In HIV-1–infected women, CD4 count declines occur during pregnancy, which has been attributed to hemodilution. However, for women who have not initiated antiretroviral therapy, it is unclear if CD4 declines are sustained beyond pregnancy and accompanied by increased viral levels, which could indicate an effect of pregnancy on accelerating HIV-1 disease progression.
In a prospective study among 2269 HIV-1–infected antiretroviral therapy-naive women from 7 African countries, we examined the effect of pregnancy on HIV-1 disease progression. We used linear mixed models to compare CD4 counts and plasma HIV-1 RNA concentrations between pregnant, postpartum, and nonpregnant periods.
Women contributed 3270 person-years of follow-up, during which time 476 women became pregnant. In adjusted analysis, CD4 counts were an average of 56 (95% confidence interval: 39 to 73) cells/mm3 lower during pregnant compared with nonpregnant periods and 70 (95% confidence interval: 53 to 88) cells/mm3 lower during pregnant compared with postpartum periods; these results were consistent when restricted to the subgroup of women who became pregnant. Plasma HIV-1 RNA concentrations were not different between pregnant and nonpregnant periods (P = 0.9) or pregnant and postpartum periods (P = 0.3). Neither CD4 counts nor plasma HIV-1 RNA levels were significantly different in postpartum compared with nonpregnant periods.
CD4 count declines among HIV-1–infected women during pregnancy are temporary and not sustained in postpartum periods. Pregnancy does not have a short-term impact on plasma HIV-1 RNA concentrations.
*Department of Global Health, University of Washington, Seattle, WA;
†Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA;
‡Department of Obstetrics & Gynaecology, University of Nairobi, Nairobi, Kenya;
§Wits Reproductive Health and HIV Institute (WRHI), University of the Witwatersrand, Johannesburg, South Africa;
‖Jomo Kenyatta University of Agriculture and Technology, Nairobi, Kenya;
¶Kenya Medical Research Institute, Nairobi, Kenya;
#Department of Reproductive Health, Moi University, Eldoret, Kenya; and
**Departments of †Epidemiology and
††Medicine, University of Washington, Seattle, WA.
Correspondence to: Renee Heffron, MPH, PhD, Department of Global Health, University of Washington, 325 Ninth Avenue, Box 359927, Seattle, WA 98104 (e-mail: firstname.lastname@example.org).
Preliminary data from this analysis were presented at the STI & HIV World Congress, July 15, 2013, Vienna, Austria, poster P3.200.
The authors have no conflicts of interest to disclose.
Supported by the US National Institutes of Health (Grant R03 HD068143) and the Bill and Melinda Gates Foundation (Grant 26469).
The Partners in Prevention HSV/HIV Transmission Study Team members are listed in the Acknowledgments.
Received September 13, 2013
Accepted September 13, 2013