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© The Rockefeller University Press, 0022-1007/1997/5/1865/ $5.00
The Journal of Experimental Medicine, Volume 185, Number 10, May 19, 1997 1865-1870


Brief Definitive Reports

CXCR4/fusin Is Not a Species-specific Barrier in Murine Cells for HIV-1 Entry

Kazunobu Tachibana*, Toshihiro Nakajima{ddagger}, Akihiko Sato{ddagger}, Kenji Igarashi{ddagger}, Hisatoshi Shida§, Hisashi Iizasa*,||, Nobuaki Yoshida*, Osamu Yoshie{ddagger}, Tadamitsu Kishimoto, and Takashi Nagasawa*

From the * Department of Immunology, Research Institute, Osaka Medical Center for Maternal and Child Health, Osaka 590-02, Japan; {ddagger} Shionogi Institute for Medical Science, Osaka 566, Japan; § Institute for Virus Research, Kyoto University, Kyoto 606-01, Japan; || Department of Molecular Preventive Medicine, Division of Social Medicine, Graduate School of Medicine, University of Tokyo, Tokyo 113, Japan; and Department of Medicine III, Osaka University Medical School, Osaka 565, Japan

Since some murine cells expressing human CD4 fail to internalize HIV-1, another block was thought to be located at the level of viral entry in addition to CD4. Recently, CXCR4 was shown to function as a coreceptor for T cell line-tropic HIV-1 entry. Here we demonstrated that cells expressing murine CXCR4 and human CD4 fused with cells expressing the env proteins derived from T cell line-tropic HIV-1 and were infected with T cell line-tropic HIV-1 strains. In contrast, the same cells were not infected with chimeric clones constructed by substitution of monocyte- or macrophage-tropic strain-derived env region or V3 region into T cell line-tropic HIV-1, indicating V3 loop of envelope protein is required for murine CXCR4mediated HIV-1 entry. We conclude that murine CXCR4 is not a species specific barrier to the entry of T cell line-tropic HIV-1.


Address correspondence to Takashi Nagasawa, Department of Immunology, Research Institute, Osaka Medical Center for Maternal and Child Health, 840 Murodo-cho, Izumi, Osaka 590-02, Japan.

Drs. Tachibana and Nakajima contributed equally to this work.


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