HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Szabò, B. Articles by Benedetto, A. Search for Related Content PubMed PubMed Citation Articles by Szabò, B. Articles by Benedetto, A. Agricola Articles by Szabò, B. Articles by Benedetto, A.

Tumour necrosis factor- increases the sensitivity of human immunodeficiency virus (HIV)-infected monocytic U937 cells to the complement-dependent cytotoxicity of sera from HIV type 1-infected individuals; role of the gp120 protein

¹ Department of Virology, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome
² Centre of Virology, St Camillo's Hospital, Circonvallazione Gianicolense 85, 00100 Rome, Italy
and³ Department of Microbiology, University Medical School, Debrecen, Hungary

Sera of 40 intravenous drug addicts [25 seropositive and 15 seronegative for human immunodeficiency virus (HIV)] were tested for the presence of cytotoxic antibodies against uninfected and HIV-infected monocytic U937 cells. Six of the 25 seropositive samples proved to be cytotoxic for HIV-infected target cells in the presence of complement. The pretreatment of HIV-infected U937 cells with tumour necrosis factor (TNF)- (which enhances virus production in these cells) increased the detection of serum cytotoxicity and 60% of these sera became cytotoxic. The percentage lysis was also increased after the TNF- treatment of the target cells (from 16·2 ± 4·5 to 71·2 ± 4·9). The complement-dependent cytotoxic activity of these sera was significantly reduced by pretreatment with recombinant HIV gp120 antigen. This reduction was dose-dependent in the majority of cases. Immunofluorescence studies suggested that the cytotoxic sera mainly interacted with the viral antigens localized on the membrane of HIV-infected TNF-treated U937 cells. Moreover, comparative Western blot analyses using cellular extracts from untreated and TNF-treated U937 cells showed that there was a positive correlation between the cytotoxic phenotype and the capacity of sera to recognize the gp120 protein in extracts from TNF-treated HIV-infected cells. These results suggest that in some circumstances endogenous TNF- can be a protective factor because it can render persistently infected cells highly sensitive to complement-dependent serum cytotoxicity as a result of increased expression of the relevant viral antigen (gp120) on the cell membrane.

Received 4 November 1992; accepted 9 February 1993.