Cj. Li et al., RECIPROCAL MODULATIONS BETWEEN P53 AND TAT OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1, Proceedings of the National Academy of Sciences of the United Statesof America, 92(12), 1995, pp. 5461-5464
Infection by human immunodeficiency virus type 1 (HIV-1) causes acquir
ed immunodeficiency syndrome (AIDS) after a long clinical latency. Thi
s disease is associated with a spectrum of cancers. Here we report tha
t wild-type p53 is a potent suppressor of Tat, a major transactivator
of HIV-1. Reciprocally, Tat inhibits the transcription of p53. Downreg
ulation of p53 by upregulated tat may be important for the establishme
nt of productive viral infection in a cell and also may be involved in
the development of AIDS-related malignancies.