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HHV-6
Twenty years after the discovery of Epstein-Barr virus (EBV) a new herpes virus was reported by Salahuddin and his associates (1). This new virus was isolated from Patients with AIDS and other lymphoproliferative disorders and was eventually named as human herpesvirus type-6 (HHV-6). HHV-6 is the smallest of herpesviruses (170 kb) and has been classified as beta-herpesvirus. HHV-6 has been reisolated by many laboratories and a consensus conference has classified them into subgroups A and B. The subgrouping is based on restriction endonuclease sites, and biological and immunological characteristics (2,3). Antibody to HHV-6 and therefore, possible exposure/infection is detected in <80% individuals in the Western world. (4,5). From all indication it appears that the infection by HHV-6 takes place very early in life after the acute phase the virus becomes dormant to be activated at a later time. HHV-6 can be reactivated by the usual factors e.g., immunological and environmental (6).
HHV-6 is exclusive T-cell tropic, induces and upregulates CD4 receptors and cytokine expression, enhances the killing of cells infected with other lytic viruses such as HIV-1 (4,5,9,10,15-21). There is evidence for the association of HHV-6 with at least three lymphoproliferative diseases; causative agent for childhood disease Roseola (Exanthem subitem) (7), febrile illness in young children (8), and EBV- and CMV- negative cases of mononucleosis in young adults(4,5). This is an important pathogen that can initiate pathologies mentioned before, it may also be a cofactor in several other diseases such as AIDS, cervical carcinoma, and oral carcinoma (9,13,14). HHV-6 is reactivated in infectious diseases, proliferative disorders, and immune deficiencies (4,5,8-12).
A variety of pathogens either co-infect the same cell or are present in the same environment. Type and level of viral antigens for example and the duration of their presence in that milieu can be important factors that my give rise to a particular disease. Whereas HHV-6 and HIV-1 may give rise to AIDS-like disease, HHV-6 in conjunction with HPV may result in malignancy of the cervix. HHV-6 becomes latent after the initial infection and can be reactivated by a variety of viruses and vice versa. Interaction between the viruses may take place after the reactivation of these agents.
For information on testing please see our Clinical Laboratory.
References
1. Salahuddin, S.Z., et.al., (1986) Science 234, 596-601
2. Ablashi, D.V., et al., (1993) Arch. Virol. 128, 363-366
3. Inoue, N., (1994) Infect. Agents Dis. 29, 343-360
4. Pellet, P.E., et al., (1992) Adv. Virus Res. 41, 1-52
5. Krueger, G.R.F., et al., (1994) In Vivo 8, 457-485
6. Yaminishi, K., et al., (1994) Lancet i, 1065-1067
7. Prukananopda, P., et al., (1992) N. Engl. J. Med. 526, 1445-1450
8. Asano, Y., et al., (1993) Cur. Opin. Pediatr. 5, 14-21
9. Lusso, P. and Gallo, R.C., (1995) Imunol. Today 16, 67-71
10. Lusso, P. and Gallo, R.C., (1994) Lancet 343, 555-556
11. Cone, R.W., (1993) N. Engl. J. Med. 329, 156-161
12. Drobyski, W.R., (1993) J. Infect. Dis 167, 735-739
13. Leach, C.T., et al., (1994) 169, 1281-1283
14. Yadav, M., et al., 91994) J. Natl. Cancer Inst. 86, 1792-1794
15. Razzaque, a., 91990) Oncogene 9, 1365-1370
16. Thompson, J., et al., (1994) Oncogene 9, 1167-1175
17. Lusso, P., et al., (1989) Nature 337, 370-373
18. Lusso, P., et al., (1991) Nature 349, 533-535
19. Ensoli, B., et al., (1989) EMBO J. 8, 3019-3027
20. Horvat, R.T., Wood, C., and Balachandran, N., (1989) J. Virol. 63, 970-973
21. Martin, M.E.D. et al., (1991) J. Virol. 65, 5381-53
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