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Relevant bibliographies by topics / Immunology; Immunosuppression; Viral infection

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Academic literature on the topic 'Immunology; Immunosuppression; Viral infection'

Author: Grafiati

Published: 4 June 2021

Last updated: 14 February 2022

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Journal articles on the topic "Immunology; Immunosuppression; Viral infection"

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Miller, David M., Thomas B. Thornley, Dale L. Greiner, and Aldo A. Rossini. "Viral Infection: A Potent Barrier to Transplantation Tolerance." Clinical and Developmental Immunology 2008 (2008): 1–14. http://dx.doi.org/10.1155/2008/742810.

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Transplantation of allogeneic organs has proven to be an effective therapeutic for a large variety of disease states, but the chronic immunosuppression that is required for organ allograft survival increases the risk for infection and neoplasia and has direct organ toxicity. The establishment of transplantation tolerance, which obviates the need for chronic immunosuppression, is the ultimate goal in the field of transplantation. Many experimental approaches have been developed in animal models that permit long-term allograft survival in the absence of chronic immunosuppression. These approaches function by inducing peripheral or central tolerance to the allograft. Emerging as some of the most promising approaches for the induction of tolerance are protocols based on costimulation blockade. However, as these protocols move into the clinic, there is recognition that little is known as to their safety and efficacy when confronted with environmental perturbants such as virus infection. In animal models, it has been reported that virus infection can prevent the induction of tolerance by costimulation blockade and, in at least one experimental protocol, can lead to significant morbidity and mortality. In this review, we discuss how viruses modulate the induction and maintenance of transplantation tolerance.

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Sevilla, Noemí, Stefan Kunz, Andreas Holz, Hanna Lewicki, Dirk Homann, Hiroki Yamada, Kevin P. Campbell, Juan C. de la Torre, and Michael B. A. Oldstone. "Immunosuppression and Resultant Viral Persistence by Specific Viral Targeting of Dendritic Cells." Journal of Experimental Medicine 192, no. 9 (October 30, 2000): 1249–60. http://dx.doi.org/10.1084/jem.192.9.1249.

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Among cells of the immune system, CD11c+ and DEC-205+ splenic dendritic cells primarily express the cellular receptor (α-dystroglycan [α-DG]) for lymphocytic choriomeningitis virus (LCMV). By selection, strains and variants of LCMV that bind α-DG with high affinity are associated with virus replication in the white pulp, show preferential replication in a majority of CD11c+ and DEC-205+ cells, cause immunosuppression, and establish a persistent infection. In contrast, viral strains and variants that bind with low affinity to α-DG are associated with viral replication in the red pulp, display minimal replication in CD11c+ and DEC-205+ cells, and generate a robust anti-LCMV cytotoxic T lymphocyte response that clears the virus infection. Differences in binding affinities can be mapped to a single amino acid change in the viral glycoprotein 1 ligand that binds to α-DG. These findings indicate that receptor–virus interaction on dendritic cells in vivo can be an essential step in the initiation of virus-induced immunosuppression and viral persistence.

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Sciubba, J. J. "Opportunistic Oral Infections in the Immunosuppressed Patient: Oral Hairy Leukoplakia and Oral Candidiasis." Advances in Dental Research 10, no. 1 (April 1996): 69–72. http://dx.doi.org/10.1177/08959374960100011401.

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Several opportunistic infections associated with immunosuppression are noted to occur secondary to an altered relationship between host and organism. In relation to diminished host immunologic defenses, associated commensal organisms may evolve to a pathogen state. Candidiasis. a common oral marker disease reflective of immunosuppression, results from dysfunction of complex cellular interactions keyed by depressed T-cell activity or function. Certain viral infections may also serve as probable markers of immunosuppression. One such infection is typified by the development of oral hairy leukoplakia, a condition highly correlated to HIV infection in most, but not all, patients. Detection of Epstein-Barr virus particles and subsequent molecular analytic verification of such and the absence of other potential viral candidates, such as papilloma and human immunodeficiency viruses, have led to a general acceptance of this virus as the cause of this condition.

