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M94A3282.TXT
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1994-10-25
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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).