Since antepartum cultures for asymptomatic shedding of HDV from women with elicitable histories of recurrent genital HSV infections do not predict shedding of HSV at delivery, and since up to 77% of mothers of infants infected with HSV do not have an elicitable history of recurrent genital infections, it is proposed to change tactics, identify a high risk population antepartum, and screen for shedding of HSV at delivery. Specific infants exposed to HSV could then be evaluated and, when appropriate, treated. Detection of shedding at delivery is complicated by the fact that HSV has been isolated from the infant only as frequently as from the mother. Amniotic fluid entrapped in the infant's mouth may be best sample and one obtainable in large quantity as compared to swab cultures. Asymptomatic shedding occurs at least as frequently from the lesion site as from the cervix in women with overt genital recurrences; the same may be true in women who are unaware of having genital HSV infections. Since HSV causes 98% of recurrent genital infections in the U.S., it is proposed that women with antibody to HSV 2 be selected as a high risk group using a serological ELISA assay augmented by the use of an avidin-biotin-perioxidase complex. The rate of asymptomatic shedding in those who never perceive overt recurrences will be compared with those who have overt recurrences, those with HSV 1 antibody only, and women with partners with genital HSV infections. The best site(s) to examine for asymptomatic shedding will be assessed by otaining multiple cultures from the mother and infant. Asymptomatic shedding or initial infection during pregnancy will be studied in asymptomatic women with partners with overt genital recurrences and correlated with the woman's part immunological experience with HSV 1 and 2. The ongoing effort to assess the source of HSV infection in infected infants will continue. In view of our belief that the high prevalence of serious HSV infection in the first month of life is related to responses in host resistance rather than solely maternal exposure, and to determine why premature infants are disproportionately represented among infected infants, we plan a re-evaluation of methodology which might prove useful in quantitating early host defenses (quality of passively acquired antibody (HSV 1 vs HSV 2; to glycoproteins vs other proteins) and macrophage/monocyte function). Using an ELISA blot from SDS-PAG gels to assess antibody, a neutralization assay, production and responses of monocytes to an HSV induced chemotactic agent, neutralization and lymphocyte transformation responses, early vs late immune responses will also be studied in treated infants.
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