Simultaneous pulmonary infection with respiratory syncytial virus and human cytomegalovirus.

prevented or treated if safe and effective methods are available. In Japan, most (probably all) children when they develop varicella visit their doctor because parents know that children with the disease are often uncomfortable, febrile, irritable, and unhappy and they look to doctors to prevent or reduce these problems. There is also an increasing number of children who receive a live varicella vaccine, which costs approximately 10 000 yen (about C65) in Japan. More than 200 000 children received the vaccine in 1993, which clearly indicates a strong parental need to have their children free from the disease. Dr Conway questions whether a rise in antibody titre from <4 to 8 reflects seroconversion. We believe it is an obvious seroconversion and a significant (a fourfold) increase in the antibody titres, which would surely be supported by clinical virologists. We followed up children who did not show seroconversion and found that most of them had antibody activity two to three months later (unpublished data), which suggests that administration of acyclovir in the incubation period tends to postpone development of immune response to the virus. We also found that immunity to the virus persisted for at least one year in most of the children treated with acyclovir (unpublished data). It is therefore possible that the actual seroconversion rate is higher than reported. As suggested by Dr Conway the optimal dose of acyclovir that prevents the disease but induces virus immunity should be established. It is unlikely that immunity in children treated with acyclovir tends to decline or diminish, thereby creating a risk of more severe varicella or early zoster later in life. Reduced frequency and severity of the skin rash in children treated with acyclovir suggests that the drug prevents or reduces blood borne dissemination of the virus and infection of skin with the virus.2 4 Possibly, the drug suppresses replication of the virus in the lung, liver, spleen, and other organs before or during the second viraemia.5 Many of the children given acyclovir developed the virus antibodies and most of them had no signs and symptoms of varicella. All this suggests that subclinical infection is occurring. As fluorescent antibody to membrane antigen assay measures antibodies to glycoproteins or late antigens of the virus, it is reasonable to consider that a limited virus replication conferred specific memory to the virus in the immune system of children treated with acyclovir. Moreover, it is likely that the immunity will persist for a long time, as subclinical infection in a natural setting and infection with live varicella vaccine provide a long lasting immunity to the virus and protect the infected individual from the disease. ' Little is known about the mechanism by which the virus establishes latency in sensory ganglia. However, it is generally believed that the virus may arrive at the sensory ganglia not only via a nerve but also via the haematogenous route during the viraemic phase of varicella. It is unlikely that acyclovir treatment during the incubation period predisposes the host to a higher risk of reactivation of disease (herpes zoster), as there was protection against rash and probably a reduced degree of viraemia in treated patients.