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001-es BibID:BIBFORM019692
Első szerző:Bácsi Attila (immunológus)
Cím:Placental macrophage contact potentiates the complete replicative cycle of human cytomegalovirus in syncytiotrophoblast cells : role of interleukin-8 and transforming growth factor-beta 1 / Bácsi A., Aranyosi J., Beck Z., Ebbesen P., Andirkó I., Szabó J., Lampé L., Kiss J., Gergely L., D. Tóth F.
Dátum:1999
ISSN:1079-9907
Megjegyzések:Although syncytiotrophoblast (ST) cells can be infected by human cytomegalovirus (HCMV), in vitro studies have indicated that ST cells do not support the complete viral reproductive cycle, or HCMV replication may occur in less than 3% of ST cells. The present study tested the possibility that placental macrophages might enhance activation of HCMV carried in ST cells and, further, that infected ST cells would be capable of transmitting virus to neighboring macrophages. For this purpose, we studied HCMV replication in ST cells grown alone or cocultured with uninfected placental macrophages. Our results demonstrated that HCMV gene expression in ST cells was markedly upregulated by coculture with macrophages, resulting in release of substantial amounts of infectious virus from HCMV-infected ST cells. After having become permissive for viral replication, ST cells delivered HCMV to the cocultured macrophages, as evidenced by detection of virus-specific antigens in these cells. The stimulatory effect of coculture on HCMV gene expression in ST cells was mediated by marked interleukin-8 (IL-8) and transforming growth factor-beta1 (TGF-beta1) release from macrophages, an effect caused by contact between the different placental cells. Our findings indicate an interactive role for the ST layer and placental macrophages in the dissemination of HCMV among placental tissue. Eventually, these interactions may contribute to the transmission of HCMV from mother to the fetus.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Journal Of Interferon And Cytokine Research. - 19 : 10 (1999), p. 1153-1160. -
További szerzők:Aranyosi János (1963-) (szülész-nőgyógyász) ifj. Beck Zoltán (1970-) (molekuláris biológus, mikrobiológus) Ebbesen, Peter Andirkó István Szabó Judit (1963-) (szakorvos, klinikai mikrobiológus) Lampé László (1929-2021) (szülész-nőgyógyász) Kiss Jolán Gergely Lajos (1940-) (szakorvos, klinikai mikrobiológus) Tóth Ferenc, D. (1940-2004) (mikrobiológus, élettanász)
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2.

001-es BibID:BIBFORM019702
Első szerző:Tóth Ferenc, D. (mikrobiológus, élettanász)
Cím:Bidirectional enhancing activities between human cell leukemia-lymphoma virus type I and human cytomegalovirus in human term syncytiotrophoblast cells cultured in vitro / D. Tóth F., Aboagye-Mathiesen G., Szabó J., Liu X., Mosborg-Petersen P., Kiss J., Hager H., Zdravkovic M., Andirkó I., Aranyosi J., Ebbesen P.
Dátum:1995
ISSN:0889-2229
Megjegyzések:The syncytiotrophoblast layer of the human placenta has an important role in limiting transplacental viral spread from mother to fetus. Human cytomegalovirus (HCMV) is capable of establishing a latent infection in syncytiotrophoblast cells, with restriction of gene expression to immediate-early and early proteins. We analyzed the extent of replication of human T cell leukemia-lymphoma virus type I (HTLV-I) in human term syncytiotrophoblasts infected with HTLV-I alone or coinfected with HTLV-I and HCMV. Although syncytiotrophoblasts could be infected with cell-free HTLV-I, no viral protein expression was found in the singly infected cells. On the contrary, coinfection of the cells with HTLV-I and HCMV resulted in simultaneous replication of both viruses. Bidirectional enhancing activities between HTLV-I and HCMV were mediated primarily by the Tax and immediate-early proteins, respectively. The stimulatory effect of HTLV-I Tax on HCMV replication appeared to be mediated partly by tumor necrosis factor beta and transforming growth factor beta-1. We observed formation of pseudotypes with HTLV-I nucleocapsids within HCMV envelopes, whereas HCMV was not pseudotyped by HTLV-I envelopes in dually infected syncytiotrophoblast cells. Our data suggest that in vivo dual infection of syncytiotrophoblast cells with HTLV-I and HCMV may facilitate the transplacental transmission of both viruses.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Aids Research And Human Retroviruses. - 11 : 12 (1995), p. 1495-1507. -
További szerzők:Aboagye-Mathiesen, George Szabó Judit (1963-) (szakorvos, klinikai mikrobiológus) Liu, Xiangdong Mosborg-Petersen, P. Kiss Jolán Hager Henrik Zdravkovic, Milan Andirkó István Aranyosi János (1963-) (szülész-nőgyógyász) ifj. Ebbesen, Peter
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3.

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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