Human herpesvirus-6: a short review of its biological behavior.

HHV-6 shows a widespread distribution with life-long persistence. The virus is frequently reactivated, yet remains clinically inapparent unless the patient is immunodeficient in some way. Even then, HHV-6 reactivation may simply enhance the pathogenicity of other viruses or existing autoimmune disorders rather than becoming a pathogen itself. Future clinical studies need to focus on such indirect viral influences mediated through molecular mimicry and interference with cell receptor expression, and cytokine and chemokine network regulation. Nevertheless, such disturbances may afford therapeutic intervention to disrupt herpesvirus interference and improve certain disease processes. There are only a few diseases for which an immediate causal relationship to HHV-6 infection has been suggested.