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001-es BibID:BIBFORM035804
Első szerző:Bánhegyi Dénes
Cím:Significant decrease of the enhancement/neutralization index in HIV patients during highly active antiretroviral therapy (HAART) / Bánhegyi Dénes, Bácsi Attila, Tóth Ferenc D., Prohászka Zoltán, Horváth Anna, Beck Zoltán, Kónya József, Füst George
Dátum:2003
ISSN:0165-2478
Megjegyzések:Authors studied the effect of highly active antiretroviral therapy (HAART) on balance of the antibodies that enhance or neutralize growth of HIV-1(IIIB) strain in MT-4 cells in the presence or absence of human complement. Sequential serum samples were collected from 28 patients in advanced stage of HIV disease before and during HAART. The balance of the enhancing and neutralizing antibodies was expressed by an index value (E/N I). Samples with an E/N I of <0.5 (twofold decrease in virus production) were considered as neutralizing, whereas samples with an E/N I>2.0 (twofold increase in virus production) were considered as enhancing. At the beginning of HAART serum samples from eight patients enhanced, and samples from only two patients neutralized the virus in the presence of complement, median (25th-75th percentile) value of E/N I was 1.32 (0.79-2.29). E/N I significantly (P<0.0001) dropped to 0.37 (0.19-0.57) during the follow-up period of 18.5 (10.5-23.5) months under HAART. Similar changes were detected when serum samples were tested with no complement added. The E/N I values were also markedly decreased when cultures inoculated with mixtures of HIV and purified IgG prepared from serum pools taken before and during HAART, respectively, were compared. In the last samples of 20/28 patients, neutralization was measured even in the presence of complement while enhancement was found with none of these samples. These findings suggest that HAART results in disappearance of enhancing antibodies and switches the E/N I toward neutralization.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Immunology Letters. - 89 : 1 (2003), p. 25-30. -
További szerzők:Bácsi Attila (1967-) (immunológus) Tóth Ferenc, D. (1940-2004) (mikrobiológus, élettanász) Prohászka Zoltán Horváth Anna Beck Zoltán (1970-) (molekuláris biológus, mikrobiológus) Kónya József (1964-) (szakorvos, klinikai mikrobiológus) Füst György (Budapest)
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001-es BibID:BIBFORM040072
Első szerző:Szabó Judit (szakorvos, klinikai mikrobiológus)
Cím:Soluble gC1q-R/p33, a Cell Protein That Binds to the Globular "Heads" of C1q, Effectively Inhibits the Growth of HIV-1 Strains in Cell Cultures / Szabó J., Cervenák L., D. Tóth F., Prohászka Z., Horváth L., Kerekes K., Beck Z., Bácsi A., Erdei A., Peerschke E. I. B., Füst G., Ghebrehiwet B.
Dátum:2001
ISSN:1521-6616
Megjegyzések:C1q and the outer envelope protein of HIV, gp120, have several structural and functional similarities. Therefore, it is plausible to assume that proteins that are able to interact with C1q may also interact with isolated gp120 as well as the whole HIV-1 virus. Based on this hypothesis, we studied the potential ability of the recombinant form of the 33-kDa protein, which binds to the globular "heads" of C1q (gC1q-R/p33), to inhibit the growth of different HIV-1 strains in cell cultures. gC1q-R/p33 was found to effectively and dose-dependently inhibit the production of one T-lymphotropic (X4) and one macrophage-tropic (R5) strain in human T cell lines (MT-4 and H9) and human monocyte-derived macrophage cultures, respectively. At a concentration range of 5-25 microg/ml, gC1q-R caused a marked and prolonged suppression of virus production. The extent of inhibition was enhanced when gC1q-R was first incubated with and then removed from the target cell cultures before virus infection, compared to that when the cells were infected with gC1q-R-HIV mixtures. The extent of inhibition was comparable to that of the Leu3a anti-CD4 antibody. Addition of gC1q-R to the cell cultures on day 1 or 2 after infection induced markedly less inhibition of HIV-1 growth than pretreatment of the cells just before or together with the infective HIV strains. In ELISA experiments, gC1q-R did not bind to a solid-phase recombinant gp120 while strong and dose-dependent binding of gC1q-R to solid-phase CD4 was observed. Our present findings indicate that gC1q-R is an effective inhibitor of HIV-1 infection, which prevents viral entry by blocking the interaction between CD4 and gp120. Since gC1q-R is a human protein, it is most probably not antigenic in humans. It would seem logical, therefore, to consider gC1q-R or its fragments involved in the CD4 binding as potential therapeutic agents.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Clinical Immunology. - 99 : 2 (2001), p. 222-231. -
További szerzők:Cervenak László Tóth Ferenc, D. (1940-2004) (mikrobiológus, élettanász) Prohászka Zoltán Horváth L. Kerekes K. Beck Zoltán (1970-) (molekuláris biológus, mikrobiológus) Bácsi Attila (1967-) (immunológus) Erdei A. Peerschke, E. I. B. Füst György (Budapest) Ghebrehiwet, Berhane
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