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Kawasaki, Hideya, Edward S. Mocarski, Isao Kosugi, and Yoshihiro Tsutsui. "Cyclosporine Inhibits Mouse Cytomegalovirus Infection via a Cyclophilin-Dependent Pathway Specifically in Neural Stem/Progenitor Cells." Journal of Virology 81, no. 17 (June 6, 2007): 9013–23. http://dx.doi.org/10.1128/jvi.00261-07.

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ABSTRACT The potential of neural stem and progenitor cell (NSPC) transplantation in neurodegenerative disease raises a concern about immunosuppressive agents and opportunistic neurotropic pathogens that may interfere with engraftment. Cytomegalovirus (CMV) is an important opportunistic pathogen infecting the central nervous system, where it may remain latent for life, following transplacental transmission. Cyclosporine (Cs), an immunosuppressive drug used in organ transplantation, where its use is associated with CMV reactivation, suppressed murine CMV (MCMV) infection in cultured NSPCs but not in fibroblasts. This activity of Cs appears to be mediated via cyclophilin (CyP) rather than via calcineurin. First, the calcineurin-specific inhibitor FK506 failed to suppress replication. Second, the CyP-specific inhibitor NIM811 strongly suppressed replication in NSPC. NSPCs maintained in the presence of NIM811 retained viral genomes for several weeks without detectable viral gene expression or obvious deleterious effects. The withdrawal of NIM811 reactivated viral replication, suggesting that the inhibitory mechanism was reversible. Finally, inhibition of endogenous CyP A (CyPA) by small interfering RNA also inhibited replication in NSPCs. These results show that MCMV replication depends upon cellular CyPA pathways in NSPCs (in a specific cell type-dependent fashion), that CyPA plays an important role in viral infection in this cell type, and that inhibition of viral replication via CyP leads to persistence of the viral genome without cell damage. Further, the calcineurin-signaling pathway conferring immunosuppression in T cells does not influence viral replication in a detectable fashion.

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Araki, Koichi, Shivaprakash Gangappa, Dirck L. Dillehay, Barry T. Rouse, Christian P. Larsen, and Rafi Ahmed. "Pathogenic virus-specific T cells cause disease during treatment with the calcineurin inhibitor FK506: implications for transplantation." Journal of Experimental Medicine 207, no. 11 (October 4, 2010): 2355–67. http://dx.doi.org/10.1084/jem.20100124.

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Recently, several cases of fatal lymphocytic choriomeningitis virus (LCMV) infection occurred in transplant recipients being treated with the immunosuppressive calcineurin inhibitor FK506. These findings were surprising because LCMV is a noncytolytic virus. To understand how a noncytolytic virus can cause disease under conditions of immunosuppression, we used the mouse LCMV model and found that, similar to the observations in human transplant recipients, LCMV infection of FK506-treated mice resulted in a lethal disease characterized by viremia, lack of seroconversion, and minimal lymphocytic infiltrates in the tissues. However, despite the apparent absence of an antiviral immune response, this disease was orchestrated by virus-specific T cells. FK506 did not prevent the generation and proliferation of LCMV-specific T cells but instead altered their differentiation so that these effector T cells lost the ability to control virus but were still capable of mediating disease. These pathogenic T cells initiated a cytokine storm characterized by high levels of tumor necrosis factor (TNF) and interleukin 6 (IL-6), and depletion of T cells or blockade of these inflammatory cytokines prevented the lethal disease. Our study shows that inhibiting calcineurin can generate pathogenic T cells and indicates that T cell–mediated viral disease can occur even under conditions of immunosuppression. Furthermore, we identify a potential strategy (blockade of TNF and IL-6) for treatment of transplant recipients who have acute complications of viral infection.

