Human herpesvirus 7 (HHV‑7) is a double‑stranded DNA virus in the Betaherpesvirinae subfamily closely related to human herpesvirus 6. It infects CD4 T lymphocytes and other cells and is a common but often unrecognized cause of febrile illness in childhood.
Biology and Pathogenesis
HHV‑7 has the typical herpesvirus architecture with a linear double‑stranded DNA genome enclosed within an icosahedral capsid, a tegument and an envelope bearing glycoproteins. Primary infection generally occurs during early childhood through exposure to saliva. Like HHV‑6, HHV‑7 replicates in activated CD4 T cells, as well as in salivary glands and perhaps neural tissue. The virus establishes lifelong latency in peripheral blood mononuclear cells and salivary glands. Reactivation may occur in association with immunosuppression or co‑infection with other herpesviruses. Pathogenesis is not completely understood, but studies show that by five years of age nearly all people possess antibodies to HHV‑7, indicating widespread infection and early seroconversion. The host immune response, both humoral and cellular, limits viral replication but does not eradicate latent genomes. HHV‑7 infection may interact with HHV‑6; co‑infection can influence replication and disease expression.
Clinical Relevance
HHV‑7 is implicated in exanthem subitum (roseola) and other febrile rash illnesses, though HHV‑6B remains the primary cause. Primary HHV‑7 infection may cause a prolonged febrile illness with or without rash and is associated with febrile seizures. In transplant recipients, reactivation of HHV‑7 has been linked to graft dysfunction and rejection, particularly after kidney transplantation. The virus has been detected in cases of encephalitis and myocarditis, but causality remains uncertain. Because most adults carry latent HHV‑7, it can be transmitted via blood transfusion or transplanted organs. Ongoing research is investigating the role of HHV‑7 in neurologic diseases and its interactions with other herpesviruses. HHV‑7 is a ubiquitous betaherpesvirus that infects T cells, establishes latency and usually produces mild or subclinical disease. Although it shares many characteristics with HHV‑6, its clinical associations are less well defined. Awareness of HHV‑7 and its potential to reactivate in immunosuppressed hosts is important for transplant medicine. Related Terms: Human Herpesvirus 6A, Human Herpesvirus 6B, Cytomegalovirus, Epstein–Barr Virus, Varicella‑Zoster Virus