Role of CD26/Dipeptidyl Peptidase IV in Human Immunodeficiency Virus Type 1 Infection and Apoptosis

• Published in: Proceedings of the National Academy of Sciences - PNAS Vol. 91; no. 21; pp. 9960 - 9964
• Main Authors: Morimoto, Chikao, Lord, Carol I., Zhang, Chonghui, Duke-Cohan, Jonathan S., Letvin, Norman L., Schlossman, Stuart F.
• Format: Journal Article
• Language: English
• Published: United States National Academy of Sciences of the United States of America 11.10.1994; National Acad Sciences; National Academy of Sciences
• Subjects: AIDS; AIDS/HIV; Antigens; Antigens, CD - physiology; Apoptosis; Apoptosis - immunology; Base Sequence; Biochemistry; CD4 Antigens - biosynthesis; Cell Line; Cell lines; Cell Membrane - enzymology; Cell Membrane - immunology; Dipeptidyl Peptidase 4 - biosynthesis; Dipeptidyl Peptidase 4 - physiology; DNA; Enzyme activity; HIV; HIV 1; HIV-1 - pathogenicity; HIV-1 - physiology; Human immunodeficiency virus; Humans; Immunity (Disease); Infections; Kinetics; Molecular Sequence Data; Oligodeoxyribonucleotides; Plasmids; T lymphocytes; Templates, Genetic; Transfection
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.91.21.9960

To examine the role of CD26/dipeptidyl peptidase IV (DPPIV; EC 3.4.14.5) in infection by human immunodeficiency virus type 1 (HIV-1), we utilized CD26 cDNA-transfected Jurkat T-cell lines. Both CD26-parental Jurkat cells and mutant CD26+(DPPIV-) transfected Jurkat cells were readily infected with HIV-1, whereas wild-type CD26+(DPPIV+) transfected Jurkat cells were more resistant to HIV-1 infection. Our results suggest that CD26 is not essential for HIV-1 infectivity as suggested by others but that DPPIV enzyme activity may decrease the efficiency of HIV-1 infection. Of great interest, we found that mutant CD26+(DPPIV-) transfectants and CD26-parental Jurkat cells strongly expressed CD95 (Fas/Apo-1) and were more sensitive than wild-type CD26+(DPPIV+) transfectants to the induction of apoptosis by anti-CD95 monoclonal antibody. These results suggest that CD26 may play a role in HIV-1-associated loss of CD4+cells through the process of programmed cell death.