Relevant bibliographies by topics / Cytomegaloviruses

Academic literature on the topic 'Cytomegaloviruses'

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Published: 4 June 2021
Last updated: 31 July 2024

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Journal articles on the topic "Cytomegaloviruses"

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Flores-Martínez, Yulia Alejandra, Vu Thuy Khanh Le-Trilling, and Mirko Trilling. "Nedd8-Activating Enzyme Is a Druggable Host Dependency Factor of Human and Mouse Cytomegalovirus." Viruses 13, no. 8 (August 14, 2021): 1610. http://dx.doi.org/10.3390/v13081610.

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Human cytomegalovirus causes diseases in individuals with insufficient immunity. Cytomegaloviruses exploit the ubiquitin proteasome pathway to manipulate the proteome of infected cells. The proteasome degrades ubiquitinated proteins. The family of cullin RING ubiquitin ligases (CRL) regulates the stability of numerous important proteins. If the cullin within the CRL is modified with Nedd8 (“neddylated”), the CRL is enzymatically active, while CRLs lacking Nedd8 modifications are inactive. The Nedd8-activating enzyme (NAE) is indispensable for neddylation. By binding to NAE and inhibiting neddylation, the drug MLN4924 (pevonedistat) causes CRL inactivation and stabilization of CRL target proteins. We showed that MLN4924 elicits potent antiviral activity against cytomegaloviruses, suggesting that NAE might be a druggable host dependency factor (HDF). However, MLN4924 is a nucleoside analog related to AMP, and the antiviral activity of MLN4924 may have been influenced by off-target effects in addition to NAE inhibition. To test if NAE is indeed an HDF, we assessed the novel NAE inhibitor TAS4464 and observed potent antiviral activity against mouse and human cytomegalovirus. Additionally, we raised an MLN4924-resistant cell clone and showed that MLN4924 as well as TAS4464 lose their antiviral activity in these cells. Our results indicate that NAE, the neddylation process, and CRLs are druggable HDFs of cytomegaloviruses.
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Khan, Taimoor, Abbas Khan, Syed Nouman Nasir, Sajjad Ahmad, Syed Shujait Ali, and Dong-Qing Wei. "CytomegaloVirusDb: Multi-omics knowledge database for cytomegaloviruses." Computers in Biology and Medicine 135 (August 2021): 104563. http://dx.doi.org/10.1016/j.compbiomed.2021.104563.

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McCormick, A. Louise, Christopher D. Meiering, Geoffrey B. Smith, and Edward S. Mocarski. "Mitochondrial Cell Death Suppressors Carried by Human and Murine Cytomegalovirus Confer Resistance to Proteasome Inhibitor-Induced Apoptosis." Journal of Virology 79, no. 19 (October 1, 2005): 12205–17. http://dx.doi.org/10.1128/jvi.79.19.12205-12217.2005.

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ABSTRACT Human cytomegalovirus carries a mitochondria-localized inhibitor of apoptosis (vMIA) that is conserved in primate cytomegaloviruses. We find that inactivating mutations within UL37x1, which encodes vMIA, do not substantially affect replication in TownevarATCC (Towne-BAC), a virus that carries a functional copy of the betaherpesvirus-conserved viral inhibitor of caspase 8 activation, the UL36 gene product. In Towne-BAC infection, vMIA reduces susceptibility of infected cells to intrinsic death induced by proteasome inhibition. vMIA is sufficient to confer resistance to proteasome inhibition when expressed independent of viral infection. Murine cytomegalovirus m38.5, whose position in the viral genome is analogous to UL37x1, exhibits mitochondrial association and functions in much the same manner as vMIA in inhibiting intrinsic cell death. This work suggests a common role for vMIA in rodent and primate cytomegaloviruses, modulating the threshold of virus-infected cells to intrinsic cell death.
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Staczek, J. "Animal cytomegaloviruses." Microbiological Reviews 54, no. 3 (1990): 247–65. http://dx.doi.org/10.1128/mmbr.54.3.247-265.1990.

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Staczek, J. "Animal cytomegaloviruses." Microbiological Reviews 54, no. 3 (1990): 247–65. http://dx.doi.org/10.1128/mr.54.3.247-265.1990.

