NAKAMURA Jun Okayama Univ., Medical Sch., Research Associate, 医学部, 助手 (20227903)
NII Shiro Okayama Univ., Medical Sch., Professor, 医学部, 教授 (40029757)
|Budget Amount *help
¥1,700,000 (Direct Cost : ¥1,700,000)
Fiscal Year 1995 : ¥400,000 (Direct Cost : ¥400,000)
Fiscal Year 1994 : ¥1,300,000 (Direct Cost : ¥1,300,000)
Human Herpesvirus 7 (HHV-7), a new T-lymphotropic herpesvirus, is related to, but significantly different from HHV-6. We isolated several clinical isolates from saliva samples of healthy adults, and they were identified as HHV-7. We established a method for infectious titration and a method to obtain high titer cell-free virus preparation using cord blood lymphocytes. One-step growth curves of HHV-6A,6B,and 7 were comparatively analyzed. Among 21 hematopoietic cell lines, a CD4+ CD8+ T cell line, SUP-T1, was the only cell line that supported HHV-7 replication. Virus titers of HHV-7 in SUP-T1 cells were comparable to those in cord blood lymphocytes.
Persistent production of infectious virus was observed after infection of SUP-T1 cells with HHV-7. The culture was the mixture of infected and uninfected cells with the ratio of the infected cells ranging around 10 to 20%. Interferon activity was not detected in the supernatant. However, the treatment of the culture with exogenous interferon beta dramatically reduced the production of virus and cured the culture of the persistent infection. No virus production, infected cell, or HHV-7 genome was detectable.
We studied the interaction of HIV-1 and HHV-7 using the SUP-T1 cell line and a HIV carrier cell line established from SUP-T1. Expression of the CD4 antigen was completely downregulated in the HIV-1 carrier cell line. While superinfection of HIV-1 carrier SUP-T1 cells with HHV-6 was readily accomplished, the same cells were completely resistant to superinfection with HHV-7. Furthermore, treatment of SUP-T1 cells with anti-CD4 monoclonal antibodies inhibited the growth of HHV-7. These results suggest that resistance of HIV-1 carrier SUP-T1 cells to HHV-7 is due to the absence of the CD4 antigen on the cell surface and that HIV-1 and HHV-7 use the same molecule, the CD4 antigen, as the virus receptor.