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Turning the Page on Perinatal Human Immunodeficiency Virus.

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Few recent obstetric challenges have been met with such unabashed success as has perinatal human immunodeficiency virus (HIV). Over the past two and a half decades, a combination of good… Click to show full abstract

Few recent obstetric challenges have been met with such unabashed success as has perinatal human immunodeficiency virus (HIV). Over the past two and a half decades, a combination of good science, smart policy, and dogged public health implementation has made mother-tochild HIV transmission a vanishingly rare event in most of North America and Europe. Similar progress has been made in developing Africa and South Asia, where, despite much higher disease burden and scarcer resources, international agencies have begun to call for the virtual elimination of perinatal HIV.1 Key to these successes is the fundamental finding that maternal combination antiretroviral therapy (multiple drugs targeting two or more aspects of the viral life cycle) can shut down viral replication and thereby prevent most vertical transmission. In this issue of Obstetrics & Gynecology, two articles (see pages 497 and 502) focus on treatment of pregnant women whose HIV disease is wellcontrolled on antiretroviral therapy.2,3 Boucoiran et al2 evaluated the incidence of viral rebound (defined as detectable maternal circulating viral RNA at the time of delivery) among 318 women whose viral loads had been suppressed earlier in pregnancy. This is important, they argue, because intravenous zidovudine in labor is recommended4 for women whose viral load is greater than 1,000 copies/mL, and there is often not enough time to reassess this titer on presentation for delivery; we thus are forced to rely on an earlier result to inform a decision on the labor floor. Overall, 19 women (6%) whose viral loads had been suppressed previously had a detectable viral RNA at delivery, but only six (1.9%) had viral loads greater than 1,000 copies/mL. The authors use this low but measurable rate of viral rebound to argue—dubiously in my view—for a belt-andsuspenders approach in which intravenous zidovudine is standard of care for all women with HIV presenting in labor, irrespective of the earlier viral load. By the authors’ own calculations, we would have to expose nearly 700 women to intravenous zidovudine under this strategy to prevent a single case of neonatal HIV. In a related article, Scott et al3 investigate the timing of delivery among women with suppressed viral loads in pregnancy, thus challenging the conventional wisdom that women with HIV should be delivered in the early period of term gestation. Among women whose viral loads are less than 1,000 copies/mL, Scott et al describe a very low overall risk of perinatal transmission (0.4%; 95% CI 0.2%–0.7%) that does not differ substantially according to delivery timing (0.3% for deliveries occurring between 38 and 40 weeks of gestation and 0.5% for deliveries occurring between 40 and 42 weeks; P5.77). Taken together, these two studies demonstrate the absolute triumph of science over perinatal HIV. That we are now publishing articles on how to move an exceedingly low risk into the realm of the infinitesimal is something for which we, as a discipline, should be immensely proud. See related articles on pages 497 and 502.

Keywords: human immunodeficiency; delivery; hiv; women whose; viral loads; perinatal human

Journal Title: Obstetrics and gynecology
Year Published: 2017

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