title: Impaired IL-2 expression in latent HIV-1 infection.
abstract: Regarding the T cell function in HIV-1 infection, activation of T cells is enhanced in acutely HIV-1-infected T cells upon stimuli. However, T cell immune responses underlying the activation of T cell receptor (TCR) signaling molecules and interleukin (IL)-2 production in latently HIV-1-infected cells are poorly understood. The expression and activation of TCR components and its downstream molecules in acutely and latently HIV-1-infected T cells were compared using quantitative reverse transcription polymerase chain reaction (RT-PCR) for mRNA expression and enzyme-linked immunosorbent assay (ELISA) for levels of IL-2 in phytohemagglutinin M (PHA-M). The levels of T cell surface molecules and TCR signaling molecules in latently HIV-1-infected cells were greatly decreased without changes in their mRNA levels. In addition, downstream TCR-signaling molecules in latently HIV-1-infected cells were not activated even in the presence of PHA-M. The phosphorylation of mitogen-activated protein kinases (MAPKs) in the presence of PHA-M was weakly induced in latently HIV-1-infected cells but was greater in acutely HIVNL4-3-infected cells. Finally, the production of IL-2 was significantly decreased in latently HIV-1-infected cells compared with uninfected parent cells. Thus, IL-2-related immunological functions in latently HIV-1-infected T cells were markedly impaired even in the presence of stimuli.
authors.affiliation: Division of AIDS, Korea National Institute of Health, Chungbuk, Republic of Korea.
authors.forename: YoungHyun
authors.initials: Y
authors.lastname: Shin
authors.affiliation: Division of AIDS, Korea National Institute of Health, Chungbuk, Republic of Korea.
authors.forename: Cheol-Hee
authors.initials: CH
authors.lastname: Yoon
authors.affiliation: Division of AIDS, Korea National Institute of Health, Chungbuk, Republic of Korea.
authors.forename: Hoyong
authors.initials: H
authors.lastname: Lim
authors.affiliation: Department of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang 790-784, Republic of Korea.
authors.forename: Jihwan
authors.initials: J
authors.lastname: Park
authors.affiliation: Department of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang 790-784, Republic of Korea.
authors.forename: Tae-Young
authors.initials: TY
authors.lastname: Roh
authors.affiliation: Division of AIDS, Korea National Institute of Health, Chungbuk, Republic of Korea.
authors.forename: Chun
authors.initials: C
authors.lastname: Kang
authors.affiliation: Division of AIDS, Korea National Institute of Health, Chungbuk, Republic of Korea. Electronic address: byeongsun@korea.kr.
authors.forename: Byeong-Sun
authors.initials: BS
authors.lastname: Choi
mesh_terms: D015658:HIV Infections / Q000378:metabolism*; D015497:HIV-1 / Q000502:physiology; D006801:Humans; D007376:Interleukin-2 / Q000378:metabolism*; D011948:Receptors, Antigen, T-Cell / Q000378:metabolism; D015398:Signal Transduction; D017735:Virus Latency
chemical_list: D007376:Interleukin-2; D011948:Receptors, Antigen, T-Cell
keywords: IL-2; Latent HIV-1 infection; MAPKs; TCR-downstream signaling molecules