Human immunodeficiency virus (HIV) is a causative agent of acquired immunodeficiency syndrome (AIDS) and a member of Retrovirus family. The name of "retrovirus" is said to be derived from "reverse-transcribing oncogenic virus." Living up to its name, retrovirus has contributed to oncology, especially in the field of cancer pathogenesis. Retrovirus research has led to discovery of a number of oncogenes as well. Since the discovery of HIV in 1983, however, retrovirus has also been considered as an important etiologic agent that could incapacitate the cells involved in immune responses. As of the end of 2004, the number of people living with HIV/AIDS is estimated to be as large as 40 million. Every year, nearly 5 million people are newly infected with HIV, and 3 million people die of AIDS in the world, mainly in Africa and southeastern and southern Asia. Despite extensive studies, detailed mechanisms of HIV pathogenesis are still unclear, and efforts are being made to clarify functions of various HIV proteins and identify the cellular factors that could interact with the HIV proteins. One of the HIV accessory proteins, Vpr, causes the host cell cycle arrest at G2 phase, which may play an important pathogenic role in AIDS induction. Exploiting the fission yeast Schizosaccharomyces pombe useful for cell cycle studies, I've been trying to elucidate the mechanism by which Vpr induces the G2 arrest as presented in this review.