How fast could HIV change gene frequencies in the human population?

Cromer, Deborah; Wolinsky, Steven M.; McLean, Angela R.

doi:10.1098/rspb.2009.2073

Cited by 5 publications

(5 citation statements)

References 38 publications

(84 reference statements)

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“…Unlike the gene-for-gene models of the world of plant pathology [30] this model is also not designed to consider host and pathogen co-evolution. Here, birth rates are independent of current host densities (see Figure 1A ) so a different model structure that combined pathogen evolution as explored here and host changes as explored, for example, in Cromer et al (2010) [31] , would be needed to explore co-evolution of HIV and humans.…”

Section: Resultsmentioning

confidence: 99%

Modelling the Evolution and Spread of HIV Immune Escape Mutants

et al. 2010

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During infection with human immunodeficiency virus (HIV), immune pressure from cytotoxic T-lymphocytes (CTLs) selects for viral mutants that confer escape from CTL recognition. These escape variants can be transmitted between individuals where, depending upon their cost to viral fitness and the CTL responses made by the recipient, they may revert. The rates of within-host evolution and their concordant impact upon the rate of spread of escape mutants at the population level are uncertain. Here we present a mathematical model of within-host evolution of escape mutants, transmission of these variants between hosts and subsequent reversion in new hosts. The model is an extension of the well-known SI model of disease transmission and includes three further parameters that describe host immunogenetic heterogeneity and rates of within host viral evolution. We use the model to explain why some escape mutants appear to have stable prevalence whilst others are spreading through the population. Further, we use it to compare diverse datasets on CTL escape, highlighting where different sources agree or disagree on within-host evolutionary rates. The several dozen CTL epitopes we survey from HIV-1 gag, RT and nef reveal a relatively sedate rate of evolution with average rates of escape measured in years and reversion in decades. For many epitopes in HIV, occasional rapid within-host evolution is not reflected in fast evolution at the population level.

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Section: Resultsmentioning

confidence: 99%

Modelling the Evolution and Spread of HIV Immune Escape Mutants

et al. 2010

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“…Since the human host evolves much slower, pathogen-host evolutionary conflicts have not, yet visibly affected the host. HIV-1 has been infecting humans for less than 100 years, and mathematical models of the effect of HIV on human gene frequency indicate that it is unlikely to have shaped our evolution on these timescales (Cromer et al, 2010). On the other hand, large-scale human activity should be reflected in the global spread and evolutionary patterns of the virus (host-to-parasite) as it has been documented for other pathogens (Paraskevis et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

The global spread of HIV-1 subtype B epidemic

Magiorkinis

Angelis

Mamais

et al. 2016

Infection, Genetics and Evolution

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Human immunodeficiency virus type 1 (HIV-1) was discovered in the early 1980s when the virus had already established a pandemic. For at least three decades the epidemic in the Western World has been dominated by subtype B infections, as part of a sub-epidemic that traveled from Africa through Haiti to United States. However, the pattern of the subsequent spread still remains poorly understood. Here we analyze a large dataset of globally representative HIV-1 subtype B strains to map their spread around the world over the last 50 years and describe significant spread patterns. We show that subtype B travelled from North America to Western Europe in different occasions, while Central/Eastern Europe remained isolated for the most part of the early epidemic. Looking with more detail in European countries we see that the United Kingdom, France and Switzerland exchanged viral isolates with non-European countries than with European ones. The observed pattern is likely to mirror geopolitical landmarks in the post-World War II era, namely the rise and the fall of the Iron Curtain and the European colonialism. In conclusion, HIV-1 spread through specific migration routes which are consistent with geopolitical factors that affected human activities during the last 50 years, such as migration, tourism and trade. Our findings support the argument that epidemic control policies should be global and incorporate political and socioeconomic factors.

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“…While the HIV-1 virus is known to adapt itself in humans with staggering mutation rates, especially in response to therapy, factors such as the very short time since the emergence of the recent HIV-1 epidemic make it unlikely that selection in humans in response to this specific epidemic has exerted a large, detectable effect [ 15 ]. It is however possible that these loci were subject to natural selection in the more distant past in response to other pathogens, and this has contributed to the population differences we currently observe in HIV-1 VL control.…”

Section: Introductionmentioning

confidence: 99%

Natural selection among Eurasians at genomic regions associated with HIV-1 control

et al. 2011

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BackgroundHIV susceptibility and pathogenicity exhibit both interindividual and intergroup variability. The etiology of intergroup variability is still poorly understood, and could be partly linked to genetic differences among racial/ethnic groups. These genetic differences may be traceable to different regimes of natural selection in the 60,000 years since the human radiation out of Africa. Here, we examine population differentiation and haplotype patterns at several loci identified through genome-wide association studies on HIV-1 control, as determined by viral-load setpoint, in European and African-American populations. We use genome-wide data from the Human Genome Diversity Project, consisting of 53 world-wide populations, to compare measures of FST and relative extended haplotype homozygosity (REHH) at these candidate loci to the rest of the respective chromosome.ResultsWe find that the Europe-Middle East and Europe-South Asia pairwise FST in the most strongly associated region are elevated compared to most pairwise comparisons with the sub-Saharan African group, which exhibit very low FST. We also find genetic signatures of recent positive selection (higher REHH) at these associated regions among all groups except for sub-Saharan Africans and Native Americans. This pattern is consistent with one in which genetic differentiation, possibly due to diversifying/positive selection, occurred at these loci among Eurasians.ConclusionsThese findings are concordant with those from earlier studies suggesting recent evolutionary change at immunity-related genomic regions among Europeans, and shed light on the potential genetic and evolutionary origin of population differences in HIV-1 control.

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How fast could HIV change gene frequencies in the human population?

Cited by 5 publications

References 38 publications

Modelling the Evolution and Spread of HIV Immune Escape Mutants

Modelling the Evolution and Spread of HIV Immune Escape Mutants

The global spread of HIV-1 subtype B epidemic

Natural selection among Eurasians at genomic regions associated with HIV-1 control

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