Human herpesvirus 6: molecular biology and clinical features

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Abstract
Human herpesvirus 6 (HHV-6) exists as distinct variants HHV-6A and HHV-6B. The complete genomes of HHV-6A and HHV-6B have been sequenced. HHV-6B contains 97 unique genes. CD46 is the cell receptor for HHV-6, explaining its broad tissue tropism but its restricted host-species range. HHV-6 utilizes a number of strategies to down-regulate the host immune response, including molecular mimicry by production of a functional chemokine and chemokine receptors. Immunosuppression is enhanced by depletion of CD4 T lymphocytes via direct infection of intra-thymic progenitors and by apoptosis induction. Infection is widespread in infants between 6 months and 2 years of age. A minority of infants develop roseola infantum, but undifferentiated febrile illness is more common. Reactivation from latency occurs in immunocompromised hosts. Organ-specific clinical syndromes occasionally result, but indirect effects including interactions with other viruses such as human immunodeficiency virus type 1 and human cytomegalovirus or graft dysfunction in transplant recipients may be more significant complications in this population. Recent advances in quantitative PCR are providing additional insights into the natural history of infection in paediatric populations and immunocompromised hosts.