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Bahr, Udo, and Gholamreza Darai. "Analysis and Characterization of the Complete Genome of Tupaia (Tree Shrew) Herpesvirus." Journal of Virology 75, no. 10 (May 15, 2001): 4854–70. http://dx.doi.org/10.1128/jvi.75.10.4854-4870.2001.

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ABSTRACT The tupaia herpesvirus (THV) was isolated from spontaneously degenerating tissue cultures of malignant lymphoma, lung, and spleen cell cultures of tree shrews (Tupaia spp.). The determination of the complete nucleotide sequence of the THV strain 2 genome resulted in a 195,857-bp-long, linear DNA molecule with a G+C content of 66.5%. The terminal regions of the THV genome and the loci of conserved viral genes were found to be G+C richer. Furthermore, no large repetitive DNA sequences could be identified. This is in agreement with the previous classification of THV as the prototype species of herpesvirus genome group F. The search for potential coding regions resulted in the identification of 158 open reading frames (ORFs) regularly distributed on both DNA strands. Seventy-six out of the 158 ORFs code for proteins that are significantly homologous to known herpesvirus proteins. The highest homologies found were to primate and rodent cytomegaloviruses. Biological properties, protein homologies, the arrangement of conserved viral genes, and phylogenetic analysis revealed that THV is a member of the subfamilyBetaherpesvirinae. The evolutionary lineages of THV and the cytomegaloviruses seem to have branched off from a common ancestor. In addition, it was found that the arrangements of conserved genes of THV and murine cytomegalovirus strain Smith, both of which are not able to form genomic isomers, are colinear with two different human cytomegalovirus (HCMV) strain AD169 genomic isomers that differ from each other in the orientation of the long unique region. The biological properties and the high degree of relatedness of THV to the mammalian cytomegaloviruses allow the consideration of THV as a model system for investigation of HCMV pathogenicity.
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Becker, Tanja, Vu Le-Trilling, and Mirko Trilling. "Cellular Cullin RING Ubiquitin Ligases: Druggable Host Dependency Factors of Cytomegaloviruses." International Journal of Molecular Sciences 20, no. 7 (April 2, 2019): 1636. http://dx.doi.org/10.3390/ijms20071636.

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Human cytomegalovirus (HCMV) is a ubiquitous betaherpesvirus that frequently causes morbidity and mortality in individuals with insufficient immunity, such as transplant recipients, AIDS patients, and congenitally infected newborns. Several antiviral drugs are approved to treat HCMV infections. However, resistant HCMV mutants can arise in patients receiving long-term therapy. Additionally, side effects and the risk to cause birth defects limit the use of currently approved antivirals against HCMV. Therefore, the identification of new drug targets is of clinical relevance. Recent work identified DNA-damage binding protein 1 (DDB1) and the family of the cellular cullin (Cul) RING ubiquitin (Ub) ligases (CRLs) as host-derived factors that are relevant for the replication of human and mouse cytomegaloviruses. The first-in-class CRL inhibitory compound Pevonedistat (also called MLN4924) is currently under investigation as an anti-tumor drug in several clinical trials. Cytomegaloviruses exploit CRLs to regulate the abundance of viral proteins, and to induce the proteasomal degradation of host restriction factors involved in innate and intrinsic immunity. Accordingly, pharmacological blockade of CRL activity diminishes viral replication in cell culture. In this review, we summarize the current knowledge concerning the relevance of DDB1 and CRLs during cytomegalovirus replication and discuss chances and drawbacks of CRL inhibitory drugs as potential antiviral treatment against HCMV.
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Forrest, Calum, Ariane Gomes, Matthew Reeves, and Victoria Male. "NK Cell Memory to Cytomegalovirus: Implications for Vaccine Development." Vaccines 8, no. 3 (July 20, 2020): 394. http://dx.doi.org/10.3390/vaccines8030394.

