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EN
Contribution of endothelial cells to normal immune processes (circulation of leukocytes, immune diapedesis, presentation of antigenes) as well as to pathology caused by viral diseases is described.Cytokine secretion and expression of adhesion molecules, particularly during viral infections are described.Permissiveness of endothelial cells to HIV infection is presented.Contrinution of herperviruses (CMV, HSV) to thrombosis and atherosclerosos is also considered.
EN
Utilizing animals as organ donors for humans may cause transmission of foreign species pathogens to the recipient. To minimize the risk of transmission of infectious diseases from animals to humans, the strategy of appropriate animal selection is being assessed. The aim of the selection of specific pathogen-free pigs was the differentiation of active viruses from latent ones in both the recipients and donors in search of the host gene expression profiles which would differentiate the beginning of transplant rejection from an active infection. Additionally, the researchers searched for gene profile expressions indicating the type of infection which would considerably reduce the time of detection, and the cause of disease in the recipient which would offer a better chance of a positive result of the surgery.
EN
Introduction: Two activities of innate antiviral immunity were studied: the resistance of human peripheral blood mononuclear cells (PMBCs) ex vivo to viral infection and the production of cytokines. Materials and Methods: Samples of blood were taken from healthy blood donors and from persons with frequent infections of the upper respiratory system. PMBCs were isolated by gradient centrifugation. Vesicular stomatitis virus (VSV) was used as the indicatory virus to infect PMBCs. The cytokines: IFN, TNF, and IL-6 were titrated by biological methods and IL-10 by ELISA. Results: Blood donors were divided for two groups: those with VSV-resistant and those with VSV-sensitive PMBCs and secretion of cytokines by them was compared. The resistant PMBCs produced more cytokines than the sensitive ones. A statistically significant difference, was found only in the case of the IFNs. To examine the contribution of IFNs and TNF in maintaining resistance, leukocytes from both groups were treated with specific anti-cytokine antibodies. The authors' previous study showed that the elimination of spontaneous IFN-alpha IFN-beta, IFN-gamma, and TNF-alpha from resistant leukocytes resulted in increased VSV replication This indicates the important role of cytokines. In VSV-sensitive PMBCs, anti-IFN-alpha showed the opposite effect (decreased virus replication). In the absence of spontaneous IFN-alpha, disturbances in cytokine production were observed. Conclusions: Complete resistance of PMBC to VSV infection is accompanied by higher cytokine release, The paradoxical effect of anti-IFN-alpha on virus replication in leukocytes sensitive to viral infection may be attributed to changes in the cytokine profile balance, i.e. high TNF production by VSV-infected leukocytes and a complete reduction of IL-6 production.
EN
Despite extensive biomedical studies conducted during over the last decades, viral infectious diseases remain one of the most serious world heath problems. At the moment, one can distinguish three major ways of their prevention or treatment: immunisation, chemotherapy and immunomodulation. This article presents a broad spectrum of both widely used and presently developed methods of fighting viral infections.
EN
Allogeneic hematopoietic cell transplantation (alloHCT) is the treatment of choice for various pediatric malignancies and nonmalignant diseases. The most prominent complication of allotransplantation is graft vs host disease (GvHD). The treatment of GvHD influence negatively function of immune system and increase risk of bacterial, fungal and viral infections. Clinical symptoms of viral infection may mimic GvHD and lead to inappropriate treatment. Human ctomegalovirus (CMV, Herpesviridae) has been recognized as most important viral pathogen after alloHCT. Increasing number of procedures, especially from alternative donors, requiring more intensive immunosuppression, led to identification more viral pathogens causing transplant related mortality and morbidity. Among them are adenoviruses (ADV, Adenoviridae), BK and JC viruses (Papovaviridae) and human herpes virus 6 (HHV-6, Herpesviridae). Frequency of complications caused by those pathogens is higher in children then in adults.
