to be close to 10 3 . Estimates from nucleotide diversity are about 2-fold lower. The low value of the effective population number might arise from high variability in progeny number between infected cells, from the expansion in population number from a small inoculum as the virus is transmitted between hosts, or from variable selection at linked sites. These results suggest that the population genetics of HIV are best described by stochastic models.

show abstract

Section: Methodsmentioning

confidence: 71%

Analysis of HIV-1envgene sequences reveals evidence for a low effective number in the viral population

Brown

1997

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

185

102

View full text Add to dashboard Cite

show abstract

“…Although the genetic diversity, both within subpopulations and as a whole, is likely to be lower than their equilibrium values [because of the relatively genetically homogeneous viral population at the initial bottleneck of infection (6,(55)(56)(57)(58)], the ratio of the two, as measured by F ST , reaches its equilibrium value relatively rapidly, and hence estimates of F ST , and our conclusions based on them are not expected to be greatly affected by the bottleneck of infection.…”

Section: Discussionmentioning

confidence: 99%

“…4). Many analyses of the pattern of nucleotide substitution in the viral env gene have detected evolution in response to positive selection (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16), although relatively few studies have linked these patterns of viral genetic variation to selection by defined immune responses or for changes in viral phenotype associated with coreceptor usage. In the presence of antiretroviral agents that target viral protease and reverse transcriptase, positive selection has been described in numerous studies, which demonstrate convergent evolution in different individuals of mutations that confer drug resistance (17)(18)(19)(20).…”

mentioning

confidence: 99%

Genetic drift and within-host metapopulation dynamics of HIV-1 infection

Frost

Dumaurier

Wain‐Hobson

et al. 2001

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

127

View full text Add to dashboard Cite

Most HIV replication occurs in solid lymphoid tissue, which has prominent architecture at the histological level, which separates groups of productively infected CD4 ؉ cells. Nevertheless, current population models of HIV assume panmixis within lymphoid tissue. We present a simple ''metapopulation'' model of HIV replication, where the population of infected cells is comprised of a large number of small populations, each of which is established by a few founder viruses and undergoes turnover. To test this model, we analyzed viral genetic variation of infected cell subpopulations within the spleen and demonstrated the action of founder effects as well as significant variation in the extent of genetic differentiation between subpopulations among patients. The combination of founder effects and subpopulation turnover can result in an effective population size much lower than the actual population size and may contribute to the importance of genetic drift in HIV evolution despite a large number of infected cells.H IV has an enormous evolutionary potential because of the combination of a high mutation rate (Ϸ3 ϫ 10 Ϫ5 substitutions͞site͞generation; ref. 1), a short generation time (Ϸ2.6 days; refs. 2 and 3), and a large number of infected cells within the host (10 7 -10 8 infected cells; ref. 4). Many analyses of the pattern of nucleotide substitution in the viral env gene have detected evolution in response to positive selection (5-16), although relatively few studies have linked these patterns of viral genetic variation to selection by defined immune responses or for changes in viral phenotype associated with coreceptor usage. In the presence of antiretroviral agents that target viral protease and reverse transcriptase, positive selection has been described in numerous studies, which demonstrate convergent evolution in different individuals of mutations that confer drug resistance (17)(18)(19)(20). Although specific mutations have been identified with escape from immune responses and escape from antiretrovirals, viral genetic variation reflects more than just these focused positive selection pressures and may reflect more subtle processes of within-host competition between viruses for higher replicative potential.Despite an enormous potential to respond to selection, there can be substantial differences between infected individuals in the evolution of drug resistance. For example, the frequency of single drug-resistant mutants in viral protease and reverse transcriptase before therapy can vary dramatically between hosts (21-23), apparently by random. Indirect observations of the apparently stochastic way in which multiply resistant mutants emerge during therapy are also consistent with a role of genetic drift (18,24,25). In addition, three studies of the evolution of env gene sequences have found substantially lower genetic variation than expected for a population of the order of 10 7 (24,26,27). These studies estimated the ''effective'' population size to be of the order of 10 3 , reflecting the high relatedness be...

show abstract

“…A complete replacement was observed in only one individual (child 538), but this may be related to the relatively short follow-up time. Position 308 plays a crucial role in the binding of V3-antibodies Wolfs et al, 1992). While H to R substitutions or vice versa are rare in HIV-1 subtype B, these substitutions are apparently preferred in the genetic background of HIV-1 subtype A.…”

mentioning

confidence: 99%

Evolution of human immunodeficiency virus subtype A in women seroconverting post partum and in their offspring post-natally infected by ingestion of breast milk.

Simonon¹,

Mulder-Kampinga

Perre³

et al. 1997

Journal of General Virology

View full text Add to dashboard Cite

The evolution of genomic RNA of human immunodeficiency virus type 1 (HIV-1), subtype A, was studied in three Rwandan mother-child pairs over a period of 12-30 months. In two pairs a homogeneous subtype A V3 sequence population was observed at seroconversion and the virus populations in the children resembled those in the mothers. One of these mother-child pairs was infected with an A/C recombinant virus (A p17 /C p24 ). In the third pair, a heterogeneous V3 sequence population was observed in the maternal seroconversion sample but the V3 sequence population in the child's sample was homogeneous. In each individual the intra-and intersample variation (between the seroconversion and follow-up samples) increased over time in both the V3 region and p17 gag . Independent evolution for 1-2 years did not abolish the epidemiological relationship between virus populations in mother and child.

show abstract

HIV-1 genomic rna diversification following sexual and parenteral virus transmission

Cited by 266 publications

References 10 publications

Analysis of HIV-1envgene sequences reveals evidence for a low effective number in the viral population

Analysis of HIV-1envgene sequences reveals evidence for a low effective number in the viral population

Genetic drift and within-host metapopulation dynamics of HIV-1 infection

Evolution of human immunodeficiency virus subtype A in women seroconverting post partum and in their offspring post-natally infected by ingestion of breast milk.

Contact Info

Product

Resources

About