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Honke, Nadine, Namir Shaabani, Katja Merches, Asmae Gassa, Anke Kraft, Katrin Ehrhardt, Dieter Häussinger, et al. "Immunoactivation induced by chronic viral infection inhibits viral replication and drives immunosuppression through sustained IFN-I responses." European Journal of Immunology 46, no. 2 (November 17, 2015): 372–80. http://dx.doi.org/10.1002/eji.201545765.

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Liang, Raymond. "How I treat and monitor viral hepatitis B infection in patients receiving intensive immunosuppressive therapies or undergoing hematopoietic stem cell transplantation." Blood 113, no. 14 (April 2, 2009): 3147–53. http://dx.doi.org/10.1182/blood-2008-10-163493.

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AbstractHepatitis B virus (HBV) reactivation is a serious but preventable complication of immunosuppression. Full HBV serologic profile must be obtained from all patients receiving intensive immunosuppressive therapy. In general, preemptive anti-HBV therapy is more effective than giving treatment after development of reactivation. Prompt lamivudine therapy should be given to at-risk patients who are hepatitis B surface antigen (HBsAg)–positive. It is recommended that lamivudine be continued until at least 6 months after the cessation of immunosuppression. Some patients requiring a longer duration of lamivudine therapy are at risk of developing drug resistance. The newer anti-HBV agents are effective in overcoming lamivudine resistance. Early use of these agents may be considered. HBV reactivation was observed in HBsAg-negative patients with occult HBV infection (HBV DNA-positive) who are on heavy immunosuppression. The optimal management of this group of patients is unclear. For patients receiving allogeneic HSC transplants, the HBV status of the donors requires special attention. To minimize the risk of transmission of infection to recipients, HBsAg-positive donors should receive adequate anti-HBV therapy before HSC donation. As the result of adoptive immune transfer, clearance of HBsAg is observed in HBsAg-positive patients receiving HSC transplants from donors who are positive for hepatitis B surface and core antibodies.

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Ravanel, Kissia, Claire Castelle, Thierry Defrance, T. Fabian Wild, Dominique Charron, Vincent Lotteau, and Chantal Rabourdin-Combe. "Measles Virus Nucleocapsid Protein Binds to FcγRII and Inhibits Human B Cell Antibody Production." Journal of Experimental Medicine 186, no. 2 (July 21, 1997): 269–78. http://dx.doi.org/10.1084/jem.186.2.269.

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Despite the development of an efficient specific immune response during measles virus (MV) infection, an immunosuppression occurs contributing to secondary infections. To study the role of nucleocapsid protein (NP) in MV-induced immunosuppression, we produced recombinant MV NP. Purified recombinant NP exhibited biochemical, antigenic, and tridimensional structure similar to viral NP. By flow cytometry, we showed that viral or recombinant NP bound to human and murine B lymphocytes, but not to T lymphocytes. This binding was specific, independent of MHC class II expression, and dependent of the B lymphocyte activation state. The murine IIA1.6 B cell line, deficient in the Fc receptor for IgG (FcγRII) expression, did not bind NP efficiently. Transfected IIA1.6 cells expressing either murine FcγRIIb1 or b2, or human FcγRIIa, b1*, or b2 isoforms efficiently bound NP. Furthermore, this binding was inhibited up to 90% by monoclonal antibodies 2.4G2 or KB61 specific for murine and human FcγRII, respectively. Finally, the in vitro Ig synthesis of CD40- or Ig-activated human B lymphocytes in the presence of interleukin (IL)-2 and IL-10 was reduced by 50% in the presence of recombinant NP. These data demonstrate that MV NP binds to human and murine FcγRII and inhibits in vitro antibody production, and therefore suggests a role for NP in MV-induced immunosuppression.

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Murray, S. M., L. J. Picker, M. K. Axthelm, and M. L. Linial. "Expanded Tissue Targets for Foamy Virus Replication with Simian Immunodeficiency Virus-Induced Immunosuppression." Journal of Virology 80, no. 2 (January 15, 2006): 663–70. http://dx.doi.org/10.1128/jvi.80.2.663-670.2006.