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Natural killer (NK) cells are innate lymphoid cells that recognize and eliminate virally-infected and cancerous cells. Members of the innate immune system are not usually considered to mediate immune memory, but over the past decade evidence has emerged that NK cells can do this in several contexts. Of these, the best understood and most widely accepted is the response to cytomegaloviruses, with strong evidence for memory to murine cytomegalovirus (MCMV) and several lines of evidence suggesting that the same is likely to be true of human cytomegalovirus (HCMV). The importance of NK cells in the context of HCMV infection is underscored by the armory of NK immune evasion genes encoded by HCMV aimed at subverting the NK cell immune response. As such, ongoing studies that have utilized HCMV to investigate NK cell diversity and function have proven instructive. Here, we discuss our current understanding of NK cell memory to viral infection with a focus on the response to cytomegaloviruses. We will then discuss the implications that this will have for the development of a vaccine against HCMV with particular emphasis on how a strategy that can harness the innate immune system and NK cells could be crucial for the development of a vaccine against this high-priority pathogen.
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Marschall, Manfred, Thomas Stamminger, Andreas Urban, Steffen Wildum, Helga Ruebsamen-Schaeff, Holger Zimmermann, and Peter Lischka. "In VitroEvaluation of the Activities of the Novel Anticytomegalovirus Compound AIC246 (Letermovir) against Herpesviruses and Other Human Pathogenic Viruses." Antimicrobial Agents and Chemotherapy 56, no. 2 (November 21, 2011): 1135–37. http://dx.doi.org/10.1128/aac.05908-11.

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ABSTRACTAIC246 (letermovir) is a potent anticytomegalovirus drug in clinical development. Here, we report a consistent antiviral efficacy of AIC246 against human cytomegalovirus laboratory strains, clinical isolates, and virus variants resistant to approved drugs. Furthermore, we describe a remarkable selectivity of AIC246 for human cytomegaloviruses compared to that of other alpha-, beta-, or gammaherpesviruses or nonrelated pathogenic viruses, including adeno-, hepadna-, retro-, orthomyxo-, and flaviviruses. Our data confirm and support an excellent and selective anticytomegaloviral activity of AIC246.
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Bierle, Craig J., Kaitlyn M. Anderholm, Jian Ben Wang, Michael A. McVoy, and Mark R. Schleiss. "Targeted Mutagenesis of Guinea Pig Cytomegalovirus Using CRISPR/Cas9-Mediated Gene Editing." Journal of Virology 90, no. 15 (May 25, 2016): 6989–98. http://dx.doi.org/10.1128/jvi.00139-16.

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ABSTRACTThe cytomegaloviruses (CMVs) are among the most genetically complex mammalian viruses, with viral genomes that often exceed 230 kbp. Manipulation of cytomegalovirus genomes is largely performed using infectious bacterial artificial chromosomes (BACs), which necessitates the maintenance of the viral genome inEscherichia coliand successful reconstitution of virus from permissive cells after transfection of the BAC. Here we describe an alternative strategy for the mutagenesis of guinea pig cytomegalovirus that utilizes clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9)-mediated genome editing to introduce targeted mutations to the viral genome. Transient transfection and drug selection were used to restrict lytic replication of guinea pig cytomegalovirus to cells that express Cas9 and virus-specific guide RNA. The result was highly efficient editing of the viral genome that introduced targeted insertion or deletion mutations to nonessential viral genes. Cotransfection of multiple virus-specific guide RNAs or a homology repair template was used for targeted, markerless deletions of viral sequence or to introduce exogenous sequence by homology-driven repair. As CRISPR/Cas9 mutagenesis occurs directly in infected cells, this methodology avoids selective pressures that may occur during propagation of the viral genome in bacteria and may facilitate genetic manipulation of low-passage or clinical CMV isolates.IMPORTANCEThe cytomegalovirus genome is complex, and viral adaptations to cell culture have complicated the study of infectionin vivo. Recombineering of viral bacterial artificial chromosomes enabled the study of recombinant cytomegaloviruses. Here we report the development of an alternative approach using CRISPR/Cas9-based mutagenesis in guinea pig cytomegalovirus, a small-animal model of congenital cytomegalovirus disease. CRISPR/Cas9 mutagenesis can introduce the same types of mutations to the viral genome as bacterial artificial chromosome recombineering but does so directly in virus-infected cells. CRISPR/Cas9 mutagenesis is not dependent on a bacterial intermediate, and defined viral mutants can be recovered after a limited number of viral genome replications, minimizing the risk of spontaneous mutation.
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Dissertations / Theses on the topic "Cytomegaloviruses"

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Walker, Douglas Gordon. "Characterization of immediate-early and early proteins of murine cytomegalovirus synthesized in permissive and nonpermissive cells." Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/25985.

