István Andirkó
University of Debrecen
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Featured researches published by István Andirkó.
Journal of Interferon and Cytokine Research | 2001
Attila Bacsi; Eszter Csoma; Zoltan Beck; István Andirkó; József Kónya; Lajos Gergely; Ferenc Tóth
The syncytiotrophoblast (ST) layer of the human placenta has an important role in limiting transplacental viral spread from mother to fetus. Although certain strains of human immunodeficiency virus type 1 (HIV-1) may enter ST cells, the trophoblast does not exhibit permissiveness for HIV-1. The present study tested the possibility that placental macrophages might induce replication of HIV-1 carried in ST cells and, further, that infected ST cells would be capable of transmitting virus into neighboring macrophages. For this purpose, we investigated HIV-1 replication in ST cells grown alone or cocultured with uninfected placental macrophages. The macrophage-tropic Ba-L strain of HIV-1, capable of entering ST cells, was used throughout our studies. We demonstrated that interactions between ST cells and macrophages activated HIV-1 from latency and induced its replication in ST cells. After having become permissive for viral replication, ST cells delivered HIV-1 to the cocultured macrophages, as evidenced by detection of virus-specific antigens in these cells. The stimulatory effect of coculture on HIV-1 gene expression in ST cells was mediated by marked tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) release from macrophages, an effect caused by contact between the different placental cells. Results of this study suggest an interactive role for the ST layer and placental macrophages in the dissemination of HIV-1 among placental tissue. Data reported here may also explain why macrophage-tropic HIV-1 strains are transmitted preferentially during pregnancy.
Leukemia & Lymphoma | 1998
Zoltan Beck; Attila Bacsi; Eszter Kovács; Jolán Kiss; Attila Kiss; Béla Telek; Ferenc Tóth; István Andirkó; Éva Oláh; Miklós Udvardy; Rák K
Expression of nine oncogenes was investigated in cell samples from fifteen patients with Philadelphia chromosome (Ph)-positive chronic granulocytic leukemia (CGL) both at diagnosis and at the onset of accelerated phase (AP) of the disease. The bcr-abl fusion gene, the H-ras gene and the c-myb gene were universally expressed. In comparison with the chronic phase (CP) of the disease, an increase in the levels of bcr-abl-, c-myb- and H-ras-related transcripts was found in three, two and three AP samples, respectively. Elevation of the bcr-abl-related message was associated with duplication of the Ph chromosome and amplification of the bcr-abl fusion gene in one AP sample. No CP samples were positive for c-myc or c-sis expression. On the contrary, c-myc and c-sis were expressed in three and four AP samples, respectively. The presence of c-myc-related transcript was associated with trisomy 8 with or without amplification of the c-myc oncogene in leukemia cells of two patients with CGL in AP. No changes of oncogene expression were found in four AP samples. However, we observed deletions of chromosome 13 and 17 or i(17q) in three of them, suggesting that tumor suppressor gene alterations may also be responsible for the development of AP of CGL. Our data indicate that heterogeneous alterations in oncogenes and tumor suppressor genes accompany the evolution of CGL-CP to the AP of the disease.
Journal of Interferon and Cytokine Research | 1999
Attila Bacsi; János Aranyosi; Zoltan Beck; Peter Ebbesen; István Andirkó; Judit Szabó; László Lampé; Jolán Kiss; Lajos Gergely; Ferenc Tóth
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.
AIDS Research and Human Retroviruses | 1999
Judit Szabó; Zoltan Beck; Eva Csoman; Xiangdong Liu; István Andirkó; Jolán Kiss; Attila Bacsi; Peter Ebbesen; Ferenc Tóth
The interaction between human immunodeficiency virus type 1 (HIV-1) and human T cell leukemia-lymphoma virus type I (HTLV-I) has generated substantial interest. However, there is disagreement on the in vivo consequences of the double infection. We investigated the interactions between HIV-1 and HTLV-I in monocyte-derived macrophages cultured in vitro. For study, the T cell-tropic strain IIIB and the macrophagetropic strain Ada-M of HIV-1 were used. The HTLV-I was prepared from the supernatants of the virus-producing MT-2 cell line. We found that coinfection of macrophages with T cell-tropic HIV-1 and HTLV-I significantly enhanced HIV-1 replication, whereas double infection of the cells with macrophage-tropic HIV-1 and HTLV-I resulted in marked upregulation of HTLV-I production. Stimulatory interactions between HIV-1 and HTLV-I were mediated by their trans-acting proteins. Results of study on nuclear translocation of proviral DNA showed that the tax gene product of HTLV-I was able to facilitate the nuclear import of the reverse-transcribed HIV-1(IIIB) DNA. In contrast, the HIV-1 Tat protein did not increase the intranuclear trafficking of HTLV-I DNA, which suggests another mechanism for HTLV-I enhancement by the tat gene product. In conclusion, this study provides possible mechanisms whereby coinfection of an individual with HIV-1 and HTLV-I may influence the clinical outcome of double infection.
