In 1986, a herpesvirus, now called human herpesvirus type-6 (HHV-6), was identified in cultures of peripheral blood lymphocytes from patients with lymphoproliferative diseases. The virus, which is genetically distinct but morphologically similar to other her-pesviruses, replicates in lymphoid tissue, especially CD4+ T lymphocytes and has two distinct variants, A and B. HHV-6 is more closely related to CMV than to the other earlier known herpesviruses and is the β subfamily.
HHV-6 is the most rapidly spread of the herpesviruses and is shed in the throats of 10% of babies by age 5 months, 70% by 12 months, and 30% of adults. Almost all of the pop- ulation has antibody to this virus by the age of 5 years.
HHV-6 type B is the etiologic agent of exanthem subitum (roseola), and both types A and B can cause acute febrile illnesses with or without seizures or rashes. Exanthem subitum generally occurs in infants aged 6 months to 1 year. It is characterized by fever (usually about 39oC) for 3 days, followed by a faint maculopapular rash spreading from the trunk to the extremities, which begins during defervescence.
HHV-6 also appears to reactivate in transplant recipients. It may contribute to graft rejection and clinical illnesses such as meningoencephalitis, pneumonia, and bone mar-row suppression after bone marrow transplantation. The virus reactivates in other immunocompromised patients including those with AIDS, lymphoma, and leukemia, but its clinical significance is not known.
Initially, it was thought that HHV-6 would grow only in freshly isolated B lympho-cytes, and the virus was referred to as the human B lymphotropic virus. Now it is clear that the virus infects mainly T lymphocytes. HHV-6 establishes a latent infection in T cells but may be activated to a productive lytic infection by mitogenic stimulation. Rest-ing lymphocytes and lymphocytes from normal immune individuals are resistant to HHV-6 infection. In vivo, HHV-6 replication is controlled by cell-mediated factors.
Primary virus infection can be documented by seroconversion. Active virus infection can be documented by culture, antigenemia, or DNA detection in the blood (by PCR). Be-cause asymptomatic viremic reactivation is common, it is very difficult to use these tools to identify HHV-6 as the cause of febrile or other miscellaneous syndromes.
Definitive therapy has not been established, but HHV-6 appears to be susceptible in vitro to ganciclovir and foscarnet. It is less susceptible to acyclovir, because the virus has no thymidine kinase.
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