Document 3282
 DOCN  M94A3282
 TI    Different mechanisms for persistent infection of HIV-1 in MT-4 and
       MOLT-4 cell lines.
 DT    9412
 AU    Fujinaga K; Nakaya T; Kameoka M; Kishi M; Ikuta K; Section of Serology,
       Hokkaido University, Sapporo, Japan.
 SO    Int Conf AIDS. 1994 Aug 7-12;10(1):111 (abstract no. PA0064). Unique
       Identifier : AIDSLINE ICA10/94369293
 AB    OBJECTIVE: We previously showed that persistent infection was generated
       in MT-4 cells by infection with wild-type HIV-1 only after the serial
       passage. On the other hand, MOLT-4 could survive the infection with
       wild-type HIV-1. Here, we examined different mechanisms for persistent
       infection in MT-4 and MOLT-4 cell lines, especially in terms of
       intracellular signal transduction. METHODS: The MT-4 subclone M10 and
       MOLT-4 subclone No. 8 (MOLT-#8) were used here. Persistently infected
       cells used were M10 [M10(P)] infected with the serial passage of
       wild-type HIV-1 and MOLT-#8 [MOLT-#8(P)] infected with wild-type HIV-1.
       TNF-alpha levels in the conditioned media were determined by ELISA kit
       (Genzyme). RESULTS: Both M10 and M10(P) were led to cell death by the
       treatment with more than 1 ng/ml of PMA, whereas both MOLT-#8 and
       MOLT-#8(P) were not led to cell death even by the treatment with 50
       ng/ml of PMA. A greatly amplified TNF-alpha level was observed in
       M10(P). The level was comparable with the level produced from M10
       treated with lethal dose of PMA. On the other hand, the TNF-alpha
       production was undetectable level in both MOLT-#8 and MOLT-#8(P) even
       after treatment with PMA. HIV-1 antigen expression was amplified in
       MOLT-#8(P), but not in M10(P), after treatment with PMA. DISCUSSION AND
       CONCLUSION: These results suggest that different mechanisms for
       persistent infection of HIV-1 in MT-4 and MOLT-4 might be due to
       different signal transduction pathway(s). Protein kinase C activity
       induced by HIV-1 infection might affect on this difference.
 DE    Cell Death  Cell Line  Comparative Study  Human  HIV
       Infections/*ETIOLOGY/IMMUNOLOGY/PATHOLOGY
       HIV-1/PHYSIOLOGY/*PATHOGENICITY  Protein Kinase C/METABOLISM  Signal
       Transduction  Tetradecanoylphorbol Acetate/PHARMACOLOGY  Tumor Necrosis
       Factor/BIOSYNTHESIS  MEETING ABSTRACT

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).