Abstract:
Background: Whether bacterial vaginosis (BV) and CD101 immunoglobulin-like (Ig-like)
variants independently increase HIV risk through mucosal inflammation is not well
understood. We evaluated whether the impact of BV on HIV acquisition in women differs
by the presence or absence of candidate CD101 Ig-like variants.
Methods: We used data from 2 studies of HIV serodiscordant couples in east (Kenya,
Tanzania, and Uganda) and southern (Botswana, South Africa, and Zambia) Africa, which
longitudinally assessed HIV acquisition (by ELISA) and BV (by Nugent score ≥7). We
used previously generated CD101 sequence data for each case and control participant to
create a binary variable indicating the presence/absence of any of 5 CD101 Ig-like
variants.
Results: Confirming previously shown results in this cohort, Ig-like variants increased
HIV-infection risk (adjusted hazard ratio [aHR], = 2.63; 95% confidence interval [CI],
1.41 to 4.89). BV was associated with 2.5-fold higher HIV-infection risk only in the
absence of Ig-like variants (aHR = 2.47; 95% CI, 0.99 to 6.15; P = 0.052), whereas in the
presence of Ig-like variants, BV was not associated with higher HIV-infection risk (aHR
= 0.87; 95% CI, 0.35 to 2.15; P = 0.765); however, a test for interaction was
nonsignificant (P = 0.116).
Conclusions: We hypothesized that both BV and CD101 Ig-like variants facilitate HIV
acquisition by augmenting similar genital inflammation pathways. Our findings indicate
that inflammatory mucosal effects of Ig-like variants may influence the impact of BV on
HIV risk. Host-defined inflammatory pathways may be useful targets for HIV prevention.