The antiviral effects of humoral antibodies and adenine arabinoside on encephalitis due to Herpesvirus hominis were studied in three-week-old mice. Exogenously administered antibodies to H. hominis, of rabbit or human origin, significantly reduced morbidity and mortality rates from H. hominis encephalitis if enough antibodies were given during the early phase of infection. Adenine arabinoside could also modulate the pathogenesis and reduce the mortality rate in mice with H. hominis encephalitis. Simultaneous administration of adenine arabinoside and human immune globulin resulted in an enhanced protection against H. hominis encephalitis. This increased protection was manifested by a significant reduction of mortality rate, a decrease in concentration of virus, and a lessening of histopathologic damage in the brain tissues. Mechanisms involved in the enhanced protective effects were not well defined. The use of adenine arabinoside plus human immune globulin did not completely suppress viral replication. Therefore, host recovery was probably mediated through (1) partial suppression of viral replication by adenine arabinoside, (2) neutralization of cell-free virus by antibodies, and (3) collaboration of antibodies with other host resistance factors (e.g., complement, leukocytes, nonimmune effector cells, etc.). Our data suggest that control of severe H. hominis infection may require the combined use of an antiviral agent and humoral factor and, perhaps, enhancement of host responses by other means.

SUMMARY Among 40 hospitalized infants and children with cytomegalovirus infection, 14 (35 %) had interstitial pneumonitis, 4 (10%) had wheezing or tachypnoea but without x-ray evidence of classical interstitial pneumonia, the remaining 22 (55 %) were free of pulmonary involvement. Most patients had tachypnoea and nonproductive cough of varying durations: those with underlying pulmonary pathology tended to have persistent and prolonged respiratory symptoms. Mortality and severity of the lung disease were related to the underlying immunodeficiency or concomitant pulmonary process.Clinical presentations of cytomegalovirus (CMV) infection encompass a broad spectrum of symptoms and signs ranging from asymptomatic disease to lethal congenital infection (Hanshaw et al., 1965;Starr and Gold, 1968). The most common features of congenital infection include hepatosplenomegaly, jaundice, petechiae, low birthweight, and microcephaly (Overall and Glasgow, 1970). Acquired CMV infections are often seen in patients with altered host resistance (Hill et al., 1964;Cangir and Sullivan, 1966;Sutton et al., 1967;Neiman et al., 1973), but these infections may also occur in normal hosts (Klemola et al., 1969; Jordan et al., 1973). Various manifestations of acquired CMV infection have been reported, e.g. infectious mononucleosis-like syndrome, hepatitis, postperfusion syndrome, etc. (Hanshaw et al., 1965;Embil et al., 1968;Klemola et al., 1969Klemola et al., , 1972 Jordan et al., 1973).Pneumonia occurs not infrequently in patients dying from CMV infection both in congenital disease (Medearis, 1964;McCracken et al., 1969) and in hosts with altered immunity (Hill et al., 1964;Rifkind et al., 1967

Frozen sections of Herpesvirus hominis-inoculated mouse brain provide excellent antigens for indirect immunofluorescent staining of antibodies to H. hominis in serum. Indirect immunofluorescent staining is a rapid, sensitive, and reproducible method for the measurement of antibodies to H. hominis. The method can be applied to the clinical and epidemiological studies of H. hominis infections.

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