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To determine factors that influence the occurrence of congenital cytomegalovirus (CMV) infection, the authors surveyed prospectively 8,254 infants born in eastern Iowa between October 1989 and June 1994. The authors conducted a case-control study to identify maternal risk factors, matching each CMV-infected infant with three uninfected infants according to hospital and date of birth. CMV strains were compared by using the polymerase chain reaction (PCR) to identify common sources of infection. Of the 7,229 infants cultured successfully for CMV, 35 (0.48%) were congenitally infected. Mothers of CMV-infected infants were more likely to be single (odds ratio (OR) = 3.05, p = 0.016), to work in sales (OR = 4.93, p = 0.008), or to be students (OR = 5.01, p = 0.017). Conversely, women who worked in health-care professions were less likely to have a congenitally infected infant (OR = 0.14, p = 0.049). PCR analysis indicated 27 distinct strains of CMV, but two groups of infants (two infants per group) excreted strains with indistinguishable molecular patterns. One of these pairs of infants had older siblings who attended the same child-care center during their mothers' pregnancies. The authors concluded that demographic and occupational factors influenced the risk of giving birth to an infant with congenital CMV infection. Many distinct CMV strains were identified, suggesting that major point source outbreaks had not occurred. Nonetheless, point source acquisition of CMV from child-care environments did account for some cases of congenital CMV infection in eastern Iowa.

Objective Interleukin-2 (IL-2) is a cytokine with multiple effects on lymphocytes including induction of CD4+ T cell proliferation. IL-2 administration has been shown to increase CD4 counts in HIV-infected people receiving antiretroviral therapy. GB virus C (GBV-C) is an apparently non-pathogenic flavivirus that replicates in CD4+ T cells and inhibits HIV replication in vitro by mechanisms including downregulation of HIV entry coreceptors (CCR5 and CXCR4) and induction of chemokines (RANTES, MIP-1α, MIP-1β, and SDF-1). GBV-C replication is significantly inhibited in vitro by activation of primary CD4+ cell cultures with IL-2 and phytohemagglutinin. We sought to determine if there is an interaction between GBV-C and IL-2 in vivo. Methods GBV-C viremia status was characterized in 92 HIV-infected subjects participating in a randomized trial of IL-2 and antiretroviral therapy (AIDS Clinical Trials Group Study [ACTG] 328). Changes in CD4 cell counts and HIV RNA levels in subjects assigned IL-2 were compared with those in subjects assigned antiretroviral therapy alone. Results Subjects lacking GBV-C viremia had a significantly greater rise in CD4 count with IL-2, compared to GBV-C viremic subjects (by 511 cells/mm3 at week 84; interaction p=0.02): GBV-C viremic subjects assigned IL-2 did not demonstrate a significant increase in CD4 count compared to subjects not assigned to receive IL-2 (95% CI for difference -255 to 397 cells/mm3). Conclusions GBV-C viremia was associated with a block in CD4 cell expansion following IL-2 therapy in the ACTG 328 study, and GBV-C status may be an important factor in IL-2 treatment response.

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