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The gene products produced by murine cytomegalovirus (MCMV) in infected cells prior to viral DNA synthesis are believed to control the interaction of the virus with the cells, determining whether a permissive infection results, with virus replication, or whether further virus gene expression is inhibited, resulting in a latent or abortive infection. The aim of this study was to characterize the early viral gene products that are produced in permissive and nonpermissive cells. The proteins produced in 3T3-L1 cells, permissively infected with MCMV, during the first six hours of infection (the period prior to viral DNA replication) were characterized by polyacrylamide gel electrophoresis. Ten of the proteins were classified as immediate-early (IE) and seven as early according to their time of synthesis and also according to their synthesis in the presence of actinomycin D following the reversal of a cycloheximide mediated block in protein synthesis. The estimated molecular weights ranged from 28K - 100K. The synthesis of a dominant IE protein of 100K was significantly increased, after the reversal of a cycloheximide block, compared to unenhanced conditions. The synthesis of two other major IE proteins of 96K and 89K were also significantly enhanced by this treatment. The 100K and 89K proteins partitioned with the nuclear, cytoplasmic and cytoskeletal fractions, while the 96K protein partitioned more strongly with the nuclei. These proteins were phosphorylated. The other IE proteins were synthesized in lesser amounts. The major early proteins, which had molecular weights of 39K and 36K, were also phosphorylated and were exclusively nucleus-associated. A number of the IE and early proteins had affinity for native and denatured DNA-cellulose. The same major IE and early proteins were identified in nonpermissively infected J774A.1 macrophage cells. Although 0.6% of these cells became permissively infected with MCMV and the rest appeared to be nonpermissively infected, viral DNA and late protein synthesis was not detected. The major difference between the proteins produced in 3T3-L1 cells and J774A.1 cells was the affinity of the 96K protein for denatured DNA-cellulose, which was only observed when the protein was synthesized in J774A.1 cells. The main IE and early MCMV induced proteins were also synthesized in nonpermissively infected human fibroblast cells. The only difference between the proteins produced in these cells and 3T3-L1 cells was that the 100K IE protein appeared to have a greater nuclear-affinity, when produced in the human fibroblasts, than was found when synthesized in infected 3T3-L1 cells. In conclusion, a larger number of IE and early MCMV-induced proteins were identified in infected cells than had been previously characterized. There was no evidence of restricted MCMV gene expression occurring in two different cell types that were nonpermissively infected. This appeared to indicate that, in the nonpermissive experiments described, MCMV replication was inhibited at the stage of viral DNA synthesis.
Medicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
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Vellani, Nina N. "Analyses of immediate early and early transcripts and major early region, E10, of murine cytomegalovirus." Thesis, University of British Columbia, 1991. http://hdl.handle.net/2429/32374.

