Compared with HIV-negative women, HIV-infected women have increased risk of low birthweight (LBW) and preterm delivery (PTD). We assessed whether severity of maternal HIV-1 disease was associated with LBW or PTD.
Secondary analysis of The Malaria and HIV in Pregnancy prospective cohort, which enrolled HIV-positive, pregnant Malawian women from 2000 to 2004. Included participants (n = 809) were normotensive antiretroviral treatment–naive women who delivered a live singleton infant. Binomial regression models were used to assess the unadjusted and adjusted prevalence ratios (PRs) and 95% confidence intervals (CI) of the effect of severity of HIV-1 disease, defined by viral load and CD4+ T-cell counts, on prevalence of LBW and PTD.
In unadjusted analyses, among those with malaria (n = 198), there was no association between severity of HIV-1 infection and LBW, whereas among women without malaria (n = 611), we observed a harmful association between both increasing peripheral viral load and LBW (PR: 1.44 per 1-log10 increase, 95% CI: 1.12 to 1.86) and placental viral load and LBW (PR: 1.24 per 1-log10 increase, 95% CI: 1.00 to 1.53). We observed a similar association between increasing placental viral load and PTD (PR: 1.33 per one-log10 increase, 95% CI: 1.04 to 1.69). These associations persisted in multivariate models adjusted for residence, maternal education, primigravid status, and maternal anemia.
In malaria-negative women, maternal HIV-1 disease severity was significantly associated with increased prevalence of LBW and PTD. Such an association was not found in the malaria-infected women.
*Division of Infectious Diseases, Department of Medicine, Center for Microbial Interface Biology, and Public Health Preparedness for Infectious Diseases Program, Ohio State University, Columbus, OH;
†Division of Epidemiology, College of Public Health, Ohio State University, Columbus, OH;
‡Department of Obstetrics and Gynecology, College of Medicine, Ohio State University, Columbus, OH;
§Department of Community Health, Malawi College of Medicine, Blantyre, Malawi;
‖Department of Medicine, University of Melbourne, Parkville, Victoria, Australia;
¶Department of Epidemiology, University of North Carolina, Chapel Hill, NC; and
#Departments of Microbial Infection and Immunity and Microbiology, and Center for Retrovirus Research, Ohio State University, Columbus, OH.
Correspondence to: Jesse J. Kwiek, PhD, 788 Biomedical Research Tower, 460 West 12th Avenue, Columbus, OH 43210 (e-mail: firstname.lastname@example.org).
NIH: KL2RR025754 (A.N.T.); Wellcome Trust (S.R.); R01-AI49084 (S.R.M.); R00-HD056586 (J.J.K.). The MHP cohort was funded by the NIH (R01-AI49084). This research was supported in part by NIH grants R00HD056586 to J.J.K.; A.N.T. was supported by KL2RR025754, through the Ohio State University Center for Clinical and Translational Science (OSU CCTS); the OSU CCTS is supported by the National Center for Advancing Translational Sciences, Grant 8UL1TR000090-05. The content of this article is solely the responsibility of the authors and it does not necessarily represent the official views of the NIH.
S.J.R. was supported by a Senior Fellowship from the Wellcome Trust. The remaining authors have no conflicts of interest to disclose.
A.N.T. and J.J.K. designed the study, performed the data analyses, and wrote the manuscript. W.E.A. and S.T. interpreted the data and edited the manuscript. S.R., S.M., and V.M. conducted the parent MHP cohort, interpreted the data, and edited the manuscript.
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Received April 22, 2013
Accepted June 28, 2013