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Seventy-five women with anti-hepatitis C virus (HCV) antibody were enrolled prospectively during pregnancy or at delivery for study of mother-to-child transmission of HCV. Twenty-three women were coinfected with the human immunodeficiency virus (HIV). Seventy babies were monitored for at least 6 months. HCV infection was diagnosed in six infants (8.6%), four of whom were born to anti-HIV-positive mothers. HCV RNA was first detected between 2 and 6 months, and the genotypes of infected babies matched those of their mothers (type 1: n = 4; type 3: n = 2). Identical master sequences of the hypervariable region (HVR1) were detected in a mother-infant pair. In three babies coinfected with HCV and HIV, anti-HCV disappeared between 2 and 7 months, being persistently negative in two cases monitored for 11 and 26 months. Transmitting mothers did not differ significantly from those who did not transmit the infection with anti-HIV, HCV genotypes, and viral load at delivery, but had lower rate of reactivity to C100 by the recombinant immunoblot assay (RIBA) (P < .01). This prospective study confirms transmission of HCV from anti-HIV-negative mothers (4.4% in this series). Absence of anti-C100 antibodies at delivery is apparently related to increased risk of vertical transmission. Seronegative HCV infection can be observed in children coinfected with HIV.

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Rats given monocrotaline develop severe right ventricular hypertrophy often accompanied by ascites and pleural effusions. In rats with right ventricular hypertrophy and no serous effusions ("hypertrophy" group), ventricular concentrations of noradrenaline were reduced but ventricular contents were unchanged. Atrial concentrations of noradrenaline were unaffected. Those with more severe right ventricular hypertrophy and serous effusions ("failure" group) had greatly reduced concentrations of noradrenaline in all four chambers, particularly on the right side; the right and left ventricular contents of noradrenaline were also diminished. The distributions of ir-ANP, ir-bombesin and ir-neurotensin in the normal rat heart are presented. ANP concentration fell to 33% in the right atrium and 46% in the left atrium of "failure" animals and to 57% in the right atrium of "hypertrophy" animals. Right ventricular content of ANP, normally low, increased more than two-fold in both groups, the concentration remaining unchanged. Left ventricular content of ANP decreased in the "failure" group. Concentrations of bombesin and neurotensin fell in both ventricles of both groups. Ventricular contents of bombesin did not change, but ventricular contents of neurotensin decreased, especially on the right side. Plasma ANP rose nearly six-fold while plasma bombesin and neurotensin fell in the "failure" group. Plasma peptide concentrations were unchanged in the "hypertrophy" group. The studies show the utility of the monocrotaline model in distinguishing between the effects of hypertrophy and those associated specifically with the syndrome of congestive cardiac failure.

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