Pin1 liberates the human immunodeficiency virus type-1 (HIV-1): Must we stop it?
Acquired immune deficiency syndrome (AIDS) is mainly caused by the human immunodeficiency virus type-1 (HIV-1). To our knowledge, this is the first review focusing on the vital role of Pin1 in the infection of HIV-1 and the development of AIDS. We and others have demonstrated that Pin1, the only known cis-to-trans isomerase recognizing the pThr/pSer-Pro motifs in proteins, plays striking roles in several human diseases. Interestingly, recent evidence gradually indicates that Pin1 regulates several key steps of the life cycle of HIV-1, including the uncoating of the HIV-1 core, the reverse transcription of the RNA genome of HIV-1, and the integration of the HIV-1 cDNA into human chromosomes. Whereas inhibiting Pin1 suppresses all of these key steps and attenuates the replication of HIV-1, at the same time different PIN1 gene variants are correlated with the susceptibility to HIV-1 infection. Furthermore, Pin1 potentially promotes HIV-1 infection by activating multiple oncogenes and inactivating multiple tumor suppressors, extending the life span of HIV-infected cells. These descriptions suggest Pin1 as a promising therapeutic target for the prevention of HIV-1 and highlight the possibility of blocking the development of AIDS by Pin1 inhibitors.
Key Laboratory for Space Bioscience and Biotechnology, School of Life Sciences, Northwestern Polytechnical University, Xi'an 710072, Shaanxi, PR China.
Hai
H
Hou
Affiliated Hospital, College of Medicine, Hebei University of Engineering, Handan 056002, Hebei, PR China. Electronic address: wangjingzhang1981@gmail.com.
Jing-Zhang
JZ
Wang
Affiliated Hospital, College of Medicine, Hebei University of Engineering, Handan 056002, Hebei, PR China.
Bao-Guo
BG
Liu
Affiliated Hospital, College of Medicine, Hebei University of Engineering, Handan 056002, Hebei, PR China.
Ting
T
Zhang
D000163:Acquired Immunodeficiency Syndrome / Q000201:enzymology* / Q000235:genetics; D005786:Gene Expression Regulation; D020022:Genetic Predisposition to Disease; D015497:HIV-1 / Q000502:physiology*; D006801:Humans; D000072340:NIMA-Interacting Peptidylprolyl Isomerase; D019696:Peptidylprolyl Isomerase / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D014779:Virus Replication
D000072340:NIMA-Interacting Peptidylprolyl Isomerase; C000606846:PIN1 protein, human; D019696:Peptidylprolyl Isomerase
Human immunodeficiency virus type-1; Integration; Pin1; Reverse transcription; Therapeutic target; Uncoating