Departments of Global Health, and.
Epidemiology, University of Washington, Seattle, WA.
J Acquir Immune Defic Syndr. 2020 Dec 15;85(5):584-587. doi: 10.1097/QAI.0000000000002505.
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.
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.
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).
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.
细菌性阴道病（BV）和 CD101 免疫球蛋白样（Ig 样）变体是否通过黏膜炎症独立增加 HIV 风险尚不清楚。我们评估了 BV 对女性中 HIV 获得的影响是否因候选 CD101 Ig 样变体的存在与否而不同。
我们使用了来自东非（肯尼亚、坦桑尼亚和乌干达）和南部非洲（博茨瓦纳、南非和赞比亚）的 HIV 血清学不一致夫妇的 2 项研究的数据，这些研究纵向评估了 HIV 获得（通过 ELISA）和 BV（通过 Nugent 评分≥7）。我们使用为每个病例和对照参与者生成的先前的 CD101 序列数据来创建一个二进制变量，指示是否存在任何 5 种 CD101 Ig 样变体。
证实了该队列中先前显示的结果，Ig 样变体增加了 HIV 感染风险（调整后的危险比[aHR]，=2.63；95%置信区间[CI]，1.41 至 4.89）。只有在不存在 Ig 样变体的情况下，BV 才与 HIV 感染风险增加 2.5 倍相关（aHR=2.47；95%CI，0.99 至 6.15；P=0.052），而在存在 Ig 样变体的情况下，BV 与更高的 HIV 感染风险无关（aHR=0.87；95%CI，0.35 至 2.15；P=0.765）；然而，交互检验无统计学意义（P=0.116）。
我们假设 BV 和 CD101 Ig 样变体通过增强类似的生殖道炎症途径促进 HIV 获得。我们的发现表明，Ig 样变体的炎症性黏膜效应可能影响 BV 对 HIV 风险的影响。宿主定义的炎症途径可能是 HIV 预防的有用靶点。
