SHCS

Swiss HIV Cohort Study

& Swiss Mother and Child HIV Cohort Study

Blanquart et al., Viral genetic variation explains variability in HIV-1 pathogenesis

29th November, 2017

Viral genetic variation accounts for a third of variability in HIV-1 set-point viral load in Europe.    PLoS Biology

Current estimates of HIV-1 set-point viral load (SPVL) heritability vary widely in literature, from 6% to 59%. Blanquart et al. on behalf of the BEEHIVE collaboration used a dataset of 2,028 seroconverters from 5 European countries to estimate the heritability of SPVL. The heritability was measured using models of character evolution describing how viral load evolves on the phylogeny of whole-genome viral sequences. Unique to previous studies, the samples were collected in a strict time window of 6 to 24 months after infection, from which the viral genome was also sequenced. In addition, the authors controlled for covariates, including age and sex, which may inflate estimates of heritability.

The authors estimated the heritability of set-point viral load at 31% (confidence interval 15%-43%); this is consistent with other studies based on regression of viral load in donor-recipient pairs.

In conclusion, the study-results suggests that about a third of variation in HIV-1 virulence is attributable to viral genetic variation. There was little evidence for genuine biological differences across cohorts included in this data.

PubMed

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