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ABSTRACT Foamy viruses (FV) are the oldest known genus of retroviruses and have persisted in nonhuman primates for over 60 million years. FV are efficiently transmitted, leading to a lifelong nonpathogenic infection. Transmission is thought to occur through saliva, but the detailed mechanism is unknown. Interestingly, this persistent infection contrasts with the rapid cytopathicity caused by FV in vitro, suggesting a host defense against FV. To better understand the tissue specificity of FV replication and host immunologic defense against FV cytopathicity, we quantified FV in tissues of healthy rhesus macaques (RM) and those severely immunosuppressed by simian immunodeficiency virus (SIV). Contrary to earlier findings, we find that all immunocompetent animals consistently have high levels of viral RNA in oral tissues but not in other tissues examined, including the small intestine. Strikingly, abundant viral transcripts were detected in the small intestine of all of the SIV-infected RM, which has been shown to be a major site of SIV (and human immunodeficiency virus)-induced CD4+ T-cell depletion. In contrast, there was a trend to lower viral RNA levels in oropharyngeal tissues of SIV-infected animals. The expansion of FV replication to the small intestine but not to other CD4+ T-cell-depleted tissues suggests that factors other than T-cell depletion, such as dysregulation of the jejunal microenvironment after SIV infection, likely account for the expanded tissue tropism of FV replication.

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Koga, Ritsuko, Shinji Ohno, Satoshi Ikegame, and Yusuke Yanagi. "Measles Virus-Induced Immunosuppression in SLAM Knock-In Mice." Journal of Virology 84, no. 10 (March 3, 2010): 5360–67. http://dx.doi.org/10.1128/jvi.02525-09.

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ABSTRACT Measles virus (MV) causes transient severe immunosuppression in patients, which may lead to secondary viral and bacterial infections, largely accounting for measles-related morbidity and mortality. MV is known to infect immune cells by using the human signaling lymphocyte activation molecule (SLAM; also called CD150) as a cellular receptor, but the mechanism by which MV causes immunosuppression is not well understood. We show that MV infection of SLAM knock-in mice, in which the V domain of mouse SLAM was replaced by the V domain of human SLAM, crossed with alpha/beta-interferon receptor knockout mice, reproduced many immunological alterations observed in human patients. These included lymphopenia, inhibition of T-cell proliferation and antibody production, increased production of the Th2 cytokine interleukin-4 (IL-4) and the immunosuppressive cytokine IL-10, and suppression of contact hypersensitivity. Gross redistribution of lymphocytes among lymphoid tissues was not apparent in infected mice, nor was an increase of regulatory T cells. The numbers of lymphocytes in lymph nodes remained almost unchanged after MV infection, despite enhanced apoptosis, suggesting that lymph nodes were replenished with lymphocytes from the peripheral blood, which may have contributed to the observed lymphopenia in the spleen. Blocking of IL-10 by use of an anti-IL-10 receptor antibody ameliorated suppression of contact hypersensitivity in infected mice. These results indicate that SLAM knock-in mice lacking the expression of the alpha/beta-interferon receptor serve as a useful small animal model with which to elucidate MV-induced immunosuppression.

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Dissertations / Theses on the topic "Immunology; Immunosuppression; Viral infection"

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Arnaout, Ramy A. "Mathematical models of antiviral immunity." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325989.

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Noor, Iffat. "Immunosuppression in Atlantic salmon by an extracellular protein of Aeromonas salmonicida." Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361746.

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Lissauer, Samantha Mary. "Modelling hepatitis C viral host interaction and co-infection." Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/8774/.