Journal of Interferon and Cytokine Research | 1999
Judit Szabó; Attila Bacsi; Zoltan Beck; Jolán Kiss; István Andirkó; Ferenc Tóth
Human cytomegalovirus (HCMV) is one of the most frequent opportunistic agents causing severe illness in chronic human T cell leukemia-lymphoma virus type I (HTLV-I) infection. Our previous studies have shown that coinfection of macrophages with HCMV and HTLV-I significantly enhances HCMV replication, resulting in release of infectious HCMV from dually infected cells. We found that double infection of macrophages with HCMV and HTLV-I induced a rapid production of substantial amounts of interleukin-8 (IL-8) and transforming growth factor-beta1 (TGF-beta1). Results of transfection studies demonstrated that the tax gene product of HTLV-I was able to induce secretion of IL-8 and TGF-beta1. In addition to its cytokine-inducing effect, the Tax protein could interact with HCMV synergistically to result in production of much higher levels of IL-8 and TGF-beta1 than expected on the basis of their separate activities. Treatment of dually infected macrophage cultures with neutralizing antibodies to IL-8 and TGF-beta1 led to a nearly 1000-fold decrease in release of infectious HCMV from coinfected cells. Similar results were obtained when anti-IL-8 and anti-TGF-beta1 treatments were combined in macrophage cultures transfected with the tax gene before HCMV infection. Our results suggest that the stimulatory effect of HTLV-I Tax protein on HCMV replication in coinfected macrophages is largely mediated by high levels of IL-8 and TGF-beta1 production.
American Journal of Reproductive Immunology | 2002
Ferenc D. Tóth; Attila Bacsi; Eszter Csoma; Zoltan Beck; István Andirkó; Peter Ebbesen
The phenotypic mixing between human immunodeficiency virus type 1 (HIV‐1) and vesicular stomatitis virus (VSV) has been exploited to assay the susceptibility of human term syncytiotrophoblast cells to penetration by various strains of HIV‐1. VSV (HIV‐1IIIB) and VSV (HIV‐1Ba‐L) pseudotypes were found to enter syncytiotrophoblasts. Infection of syncytiotrophoblasts was mediated by envelope glycoproteins of IIIB and Ba‐L strains of HIV‐1. Although certain strains of HIV‐1 could enter syncytiotrophoblasts, the cells did not exhibit permissiveness for HIV‐1. The next studies tested the possibility that placental macrophages might induce replication of HIV‐1 carried in syncytiotrophoblast cells and that infected syncytiotrophoblasts would be capable of transmitting virus into neighbouring macrophages. For this purpose, the macrophage‐tropic Ba‐L strain of HIV‐1 was used. Interactions between syncytiotrophoblasts and macrophages activated HIV‐1 from latency in syncytiotrophoblast cells, which delivered HIV‐1 to cocultured macrophages. The stimulatory effect of coculture on HIV‐1 gene expression was mediated by marked tumor necrosis factor‐α and interleukin‐6 release from macrophages, an effect caused by contact between the different placental cells. Results suggest an interactive role for the syncytiotrophoblast layer and placental macrophages in the dissemination of HIV‐1 among placental tissue.
Journal of Medical Virology | 2001
Attila Juhász; Éva Remenyik; József Kónya; György Veress; Ágnes Bégány; István Andirkó; Ildikó Medgyessy; J. Hunyadi; Lajos Gergely
AIDS Research and Human Retroviruses | 1995
Ferenc Tóth; George Aboagye-Mathiesen; Judit Szabó; Xiangdong Liu; Peter Mosborg-Petersen; Jolán Kiss; Henrik Hager; Milan Zdravkovic; István Andirkó; János Aranyosi; Peter Ebbesen
Journal of Medical Virology | 2002
Eszter Csoma; Attila Bacsi; Xiangdong Liu; Judit Szabó; Peter Ebbesen; Zoltan Beck; József Kónya; István Andirkó; Etelka Nagy; Ferenc D. Tóth
Virology | 1997
Ferenc D. Tóth; George Aboagye-Mathiesen; József Nemes; Xiangdong Liu; István Andirkó; Henrik Hager; Milan Zdravkovic; Judit Szabó; Jolán Kiss; János Aranyosi; Peter Ebbesen