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To estimate the risk of mother-to-child transmission of hepatitis C virus (HCV) and identify correlates of transmission, 245 perinatally exposed singleton children followed prospectively beyond 18 months of age were studied. Overall, 28 (11.4%) of the 245 children acquired HCV infection. Transmission occurred in 3 of 80 children (3.7%) whose mothers had HCV infection alone and in 25 of 165 (15.1%; P õ .01) whose mothers had concurrent infection with human immunodeficiency virus type 1 (HIV-1). The percentage of HIV-1-infected children was similar (22 of 165, 13.3%), but each virus was transmitted independently; only six infants (3.6%) were coinfected with HCV and HIV-1. The risk of HCV transmission was not associated with maternal HIV-1-related symptoms, intravenous drug use, prematurity, low birth weight, or breast-feeding, whereas it was lower with cesarean section than with vaginal delivery (5.6% vs. 13.9%, P Å .06). This suggests that transmission occurs mainly around the time of delivery.birth weight, mode of delivery, and type of feeding were also Mother-to-child transmission of hepatitis C virus (HCV) is investigated. widely documented. However, in different investigations the estimated risk of infection ranged from zero to 100% [1 -15]. This variability derives from differences in methods used toPatients and Methods define the child's infection status, duration of follow-up, and size and features of the populations studied.Patients. A cohort of 245 children born to HCV-infected Transmission of HCV may occur in utero via the transplacenwomen were enrolled at 12 participating centers. In three cental route at any time during pregnancy, at the time of delivery, ters all parturients were screened for HCV-seropositivity; in and postnatally through breast-feeding. Several factors might the remaining centers, HCV testing was mostly performed only favor or hamper infection of the offspring. Identification of for women who had a history of IVDU or were known to be these factors would allow the adoption of rational preventive HIV-1-infected. Only singleton at-risk infants identified within strategies and the offer of specific counseling, but little is the first 2 weeks of life and followed up for at least 18 months known about the timing and correlates of transmission. High were included in this study. levels of viremia [5 -7], certain HCV genotypes [8], and materData collection. Specific information was collected by nal coinfection with HIV-1 [1, 2, 4, 7, 9, 15] have been associquestionnaire on maternal risk factors for HCV infection ated with increased HCV transmission rates, although the re-(IVDU, transfusions, sexual contact with an infected partner, sults are controversial [10 -13]; breast milk does not seem to other, unknown), mother's HIV-1 infection status at delivery have a significant role [13 -15].(presence or absence of specific antibody), length of pregnancy The aim of this study was to quantitate the risk of HCV (weeks), mode of delivery (vaginal, elective/emergency cesarinfection in children born to...

Our review suggests that movement disorder may help differentiate clinically an episode of HSV-induced anti-NMDAR encephalitis from HSE relapse. Compared with adults, children have shorter latency between HSE and anti-NMDAR encephalitis and, during anti-NMDAR encephalitis, more movement disorder, fewer psychiatric symptoms, and slightly more severe disease. According to our results, immune therapy given for HSV-induced anti-NMDAR encephalitis does not predispose patients to HSE recurrence.

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About one-third of vertically HIV-1 infected infants develop AIDS within the first months of life; the remainder show slower disease progression. We investigated the relationship between the pattern of HIV-1 replication early in life and disease outcome in eleven infected infants sequentially studied from birth. Viral load in cells and plasma was measured by highly sensitive competitive PCR-based methods.Although all infants showed an increase in the indices of viral replication within their first weeks of life, three distinct patterns emerged: ( a ) a rapid increase in plasma viral RNA and cell-associated proviral DNA during the first 4-6 wk, reaching high steady state levels ( Ͼ 1,000 HIV-1 copies/10 5 PBMC and Ͼ 1,000,000 RNA copies/ml plasma) within 2-3 mo of age; ( b ) a similar initial rapid increase in viral load, followed by a 2.5-50-fold decline in viral levels; ( c ) a significantly lower ( Ͼ 10-fold) viral increase during the first 4-6 wk of age. All infants displaying the first pattern developed early AIDS, while infants with slower clinical progression exhibited the second or third pattern.These findings demonstrate that the pattern of viral replication and clearance in the first 2-3 mo of life is strictly correlated with, and predictive of disease evolution in vertically infected infants. ( J. Clin. Invest. 1996. 97:323-330.)