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Hepatitis C Virus (HCV) is a clinically important infection that leads to chronic liver disease and Human Immunodeficiency Virus (HIV) co-infected patients have more rapid progression to severe liver disease and show higher rates of HCV vertical transmission. Hepatocytes are a highly differentiated cell type and support low level HCV replication. Most studies of the viral life cycle use de-differentiated hepatoma cell lines, which are highly permissive. The mechanism behind this difference is poorly understood. We show that dimethylsulfoxide (DMSO) differentiated Huh-7 cells have a 100-fold reduction in permissivity to HCV infection. We confirm that these cells are differentiated and upregulate key liver specific markers including miR122. They are metabolically active and have intact innate signaling pathways in response to infection. We observed a 10-fold reduction in the initiation of replication and a 10-fold loss in extra-cellular particle infectivity. In contrast cell-to-cell dissemination rates were comparable and cell-contact dependent infection of differentiated cells can overcome the restrictions seen in cell-free infection. HCV cell-to-cell transmission can also be mediated by other cell types. T cells are the primary cell supporting HIV-1 infection. We have shown that HCV can bind primary and immortalized T cells and trans-infect hepatoma cells. This requires replicating HIV but is independent of co-receptor engagement. HIV-1 infection of CD4+ T cells induces a significant increase in HCV trans-infection by increased viral binding. T cells provide a vehicle for HIV-1 to promote HCV infectivity, transmission and persistence.

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Huang, Kenneth Hsing-Chung. "Immune correlates of viral control in chronic HIV infection." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111908.

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There are currently an estimated 33.2 million people living with human immunodeficiency virus (HIV) worldwide. For these individuals, long-term use of combination antiretroviral therapy (cART) is not feasible for a variety of reasons including major adverse complications, multi-drug resistance, poor adherence, and high cost. Hence, development of novel therapeutic strategies that can reduce the life-long dependency on cART is highly desired. In order to develop effective therapeutic strategies such as a therapeutic vaccine, we need to have a greater understanding of the immune correlates of viral control in chronic HIV infection. In this thesis, we used treatment interruption (TI) as a tool to test the efficacy of several therapeutic approaches and immune parameters for their association with effective control of viral replication.
In Chapter 2 we showed that cART intensification and Remune vaccination resulted in reduced viral load (VL) plateau during sequential TIs. Although HIV-specific immune responses measured by interferon-gamma (IFN-gamma) enzyme-linked immunospot assay (ELISPOT) increased in the same time frame, neither their breadth nor magnitude correlated with the decrease in VL plateau. In Chapter 3 the effect of ALVAC-vCP1425 plus Remune vaccination on HIV proteome-wide HIV-specific responses was monitored using a dual color IFN-gamma/interleukin-2 (IL-2) ELISPOT assay. We observed an increase in the magnitude of HIV-specific IFN-gamma/IL-2 responses, as well as in the breadth of Gag-specific IFN-gamma responses in the vaccinated groups compared to placebo groups. A shift towards an increased contribution of Gag-specific responses to total HIV-specific vaccine induced immune response was associated with longer delay to viral rebound during TI. In Chapters 4 and 5, we examined baseline pre-TI immune parameters and their association with viral rebound and CD4 count change during TI in HIV-infected individuals in the chronic phase of infection experiencing virologic failure before TI (Chapter 4) or with different levels of VL control while on therapy prior to TI (Chapter 5). We saw that chronic antigen stimulation from persistent viremia as well as co-infections such as with cytomegalovirus are associated with T-cell senescence, which may result in less favourable clinical outcomes during TI.
Consequently, results from this thesis contribute to further understanding of immune correlates of viral control in chronic HIV infection. New therapeutic vaccines and interventions should induce polyfunctional HIV-specific immune responses, broad Gag-specific immune responses, as well as reducing chronic antigen stimulation to prevent irreversible T-cell exhaustion. Taken together, these insights could potentially lead to the development of novel treatment interventions that could effectively control viral replication off cART.

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Lin, Adora A. "The CD4+ T cell response to CNS viral infection." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1235330516.

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Dhenni, Rama B. S. "Role of Granzyme B in the Susceptibility to Secondary Bacterial Infection after Viral Infection." University of Cincinnati / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1460446984.

