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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:	BIBFORM019700
Első szerző:	Tóth Ferenc, D. (mikrobiológus, élettanász)
Cím:	Epstein-Barr virus permissively infects human syncytiotrophoblasts in vitro and induces replication of human T cell leukemia-lymphoma virus type I in dually infected cells / D. Tóth F., Aboagye-Mathiesen G., Nemes J., Liu X., Andirkó I., Hager H., Zdravkovic M., Szabó J., Kiss J., Aranyosi J., Ebbesen P.
Dátum:	1997
ISSN:	0042-6822
Megjegyzések:	Epstein-Barr virus (EBV) and human immunodeficiency virus type 1 (HIV-1), as well as human T-cell leukemia-lymphoma virus type I (HTLV-I), may interact in the pathogenesis of human retroviral infections. The placental syncytiotrophoblast layer represents a barrier protecting the fetal compartment from exposure to retroviruses. We studied the interactions of EBV with HIV-1 and HTLV-I in human term syncytiotrophoblast cells to investigate the significance of double infections in transplacental transmission of human retroviruses. We found that syncytiotrophoblast cells could be productively infected with EBV. Dual infection of the cells with EBV and HTLV-I resulted in full replication cycle of otherwise latent HTLV-I. In contrast, the restricted permissiveness of syncytiotrophoblasts for HIV-1 was not influenced by coinfection of the cells with EBV. Infection of syncytiotrophoblast cells with EBV, but not HTLV-I, induced interleukin-2 and interleukin-6 secretion, and augmented secretion occurred on coinfection with both viruses. Coinfection of syncytiotrophoblast cells with EBV and HTLV-I induced tumor necrosis factor-beta and transforming growth factor-beta 1 secretion, but infection with either virus alone did not lead to secretion of these cytokines. Permissive replication cycle of HTLV-I was induced by the EBV immediate-early gene product Zta. Pseudotype formation between EBV and HTLV-I in coinfected syncytiotrophoblast cells was not found. Our data suggest that activation of HTLV-I gene expression by EBV in coinfected syncytiotrophoblast cells may be a mechanism for transplacental transmission of HTLV-I.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban külföldön készült közlemény
Megjelenés:	Virology. - 229 : 2 (1997), p. 400-414. -
További szerzők:	Aboagye-Mathiesen, George Nemes József Liu, Xiangdong Andirkó István Hager Henrik Zdravkovic, Milan Szabó Judit (1963-) (szakorvos, klinikai mikrobiológus) Kiss Jolán Aranyosi János (1963-) (szülész-nőgyógyász) ifj. Ebbesen, Peter
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