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 January of １９９７ a series of fundamental research to answer the question how and what mechanisms retroviral infection may lead to several diseases including acquired immunodeficiency syndrome（AIDS）and adult T‐cell leukemia （ATL）.

Study on the mechanism of transactivation of several cellular genes by HTLV‐I‐Tax and HIV‐Tat
　　HTLV‐I and HIV are known to be causative agents for ATL and AIDS, respectively. HTLV‐I‐Tax and HIV‐Tat are nuclear proteins which transcriptionally trans activate not only their own enhancers in the long terminal repeat but also a number of cellular genes. We have previously demonstrated the capacity of the Tax of HTLV‐I to modulate the expression of various cellular genes: the cytokine genes for IL‐１α, IL‐６， IL‐８， IL‐１０， and the cell adhesion molecule gene for ICAM‐１． We are now intending to study the mechanisms of transactivation of cellular genes including IL‐８， IL‐１０， ICAM‐１， and iNOS by Tax or Tat.

Study on the mechanism of Tax independent NF‐κB activation
　　HTLV‐I‐infected cells have been shown to have high levels of active NF‐κB and Tax has been demonstrated to active some cellular genes by causing an increase in HF‐κB levels. However, in the ATL samples, viral mRAN are not detected. These results indicate that the celluar genes are constitutively overexpressed in the absence of Tax in vivo. These findings imply that there is another mechanism independent of Tax underlying the NF‐κB activation in fresh ATL cells. The mechanism of Tax independent NF‐κB activation is under investigation by using TL‐Oml cells.

Study on mechanism of apotosis induction in HIV or HTVL‐I infection
　　Generally, the length of time between HIV infection and development of AIDS is considered to be　１０ years on average. HIV infection is accompanied by the progressive loss of CD４ Tcells. Apoptosis, a form of programmed cell death, has been implicated in pathogenicity related to infection with HIV. HTLV‐I Tax also leads to apoptotic cell death. Apoptotic pathway and its mechanism which account for the pathophysiology in HIV or HTLV‐I infected individuals are under investigation by using Tcells transfected to constitutively express Tat or Tax.