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Stacey, Maria A. "Investigation of mammalian and viral Interleukin-10 family members during cytomegalovirus infection." Thesis, Cardiff University, 2012. http://orca.cf.ac.uk/40250/.

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Human cytomegalovirus (HCMV) infection in newborns and immunocompromised individuals with immature or deficient immune systems can cause life-threatening diseases. The clinical and subsequent economical burden of HCMV infection led the US Institute of Medicine designating a vaccine for HCMV as the highest level of priority. Complex virus-host interactions have developed over millions of years of co-evolution, making the understanding of the pathogenesis of HCMV disease particularly challenging. Consequently, a crucial factor in aiding the development of effective vaccinations and therapies to significantly reduce morbidity and mortality associated with HCMV infection is elucidating what immune mechanisms contribute to/impede protection against infection. For example, is the induction of immunomodulatory agents such as cytokines beneficial or harmful to the host during infection? Given the known immunosuppressive properties of one such cytokine, interleukin-10 (IL-10), in conjunction with the evolutionary acquisition by HCMV of its own IL-10 homologue, I hypothesised that mammalian- and viral-IL-10 suppress protective immunity during acute CMV infection. Utilising a mouse model of CMV infection, I revealed a surprising antiviral role for IL-10 during acute infection in vivo, which was achieved via limitation of activation-induced death of NK cells. The IL-10-related cytokine interleukin-22 (IL-22) provides critical protection against certain infectious agents and I therefore hypothesised that IL-22 provides protective immunity during acute CMV infection. Utilising the murine infection model once more, I discovered a tissue-specific antiviral role for IL-22 during acute infection in vivo and made the surprising finding that neutrophils play a protective role during infection. I also demonstrated that neutrophils can directly inhibit viral replication in vitro. Thus, novel insights into cytokine biology in the context of viral infections in vivo revealed by these studies highlighted important considerations for future research into herpesvirus infections, and has major implications for the treatment of this important infectious disease.

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Levitskaya, Jelena Vladimirovna. "T-cell mediated control of Epstein-Barr virus infection : viral mechanisms of immune escape /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3335-9/.

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Fernandez, Maria Helen. "The role of viral variation on CD4âº T cell recognition in HIV-1." Thesis, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325677.

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Mays, Jacqueline Wiesehan. "Psychsocial Stress Modulation of the Murine Anti-Viral Immune Response During a Primary Influenza Infection and the Impact on Immunologic Memory." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1241712390.

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Books on the topic "Immunology; Immunosuppression; Viral infection"

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Friedman, Herman, Thomas W. Klein, and John J. Madden. Neuroimmune circuits, drugs of abuse, and infectious diseases. New York: Kluwer Academic, 2002.

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Norbert, Gilmore, Wainberg Mark A, Medical Research Council (Canada), Canada. National Advisory Committee on AIDS., and Workshop on Viral Mechanisms of Immunosuppression (1984 : Montréal, Quebec), eds. Viral mechanisms of immunosuppression: Proceedings of a workshop. New York: Liss, 1985.

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GILMORE, N. Gilmore Viral Mechanisms of Immunosuppression. John Wiley & Sons Inc, 1985.

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Kotton, Camille Nelson. Infection. Edited by Jeremy R. Chapman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0284_update_001.

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The immunosuppression which makes organ transplantation possible increases the risk of infections, both ordinary and opportunistic. The accurate diagnosis and management of infection after organ transplantation reduces morbidity and improves survival. Infections can be acquired in the hospital (i.e. nosocomial infections), from the transplant itself, from the blood product donor, from reactivation of latent infection in the host or from community exposure. Although viral infections are the most common, bacterial, fungal, and parasitic infections are also seen. While the intensity of immunosuppression is at its highest for a year after solid organ transplant, most opportunistic infections occur in the first 6 months.

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Burton, Dennis R. Antibodies in Viral Infection (Current Topics in Microbiology and Immunology). Springer, 2001.

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Chemokines and Viral Infection (Current Topics in Microbiology and Immunology). Springer, 2006.

