Human herpesvirus 6: Relevance of infection in the immunocompromised host

Human herpesvirus 6 (HHV-6) is highly seroprevalent and primary infection usually occurs in early childhood. Two variants of HHV-6 exist (A and B) which have colinear and highly homologous genomes. Similar to other herpesviruses, HHV-6 has enhanced pathogenicity in the immunocompromised host. In solid organ and bone marrow transplant recipients, active HHV-6 infection is common and case reports suggest the virus can cause disease, including encephalitis and bone marrow suppression. Prospective studies, however, suggest that the overall burden of HHV-6 disease after transplantation is more focused on indirect effects, such as triggering allograft rejections. There is growing evidence for interactions among the beta-herpesviruses (cytomegalovirus, HHV-6 and HHV-7), resulting in an increased risk of cytomegalovirus disease and opportunistic infections. HHV-6 has been proposed as a cofactor in HIV disease although there are contradictory findings on its ability to upregulate HIV replication. The virus may be susceptible to existing antiviral agents, although clinical trials are required to determine if therapeutic intervention is beneficial.