Human Herpesvirus Type 6, Integrated

Since the first isolation of human herpesvirus-6 (HHV-6) by Salahuddin et al. (1986), widespread infection by this virus has become apparent. As with other herpesviruses, HHV-6 remains latent in the host after primary infection. Transmission of HHV-6 via the saliva from mother to infant is thought to be the most common route. Besides being an infectious agent, HHV-6 has been cited as a possible etiologic factor or as a modulating element of certain human neoplastic diseases, particularly lymphoproliferative disorders. Bandobashi et al. (1997) reported the case of a woman with HHV-6-infected Burkitt lymphoma (113970). FISH showed that the viral genome was integrated into 22q13. The patient's asymptomatic husband also carried HHV-6 DNA integrated at 1q44. To assess the possibility of chromosomal transmission of HHV-6 DNA, Daibata et al. (1999) looked for HHV-6 DNA in the peripheral blood of the couple's daughter. She had HHV-6 DNA on both 22q13 and 1q44, identical to the site of viral integration in her mother and father, respectively. The findings suggested that her viral genomes were inherited chromosomally from both parents. The 3 family members were all seropositive for HHV-6 but showed no serologic signs of active infection. Daibata et al. (1999) proposed a novel latent form for HHV-6, in which integrated viral genome can be chromosomally transmitted. The possible role of this integrated HHV-6 in the pathogenesis of lymphoproliferative diseases remained to be explored.