Human herpesvirus 6 (HHV-6) was first isolated and characterized in 1986. It infects predominately T-lymphocytes of the CD4 (helper) type, but also B-lymphocytes, megakaryocytes, and probably other cells. It is the sixth described member of the Herpesvirus family (the others being HSV-1, HSV-2, EBV, CMV, and varicella-zoster). Infection takes place mainly in the first 2-3 years of life, with antibodies detected in 52% to “almost all” (over 90%) of young children and up to 80% of adults. Similar to the other herpesviruses, a lifelong low-grade or latent infection is produced and reactivation may occur. HHV-6 is now well accepted as the cause of exanthema subitum (roseola infantum). Evidence has been presented for possible involvement in other conditions, such as heterophil-negative mononucleosis, transient febrile illnesses in children, and a type of chronic fatigue syndrome with CNS involvement centered in Nevada and California. One report suggests a role in idiopathic bone marrow transplant failure, seen in about 20% of bone marrow transplants. There is some reported serologic evidence of HHV-6 reactivation associated with CMV infection.

Tests have been described to detect HHV-6 IgG antibody, mostly fluorescent immunoassay and ELISA. Tests for antigen in patient peripheral blood monocytes have also been described, both fluorescent immunoassay and nucleic acid probe with PCR amplification. These tests are currently available only in research laboratories or large reference laboratories.

HHV-7 was identified in 1990. It is frequently found in saliva and apparently causes frequent subclinical infection similar to HHV-6. Also similar to HHV-6, HHV-7 has been reported to cause some cases of exanthema subitum in young children. Serologic testing for IgG antibody has been reported using indirect immunofluorescent methodology.