Document 3150 DOCN M94A3150 TI Inhibition of human herpesvirus 7 infection by anti-CD4 monoclonal antibodies and HIV-1 gp120. DT 9412 AU Yasukawa M; Yakushijin Y; Furukawa M; Hato T; Takada K; Fujita S; First Dep. Int. Med., Ehime University School of Medicine, Japan. SO Int Conf AIDS. 1994 Aug 7-12;10(1):141 (abstract no. PA0184). Unique Identifier : AIDSLINE ICA10/94369425 AB OBJECTIVE: We have recently found that human herpesvirus (HHV)-7 shows tropism to CD4+ T cells, but not to CD4- cells, and that the transport of intracytoplasmic CD4 molecules to the cell surface is impaired in HHV-7-infected cells (J. Immunol. in press). Based on these findings, we speculated that the CD4 molecule might be the receptor for HHV-7, and the present study was performed to verify this possibility. METHODS: The ability of anti-CD4 V1 domain monoclonal antibodies (mAbs) to inhibit the replication of HHV-7 was examined by detection of cytopathic effect, indirect immunofluorescence, 50% tissue culture infection dose and quantitative PCR for the virus genome. Similarly, the effect of HIV-1 gp120 on the replication of HHV-7 was examined. RESULTS: Anti-CD4 V1 domain mAbs, which inhibit HIV-1 infection, also appeared to inhibit the replication of HHV-7. None of anti-CD4 mAbs affected the replication of HHV-6. Pretreatment of CD4+ T cells with recombinant HIV-1 gp120 also resulted in inhibition of HHV-7 infection. DISCUSSION AND CONCLUSIONS: These data strongly suggest that the CD4 molecule is the major receptor for HHV-7, and that HIV-1 and HHV-7 compete for CD4 as their binding receptor. The identification of the HHV-7 structure binding to CD4 molecule would shed light on the development of the subcomponent peptide derived from HHV-7, which selectively inhibits HIV binding but not affect CD4+ T-cell functions. DE Antibodies, Monoclonal/*PHARMACOLOGY Antigens, CD4/IMMUNOLOGY/*PHYSIOLOGY Comparative Study Herpesvirus 7, Human/DRUG EFFECTS/*PHYSIOLOGY/PATHOGENICITY Human HIV Envelope Protein gp120/*PHARMACOLOGY HIV-1/*PHYSIOLOGY Receptors, Virus/DRUG EFFECTS/PHYSIOLOGY Recombinant Proteins/*PHARMACOLOGY T-Lymphocytes/DRUG EFFECTS/IMMUNOLOGY/*MICROBIOLOGY T4 Lymphocytes/DRUG EFFECTS/IMMUNOLOGY/*MICROBIOLOGY Virus Replication/*DRUG EFFECTS/IMMUNOLOGY MEETING ABSTRACT SOURCE: National Library of Medicine. NOTICE: This material may be protected by Copyright Law (Title 17, U.S.Code).