Department of AIDS Research
This department was newly added to the institute in １９７８ as a research division open to visiting professors from other universities and institutes. It is run by concurrent research staff for the present. We have planned and started from August of２００２ a series of fundamental research to answer the question how and what mechanisms human immunodeficiency virus and murine leukemia virus enter into host cells. In addition, we are studying the application of these retrovirus to human gene therapy.
Members
- Visiting Professor Naoki Yamamoto
- Visiting Associate Professor Hironori Sato
- Assistant Professor Yoshinao Kubo
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Activities
Study on the mechamism of viral entry into host cells by retroviruses.
Human immunodeficiency virus (HIV) is known to be a causative agent for acquired immunodeficiency syndrome. After the HIV recognizes CD４and chemokine receptor, for example CXCR４，it enters into target cells mediated fusion between virus envelope and cell membrane. Murine leukemia virus (MLV) recognizes CAT１as the infection receptor, and enters into host cells by same manner. It is most likely that the environment around the receptors influences the infection efficiency. In this context, we are studying the effect of receptor glycosylation and lipid factors proximal to the receptor on the HIV and MLV infection. On the other hand, there are some evidences showing that actin-dependent clustering of the receptors is involved in the retrovirus infection. The receptors, however, do not directly associate with actin. We try to identify the cellular molecule that functions as a linker between the receptor and actin.
Application of HIV envelope gene to gene therapy.
HIV enters into target cells by fusion between virus envelope and cell membrane. This reaction is catalyzed by envelope glycoprotein encoded by the viral genome. When the envelope gene is introduced to susceptible cells expressing CD４and CXCR４，syncytium formation is induced by its membrane fusion activity, and die. Recently, CD４-independent HIV has been isolated. When the envelope gene of the CD４-independent HIV is introduced to cells expressing CXCR４but not CD４，syncytium and cell death was induced. It has been reported that CXCR ４ is up-regulated in mammary tumor. This suggests that the CD４-independent HIV envelope protein specifically induces cell death of mammary tumor cells. We are studying the application of the CD４-independent HIV envelope as a novel therapeutic gene for mammary tumor.