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Murine cytomegalovirus (MCMV) is used as a biological model for human cytomegalovirus (HCMV). Latency, persistence and reactivation are same of the important aspects of the murine model that share analogies with human CMV infections. In order to elucidate the molecular mechanisms leading to these events, in-depth analyses of the murine model are required at the transcriptional level. During the MCMV replication cycle, there is a sequential expression of different regions of the viral genome, hence the transcripts are divided into three kinetic classes; the immediate early (IE), early (E) and late (L). This study presents the analyses of MCMV (Smith strain) transcripts of the major IE and E transcriptional units, and a more detail analysis of one of the major E regions, E10. The IE and E transcripts were studied by probing them with Ctoitplementary DNAs (cDNAs). The cDNAs were prepared from mRNA isolated from the IE and E phases of the viral replication cycle and cloned into the bacteriophage Lambda gt10. Ten E cDNAs were mapped to specific locations of the virus genome, and these represented transcripts from the major E regions in Hindlll fragments A, B, E, F, and I-J. Five E cDNAs, each representing a different major E region, and two IE cDNAs representing the major IE region, were applied as probes in one of the studies to determine the relative transcript levels during the course of infection of 3T3L1 fibroblast cells with MCMV. The major E transcriptional units were investigated further in a study where Northern blots of RNAs, isolated from different phases of the viral replication cycle, were probed with the five E cDNAs. This study revealed transcripts that were temporally regulated since they were present only during the E and usually L phases of the viral replication cycle. In addition, the quantities of these transcripts varied depending on the phase. However, all five cDNAs detected more than one transcript which indicates complex splicing events, overlapping genes, multiple initiation sites and/or the presence of gene(s) in the complementary DNA strand. One of the E cDNAs, E10, corresponding to a transcript from a major E region of Hindlll fragment I-J, was selected for further analysis. The E10 cDNA detected four transcripts of 9.5, 6.9, 4.7 and 2.1 kb in size, which were found to be transcribed from the same DNA strand. The DNA sequence of this E10 cDNA was determined and shown to contain 3223 nucleotides, however it lacked a polyadenylation signal and a poly A tract at the 3' end. The missing 3' terminus, designated as E10-A, was isolated using the polymerase chain reaction (PCJR) method and its DNA sequence of 1422 nucleotides was also determined. The combined sequence of E10 and E10-A (total of 4606 nucleotides) was designated as E10-C and is presented in this thesis. The E10-C cDNA (4.6kbp) most likely represents the 4.7 kb transcript. The E10-C cDNA sequence has one minor and one major open reading frame (ORF). The minor ORF is initiated by the first ATG triplet (nucleotide position 114) while the major ORF is initiated by the second triplet (nucleotide position 155). Since the sequence preceeding the second ATG triplet is in "good context" with regard to the translation initiation consensus sequence, it is most likely that the major ORF is translated. The major ORF (3600 bases) encodes a 1200 amino acid polypeptide, the putative E10 protein of approximately 135 kd in size. A protein close to that size was detected in one of the experiments in which RNAs, that were hybrid-selected by the E10 cDNA and eluted, were translated in vitro. The putative E10 protein lacks homology with any other protein in the data banks (SWISSPRT and GENPEPT). Portions of the viral genomic fragments Hindlll I and J were also sequenced to reveal the orientation of the gene coding for the E10 cDNA and its related transcripts.
Medicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
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Kansara, Viral Mitra Ashim K. "Ocular delivery of peptide ganciclovir prodrugs following subconjunctival injection evaluation of episcleral drug delivery approach /." Diss., UMK access, 2007.

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Thesis (Ph. D.)--School of Pharmacy. University of Missouri--Kansas City, 2007.
"A dissertation in pharmaceutical sciences and pharmacology." Advisor: Ashim K. Mitra. Typescript. Vita. Title from "catalog record" of the print edition Description based on contents viewed May 23, 2008. Includes bibliographical references (leaves 210-225). Online version of the print edition.
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Chaudry, Tanya N. "Characterisation of PP71 homologues encoded by mammalian cytomegaloviruses." Thesis, Connect to e-thesis, 2008. http://theses.gla.ac.uk/377/.

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Thesis (Ph.D.) - University of Glasgow, 2008.
Ph.D. thesis submitted to the Division of Virology, Institute of Biomedical and Life Sciences, University of Glasgow, 2008. Includes bibliographical references. Print version also available.
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Jun, Min Medical Sciences Faculty of Medicine UNSW. "Analysis of human cytomegalovirus susceptibility to novel antiviral agents." Publisher:University of New South Wales. Medical Sciences, 2008. http://handle.unsw.edu.au/1959.4/41443.

