Neurologic symptoms, MRI findings, and lymphocyte phenotyping studies suggest that the patients may have been experiencing a chronic, immunologically mediated inflammatory process of the central nervous system. The active replication of HHV-6 most likely represents reactivation of latent infection, perhaps due to immunologic dysfunction. Our study did not directly address whether HHV-6, a lymphotropic and gliotropic virus, plays a role in producing the symptoms or the immunologic and neurologic dysfunction seen in this illness. Whether the findings in our patients, who came from a relatively small geographic area, will be generalizable to other patients with a similar syndrome remains to be seen.
The recent isolation of human herpesvirus 7 (HHV-7) from activated CD4+ T lymphocytes of a healthy individual raises questions regarding the prevalence of this virus in humans and its immunological relationship to previously characterized human herpesviruses. We report that HHV-7 is a ubiquitous virus which is immunologically distinct from the highly prevalent T-lymphotropic HHV-6. Thus, (i) only two of six monoclonal antibodies to HHV-6 cross-reacted with HHV-7-infected cells, (ii) Western immunoblot analyses of viral proteins revealed different patterns for HHV-6-and HHV-7-infected cells, (iii) tests of sequential serum samples from children revealed seroconversion to HHV-6 without concomitant seroconversion to HHV-7, and (iv) in some instances HHV-7 infection occurred in the presence of high titers of HHV-6 antibodies, suggesting the lack of apparent protection of children seropositive for HHV-6 against subsequent infection with HHV-7. On the basis of the analyses of sera from children and adults it can be concluded that HHV-7 is a prevalent human herpesvirus which, like other human herpesviruses, infects during childhood. The age of infection appears to be somewhat later than the very early age documented for HHV-6.
The Z29 and U1102 strains of human herpesvirus 6 (HHV-6) were compared for their ability to replicate in fresh peripheral blood lymphocytes (PBL) and in continuous T cell lines. The replication of both strains in PBL was enhanced by mitogenic activation of cell growth. U1102 replicated in the continuous T cell lines, J JHAN and HSB-2, whereas no Z29 replication was observed in these cell lines as judged by infectious virus yields, the presence of viral antigens, and viral DNA replication. The two strains were compared with respect to their ability to react in immunofluorescence assays with monoclonal antibodies (MAbs) prepared against the GS strain of HHV-6. These MAbs are directed against six different polypeptides including three glycoproteins. All MAbs reacted with cells infected with the U1102 strain. The Z29-infected cells reacted with four MAbs but failed to react with MAbs specific for an 82- to 105-kDa major surface glycoprotein and with one MAb reactive with a nonglycosylated 180-kDa protein. Taken together, the two strains of HHV-6 exhibit variations with regard to their growth and antigenic properties.
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