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Aging, Immunity, and Infection. Springer-Verlag: New York, 2009.

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Albright, Joseph F. Aging, Immunity, and Infection. Humana, 2012.

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Fungal Infections in the Immunocompromised Patient (Infectious Disease and Therapy). Informa Healthcare, 2005.

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1947-, Wingard John R., and Anaissie Elias J, eds. Fungal infections in the immunocompromised patient. Boca Raton: Taylor & Francis, 2005.

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Book chapters on the topic "Immunology; Immunosuppression; Viral infection"

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Kawamura, Tatsuyoshi. "Viral Infection." In Immunology of the Skin, 295–324. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55855-2_19.

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Kurstak, Edouard. "Immunology of hepatitis B virus infection." In Viral Hepatitis, 105–10. Vienna: Springer Vienna, 1993. http://dx.doi.org/10.1007/978-3-7091-4437-4_13.

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Sissons, J. G. P. "The Immunopathology of Viral and Bacterial Infections." In Immunology of Infection, 133–57. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1430-1_7.

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Hierholzer, T. C. "Rapid Diagnosis of Viral Infection." In Rapid Methods and Automation in Microbiology and Immunology, 556–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76603-9_66.

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Roberts, Hannah, and Stuart E. Turvey. "Predisposition to Severe Viral Infection, STAT2 Deficiency." In Encyclopedia of Medical Immunology, 1–3. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-9209-2_52-1.

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Roberts, Hannah, and Stuart E. Turvey. "Predisposition to Severe Viral Infection, MCM4 Deficiency." In Encyclopedia of Medical Immunology, 1–4. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-9209-2_53-1.

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Roberts, Hannah, and Stuart E. Turvey. "Predisposition to Severe Viral Infection, STAT2 Deficiency." In Encyclopedia of Medical Immunology, 546–49. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-8678-7_52.

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Roberts, Hannah, and Stuart E. Turvey. "Predisposition to Severe Viral Infection, MCM4 Deficiency." In Encyclopedia of Medical Immunology, 543–46. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-8678-7_53.

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Ng, Cherie T., and Michael B. A. Oldstone. "IL-10: Achieving Balance During Persistent Viral Infection." In Current Topics in Microbiology and Immunology, 129–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-43492-5_6.

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Ludewig, B. "Dendritic Cell Vaccination and Viral Infection — Animal Models." In Current Topics in Microbiology and Immunology, 199–214. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-662-06508-2_9.

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Conference papers on the topic "Immunology; Immunosuppression; Viral infection"

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Shakhgildyan, V. I., M. S. Yadrikhinskaya, А. А. Orlovsky, О. Y. Shipulina, E. A. Domonova, and Е. В. Yarovaya. "CYTOMEGALOVIRUS DNA CONCENTRATION IN BIOLOGICAL SAMPLES AS A KEY TO THE DIAGNOSIS OF CMV PNEUMONIA IN HIV-INFECTED PATIENTS." In Молекулярная диагностика и биобезопасность – 2020. ФБУН Центральный НИИ эпидемиологии Роспотребнадзора, 2020. http://dx.doi.org/10.36233/978-5-9900432-9-9-86.

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Abstract:

According to examination and follow-up results of 5485 HIV-positive hospitalized patients (3333 of which were diagnosed with AIDS) we have identified the frequency of clinically evident CMV-infection as well as the frequency and character of CMV related lung disease. Statistically significant correlation between viral load, degree of immunosuppression, CMV replication rate and CMV pneumonia development risk has been determined. Qualitative PCR assay for CMV DNA in plasma and respiratory samples was found to have high sensitivity and low specificity for diagnosing CMV-pneumonia. We identified quantitative PCR CMV DNA values in blood cells, plasma, bronchoalveolar lavage, bronchi samples and sputum that confirm the diagnosis of CMV pneumonia with 95% and 99% probability, and exclude CMV related lung damage in HIV patients with 90% and 99% probability.

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