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001-es BibID:	BIBFORM019703
Első szerző:	Prohászka Zoltán
Cím:	Two parallel routes of the complement-mediated antibody-dependent enhancement of HIV-1 infection / Prohászka Z., Nemes J., Hidvégi T., D. Tóth F., Kerekes K., Erdei A., Szabó J., Ujhelyi E., Thielens N., Dierich M. P., Spath P., Ghebrehiwet B., Hampl H., Kiss J., Arlaud G., Füst G.
Dátum:	1997
ISSN:	0269-9370
Megjegyzések:	To study the mechanism of the complement-mediated antibody-dependent enhancement (C'-ADE) of HIV infection which may play a significant role in the progression of HIV-disease. METHODS: In vitro complement activating and complement-mediated HIV-infection enhancing abilities of three human anti-gp41 monoclonal antibodies (MAb) were tested. C'-ADE was estimated using HIV-1IIIB and CR2 (CD21)-carrying MT-4 target cells. Normal human serum (NHS), purified C1q, C1q-deficient (C1qD) and C2-deficient (C2D) human sera were applied as complement sources. RESULTS: All MAb mediated increased C1q binding to solid-phase gp41. All MAb had a marked dose-dependent and strictly complement-mediated HIV-infection enhancing effect. Mixtures of the MAb with purified C1q also significantly increased HIV-1 infection. C1qD serum had a markedly lower enhancing effect than NHS, which could be raised to normal level by addition of purified C1q. Pretreatment of the target cells with anti-CR2 antibodies only partially inhibited the enhancing effect of the MAb plus normal human serum. CONCLUSION: These novel findings indicate that besides the well-known facilitation of entry of HIV-1 by the interaction between virus-bound C3 fragments and CR2 present on the target cells, fixation of C1q to intact virions also results in an enhanced productive HIV-1 infection in the MT-4 cell cultures.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	Aids. - 11 : 8 (1997), p. 949-958. -
További szerzők:	Nemes József Hidvégi Tünde Tóth Ferenc, D. (1940-2004) (mikrobiológus, élettanász) Kerekes Krisztina Erdei Anna Szabó Judit (1963-) (szakorvos, klinikai mikrobiológus) Ujhelyi Eszter Thielens, Nicole Dierich, Manfred P. Spath Peter Ghebrehiwet, Berhane Hampl, Hartmut Kiss Jolán Arlaud, Gerard Füst György (Budapest)
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001-es BibID:	BIBFORM045393
Első szerző:	Szabó Judit (szakorvos, klinikai mikrobiológus)
Cím:	Strong correlation between the complemet-mediated antibody-dependent enhancement of HIV-1 infection and plasma viral load / Szabó J., Prohászka Z., D. Tóth F., Gyuris Á., Segesdi J., Bánhegyi D., Ujhelyi E., Minárovits J., Füst G.
Dátum:	1999
ISSN:	0269-9370
Megjegyzések:	We have previously demonstrated that complement-mediated antibody-dependent enhancement (C-ADE) of HIV-1 infection correlates with accelerated immunosuppression and disease progression in HIV-1-infected individuals. In the present work the relationship between C-ADE and plasma HIV-1 RNA concentrations was studied to determine the effect of C-ADE on viral replication. METHODS: Three studies were performed: (a) C-ADE and HIV-1 RNA concentrations were determined in the serum and plasma aliquots taken at the same time from 98 HIV patients, mostly in the advanced stage of the disease; (b) the above two parameters as well as HIV enzyme-linked immunosorbent assay (ELISA)-reactive antibodies (Abbott HIV 1/2 test), and p24 antigen levels (Abbott antigen test; Abbott, Delkenheim, Germany) were determined in four seroconversion panels purchased from the Boston Biomedica firm; (c) changes of HIV-1 RNA concentration and C-ADE during a 17 month follow-up period were determined in 18 HIV-infected patients. C-ADE was measured by the method previously established in our laboratories. The results were expressed by an enhancement/neutralization index (E/NI). HIV-1 RNA levels were determined with the Amplicor monitor kit (Roche, Basel, Switzerland), and in some experiments with the nucleic acid sequence based amplification (Organon Teknika, Turnhout, Belgium) kits. RESULTS: (a) We found a highly significant (P<0.0001) positive correlation between E/NI values reflecting the extent of HIV-1 infection enhancement and plasma HIV-1 RNA levels. Both E/NI and HIV-1 RNA levels negatively correlated to the CD4 cell counts. (b) C-ADE was first detected just before, or concomitantly with, seroconversion in 4/4 seroconversion panels. (c) Both E/NI values and HIV-1 RNA levels significantly (P<0.001) increased during a 17 month observation period in 18 HIV-infected patients. CONCLUSION: We found strong association between the extent of the complement-mediated antibody-dependent enhancement of HIV-1 infection and the plasma viral load in HIV patients. On the basis of these findings, C-ADE correlates with HIV replication in vivo, and potentially contributes to the progression of HIV disease.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Aids. - 13 : 4 (1999), p. 1841-1849. -
További szerzők:	Prohászka Zoltán Tóth Ferenc, D. (1940-2004) (mikrobiológus, élettanász) Gyuris Á. Segesdi J. Bánhegyi Dénes Ujhelyi Eszter Minárovits János Füst György (Budapest)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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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
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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