Race E, Stein CA, Chargelegue D, Oxford JS, Aston R; International Conference on AIDS.

Int Conf AIDS. 1994 Aug 7-12; 10: 113 (abstract no. PA0333).

Retroscreen Ltd., Lond Hosp Med Coll, UK.

OBJECTIVE: To investigate the mode of action of peptide T. METHODS: TNF-alpha was obtained from Peptech (UK) as a 500 micrograms/ml solution with a specific activity of 3.2 x 10(7) units/mg. The laboratory strain HIV-1RF was quantified on C8166 cells, cultivated in RPMI 1640 with sodium bicarbonate plus 1 mM L-Glutamine, 50 u/ml Penicillin, 50 micrograms/microliter Streptomycin, 25 mM Hepes buffer and 10% FCS. Peripheral blood mononuclear cells (PBMC) were isolated from blood packs by density gradient centrifugation (Ficoll Paque, Pharmacia). PHA stimulated cells were maintained 10 u/ml of Il2. RESULTS AND CONCLUSIONS: The virus assay system was optimised for using varying multiplicities of infection to allow a sensitive detection of a potentiation of HIV-1 replication by TNF alpha. In the absence of Peptide T, TNF-alpha, at concentrations of 10 IU/ml and above stimulated the production of HIV-1 in culture after 6 days. The addition of Peptide T to the assay systems significantly reduced this effect even at low concentrations (0.01 mM). At concentrations of 1 mM and above Peptide T completely inhibited the enhancement of viral p24 levels by the TNF-alpha. Peptide T also showed some inhibitory activity against HIV-1 in the absence of TNF-alpha with p24 levels in the culture containing 0.01 mM and above of Peptide T, being less than half of p24 in the control.

Publication Types:

• Meeting Abstracts

Keywords:

• Acquired Immunodeficiency Syndrome
• HIV Infections
• HIV-1
• Interleukin-2
• Peptide T
• TNF protein, human
• Tumor Necrosis Factor-alpha

Other ID:

• 94371057

UI: 102209887

From Meeting Abstracts