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An abstract of the article "Transmission of Hepatitis B virus (HBV) minor variants in children born to HBV/HIV co-infected mothers," by Woottichai Khamduang and colleagues, is presented.

Background In Thailand where virtually all pregnant women are infected with HCMV, about 2% of infants are congenitally infected with HCMV. However, the transmission rate among infants born to HIV-1 infected mothers is not well known. Our objectives were to evaluate HCMV transmission rates in infants born to HIV-1 infected mothers, and to identify maternal and newborn risk factors associated with infant HCMV infection. Materials and methods Ninety-seven HIV-1 transmitting mothers were matched on maternal plasma HIV-1 RNA before zidovudine prophylaxis initiation with 194 non-transmitting mothers enrolled in PHPT-1, an HIV prevention trial in Thailand. Infant HCMV infection was assessed by anti-HCMV IgM and/or HCMV DNA within 6 months of age and by IgG serology at 18 months. Congenital HCMV infection was defined as the presence of HCMV IgM and/or a positive DNA PCR within 10 days of life. Univariate odds ratio (95% confidence intervals) were calculated for potential risk factors among maternal (age, HIV and immunological stage, pregnancy history, pregnancy complications, induction of labor, mode of delivery, past/present sexual transmitted diseases, CD4/CD8 T-lymphocyte counts) and infant characteristics (HIV status, sex, prematurity and birth weight). Adjusted odds ratios were calculated using logistic regression with stepwise selection of variables with less than 0.20 p value association. Results The prevalence of congenital HCMV infection was 16% (10/62) in HIV-1 infected infants and 5% (5/105) in uninfected infants, p=0.013. The prevalence of HCMV infection by 18 months of age was 83% (62/75) in HIV-1 infected infants and 62% (112/182) in uninfected infants, p=0.001. Upon univariate analysis, among the maternal factors, only vaginal delivery was associated with HCMV infection in infants (OR: 2.5; 95%CI: 1.3-4.7). Among infants' factors, HIV infection (OR: 3.3; 95%CI: 1.7-7.0) and prematurity (OR: 3.5; 95%CI: 1.0-18.8) were associated with HCMV. Upon multivariate analysis only vaginal delivery (OR: 2.5; 95%CI: 1.3-4.5) and infant HIV infection (OR: 3.3; 95%CI: 1.7-6.4) remained independently associated with HCMV infection in infants. Conclusions Infant HIV infection and vaginal delivery are the main risk factors for HCMV infection in children born to HIV-1 infected mothers. The clinical consequences of congenital and postnatal HCMV infection on HIV disease progression need to be assessed. [ABSTRACT FROM AUTHOR]

Our objective was to analyze, in formula-fed infants, correlates of HIV mother-to-child transmission, including cytomegalovirus (CMV) infection. HIV-infected infants were matched with HIV uninfected by maternal HIV RNA in a case-control design. Infant CMV infection was determined by CMV IgG at 18 months and timed by earlier CMV IgM or CMV DNA. Correlations were assessed using logistic regression. In utero HIV infection was independently associated with congenital CMV infection (P = 0.01), intrapartum HIV infection with congenital-plus-intrapartum/neonatal CMV infection (P = 0.01), and overall HIV with overall CMV infection (P = 0.001), and prematurity (P = 0.004). Congenital and acquired CMV infections are strong independent correlates of mother-to-child HIV transmission.

The evolution of hematological parameters in HIV-1-exposed uninfected infants according to various durations of perinatal zidovudine exposure was studied. We used data prospectively collected among 1122 HIV-uninfected formula-fed infants born to HIV-infected mothers who participated in a clinical trial to prevent perinatal transmission in Thailand (PHPT-1). Infants were exposed to different durations of zidovudine both in utero and after birth. Hemoglobin level and leukocyte, absolute neutrophil, and lymphocyte counts were measured at birth and at 6 weeks of age. The association between hematological parameters at birth and the duration of zidovudine exposure in utero was studied using a linear regression model, and changes between birth and 6 weeks of age and the duration of postnatal zidovudine exposure using mixed effects models. At birth, the hemoglobin level was lower in newborns exposed to zidovudine for more than 7.5 weeks in utero (adjusted regression coefficient: -0.6 g/dl; 95% confidence interval: -1.1 to -0.1). Six weeks after birth, the hemoglobin level had decreased faster in infants administered zidovudine for more than 4 weeks (adjusted regression coefficient: -0.1 g/dl; 95% confidence interval: -0.2 to -0.1). The duration of perinatal zidovudine exposure was not associated with the evolution of leukocyte, neutrophil, and lymphocyte counts. Despite the differences in hemoglobin levels, grade 3 or 4 anemia did not significantly differ by maternal or infant zidovudine duration. The clinical impact appeared modest, but longer exposure may warrant close monitoring.