The Effect of Prenatal Highly Active Antiretroviral Therapy on the Transmission of Congenital and Perinatal/Early Postnatal Cytomegalovirus Among HIV-Infected and HIV-Exposed Infants
ABSTRACT Before highly active antiretroviral therapy (HAART), congenital cytomegalovirus (CMV) rates were higher among human immunodeficiency virus (HIV)-exposed infants than unexposed infants. This study examines congenital and perinatal/early postnatal (P/EP) CMV among HIV-exposed infants pre- and post- HAART.
Infants born to HIV-infected women were evaluated for congenital CMV (CMV-positive culture in first 3 weeks of life) and P/EP CMV (positive culture in first 6 months of life). Prenatal maternal HAART was defined as triple antiretroviral therapy (ART) with at least 1 nonnucleoside reverse-transcriptase inhibitor or protease inhibitor.
Among 414 infants evaluated, 1678 CMV assessment days were completed (mean = 3 assessment days per infant). Congenital CMV rates did not differ by time period, HAART use, or infant HIV infection status. P/EP CMV rates were greater for the 1988-1996 birth cohort (17.9%) compared with the 1997-2002 birth cohort (8.9%) (P < .01), HIV-infected versus uninfected infants (P < .01), and infants with no maternal ART versus those with ART (P < .01). Controlling for potential confounders, P/EP CMV was associated with no maternal ART (odds ratio = 4.7; P < .01), and among those with no maternal ART, P/EP CMV was associated with maternal CD4 count ≤200 cells/μL (P < .01). For HIV-uninfected infants with P/EP CMV, symptoms including splenomegaly, lymphadenopathy, and hepatomegaly were associated with no maternal HAART versus those with HAART (41% vs 6%; P < .05).
Although congenital CMV rates did not change, the post-HAART era showed reduced P/EP CMV and occurrence of related clinical symptoms. These findings underscore the importance of prenatal HAART for all HIV-infected pregnant women.
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ABSTRACT: Background. A high rate of congenital CMV has been documented in HIV exposed infants in industrialized settings, both in pre- and post-HAART era. Only limited data on the birth prevalence of congenital CMV among infants of HIV-infected women on prenatal antiretroviral (ARV) prophylaxis are available from sub-Saharan Africa, despite a high prevalence of both infections. We evaluated the prevalence of congenital CMV in HIV-exposed infants in the Western Cape, South Africa. Methods. HIV-infected mothers were recruited in the immediate postnatal period at a referral maternity hospital between April and October 2012. Maternal and infant clinical data and newborn saliva swabs were collected. Saliva swabs were assayed by real-time PCR for CMV. Data were analyzed using univariate and multivariate logistic regression analyses to determine specific demographic, maternal and newborn characteristics associated with congenital CMV. Results. CMV was detected in 22/748 newborn saliva swabs (2.9%; 95% CI, 1. 9-4.4%). Overall, 96% of mothers used prenatal ARV prophylaxis (prenatal AZT 43.9%, HAART 52.1%). Maternal age, gestational age, prematurity (< 37 weeks gestation), type of ARV prophylaxis, length of ARV prophylaxis, birth weight, small for gestational age and infant feeding choice were not significantly different between CMV-infected and uninfected infants. Maternal CD4 count less than 200 cells/μL during pregnancy was independently associated with congenital CMV (aOR 2.9; 95% CI, 1.2-7.3). A negative correlation between CMV viral load in saliva and maternal CD4 count was observed (r=-0.495, n=22, p=0.019). Conclusions. The birth prevalence of congenital CMV was high despite prenatal ARV prophylaxis, and was associated with advanced maternal immunosuppression.Clinical Infectious Diseases 02/2014; 58(10). DOI:10.1093/cid/ciu096 · 9.42 Impact Factor
Tropical Medicine & International Health 04/2014; DOI:10.1111/tmi.12317 · 2.30 Impact Factor
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ABSTRACT: HIV-1 and CMV are important pathogens transmitted via breastfeeding. Furthermore, perinatal CMV transmission may impact growth and disease progression in HIV-exposed infants. Although maternal antiretroviral therapy reduces milk HIV-1 RNA load and postnatal transmission, its impact on milk CMV load is unclear. We examined the relationship between milk CMV and HIV-1 load (4-6 weeks postpartum) and the impact of antiretroviral treatment in 69 HIV-infected, lactating Malawian women and assessed the relationship between milk CMV load and postnatal growth in HIV-exposed, breastfed infants through six months of age. Despite an association between milk HIV-1 RNA and CMV DNA load (0.39 log10 rise CMV load per log10 rise HIV-1 RNA load, 95% CI 0.13-0.66), milk CMV load was similar in antiretroviral-treated and untreated women. Higher milk CMV load was associated with lower length-for-age (-0.53, 95% CI: -0.96, -0.10) and weight-for-age (-0.40, 95% CI: -0.67, -0.13) Z-score at six months in exposed, uninfected infants. As the impact of maternal antiretroviral therapy on the magnitude of postnatal CMV exposure may be limited, our findings of an inverse relationship between infant growth and milk CMV load highlight the importance of defining the role of perinatal CMV exposure on growth faltering of HIV-exposed infants.Infectious Diseases in Obstetrics and Gynecology 03/2014; 2014:989721. DOI:10.1155/2014/989721