EN
Different infections are the most common complication of immunosuppressive therapy. In this context, the effect of cyclosporine A (CsA) on the innate antiviral immunity of mice was studied. The presence of immunity was shown by infection of resident peritoneal cells (RPC) of BALB/c mice with herpes virus type 1 (HSV-1) and vesicular stomatitis virus (VSV). While the cells infected immediately after isolation were resistant to the viruses, the cells cultured for several days before infection lost immunity. The lack of activity to neutralize HSV-1 and VSV in the sera of the mice excluded a participation of specific antibodies in the resistance. To study the effect of CsA on innate immunity, BALB/ c mice were intraperitoneally (i. p.) injected with cyclosporine (20 or 100 mug/ mouse, twice a day) for three days. The other group of animals was injected in the same way with PBS only. Then the peritoneal cells were isolated and infected with VSV immediately after cell isolation. The kinetics of viral replication in the control and the CsA-treated groups was compared. While in the cells from the control group VSV did not multiply, in the cells from the CsA-treated mice the virus reached considerable titers. The cyclosporine effect on VSV replication was dose-dependent and statistically significant. We conclude that innate antiviral immunity was suppressed in the cyclosporine-treated mice and that this mechanism may be involved in the high susceptibility of patients to viral infections during immunosuppressive therapy.
EN
Activation of nuclear factor (NF)-kappaB transcription factors family in response to different stimuli such as inflammatory cytokines, stress inducers or pathogens? products results in host innate and adaptive immunity. NF-kappaB plays a central role in promoting the expression of genes involved in inflammatory, immune and apoptotic processes, including those encoding cytokines, chemokines, cytokine receptors or proteins involved in antigen presentation. Although the main function of NF-kappaB is to activate specific genes in the cells of the immune system, its role in controlling the host cell cycle makes NF-kappaB an interesting target for pathogenic viruses. Some viruses take advantage of anti-apoptotic properties of NF-kappaB to escape host defence mechanisms, other use apoptosis to spread. This review describes the role of NF-kappaB family in immune responses, mechanism of NF-kappaB activation and different strategies that viruses have developed to modulate NF-kappaB pathway in order to facilitate and enhance viral replication and avoid host immune responses.
EN
The natural antiviral immunity of human lymphocytes, leukocyte from peripheral blood and whole-blood cultures was studied using the method of infection with two viruses belonging to different taxonomic groups, vesicular stomatitis virus (VSV) and encephalomyocarditis virus (EMCV). The kinetics of virus replication in both kinds of cultures and the dependence of culture infection on pre-infection incubation time were studied. When the cultures were infected immediately after preparation, most of them were found to be resistant to the viruses. However, when they were infected after several (1-5) days of incubation, VSV and EMCV multiplied in the cultures to high titers. The time of losing the resistance was individually differentiated. The results indicate the presence of a non-specific antiviral immunity characteristic for individuals. The antiviral immunity of healthy donors was compared with that of people suffering from recurrent infections of the upper respiratory tract. This latter group expressed statistically significant lower innate immunity than healthy donors. However there were no differences in interferon (IFN) and tumor necrosis factor (TNF) production between these groups. In order to examine the contribution of the endogenous IFNs and TNF alpha in maintaining innate immunity, specific antibodies against IFN alpha, IFN beta, IFN gamma and TNF alpha were added to VSV-infected leukocytes resistant to infection. The antibodies reduced the antiviral resistance in 9 of 16 experiments. The results suggest that both: endogenous interferons and TNF alpha may participate in the constitution of innate immunity, though they are not the only mediators of it.
EN
This study presents news about machanisms of antibody responses and call-mediated immunity in human placenta.The cytokins such as TNFs, ILs, CSFs, produced by the placental cells, may play a role in protection against viral pathogens.The immunological function at the materno/fetal interface probably is associated with a phase of embryonic development.
EN
This paper deals with the viral infections of the fetus and properties of the human placenta acting as an immunological and anatomic barrier.Natural immunity, discussed in this chapter, regards to two principal mechanisms of immunity against viruses:production of IFN and natural cytotoxity..
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