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Human cytomegalovirus (CMV) is a significant infectious agent causing disease in immunocompromised HIV-infected patients, transplant recipients, and neonates. The current antiviral therapeutic strategy against CMV is limited in its utility due to the inherent toxicity and lack of bioavailability of currently available anti-CMV agents, ganciclovir (GCV), cidofovir (CDV), and foscarnet (FOS). The development of the prodrug of GCV, valganciclovir (val-GCV), has vastly improved the bioavailability profile of GCV. However, val-GCV demonstrates limited effectiveness against tissue-invasive CMV diseases as side effects involved with traditional intravenously administered GCV such as haematologic and reproductive toxicities remain. In addition, the emergence of antiviral resistant CMV mutant strains due to prolonged treatment with currently available antivirals necessitates the development of novel anti-CMV agents with reduced toxicity and improved bioavailability. In this study, select groups of novel compounds were analysed for their potential for further development as anti-CMV agents. Three groups of compounds were identified based on two screening methods which included the computer simulated screening process of compounds known as in silico screening and the traditional method of random screening. The first group of compounds (CATi) were identified by in silico screening against the CMV DNA polymerase catalytic aspartate triad, resulting in the identification of 31 compounds with the potential for inhibitory activity against CMV. The second group of compounds (PRO-i) were identified through in silico screening against the CMV protease, identifying a total of 18 lead compounds exhibiting structural complementarity with CMV protease. The third and final group of compounds (TPEX) were identified through random screening and consisted of plant extracts purified from tropical plants. All three compounds were initially screened for cytotoxicity against human fibroblasts. Plaque reduction assays were performed using compounds with acceptable levels of cytotoxicity to determine the ability of the compounds to inhibit the replication of the laboratory antiviral sensitive CMV strain, Towne. Two of the PRO-i compounds demonstrated good antiviral activity against CMV. Eleven percent (2/18) of the PRO-i compounds inhibited CMV replication, with PRO-i-43 and PRO-i??-44 displaying mean 50% inhibitory concentrations (IC50) of 4.8 ?? 1.2 ??M and 8.04 ??M, respectively. PRO-i-43 and PRO-i-44 are thus good candidates for further development as novel antiviral agents against CMV. The majority of CATi and TPEX compounds displayed significant cytotoxicity against human fibroblasts and compounds with acceptable levels of cytotoxicities did not significantly inhibit CMV replication. However, the identification of compounds with low cytotoxicities provides a good foundation for further development of novel anti-CMV agents with superior antiviral activity. In silico screening against three-dimensional viral protein models is a useful strategy for the identification of novel antiviral agents with the potential for inhibitory activity against CMV. Structural modification to produce potent derivatives of the identified anti-CMV compounds (PRO-i-43 and PRO-i-44) is a good option for the further development of novel antiviral agents against CMV. Such further examination of the identified compounds with anti-CMV activity is required to investigate their activity against not only antiviral sensitive CMV strains but also resistant CMV strains. Further investigations will yield new insights into their target, allowing further identification of compounds with potential anti-CMV activity with pharmaceutical application.
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Andrews, Daniel Mark. "Effects of murine cytomegalovirus infection on dendritic cell functionality and natural killer cell responses." University of Western Australia. Centre for Ophthalmology and Visual Science, 2004. http://theses.library.uwa.edu.au/adt-WU2005.0003.

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Cytomegaloviruses (CMVs) are ubiquitous in nature, having evolved over many millenia with their hosts. While in healthy hosts most infections with CMV are asymptomatic, the virus can cause severe disease in immunocompromised hosts. Thus, the increase in organ transplantation and the HIV/AIDS pandemic have established human CMV (HCMV) as a clinically important pathogen. Indeed, HCMV infections are now the major cause of morbidity and mortality among immunocompromised patients, which has led to more research targeting CMV for effective anti-viral treatment. The discovery that cytomegaloviruses encode several genes which are involved in immune escape has prompted a new area of research, aimed at understanding immune escape mechanisms for exploitation as potential anti-viral therapeutics. By targeting the viral proteins directly, or their receptors in the host, it may be possible to treat CMV disease by agonistic/antagonistic therapy. The first part of this thesis describes the first demonstration of anti-NK1.1 staining in situ to identify NK cells using a modified in vivo perfusion/fixation method. Using this method, we have compared the acute NK1.1+ cellular response to wild-type MCMV infection in the visceral organs of genetically susceptible intra-NK complex recombinant BALB.B6-CT6 (Cmv1s, NK1.1+) mice with resistant C57B⁄J (Cmv1r, NK1.1+) and BALB.B6-Cmv1r mice (Cmv1r, NK1.1+). Expression of viral antigens and the consequences of infection on other cellular subsets, were also analyzed in this study. The data show that in susceptible mice (Cmv1s) MCMV infection is predominent in the marginal zone of splenic white pulp, resulting in local changes in various cellular constituents, including macrophages, NK cells and DC. In the liver, distinct foci of infection were comprised of large numbers of macrophages and NK1.1+ cells surrounding infected cytomegalic cells. In resistant mice (Cmv1r), 6 MCMV infection predominantly affected the red-pulp of the spleen and was associated with increased accumulation of NK1.1+ cells and macrophages at sites of viral infection
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Sumaria, Nital. "The relevance of specific molecular and cellular effectors during murine cytomegalovirus infection." University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0116.

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[Truncated abstract] The design and development of effective anti-viral immunotherapies requires a comprehensive understanding of the cellular and molecular processes that are involved in the generation and regulation of immune responses. The fundamental objective of the immune system is to successfully complete the task of eliminating/controlling the invading pathogen without causing overt pathology. Cytomegaloviruses (CMVs) are large DNA viruses that are able to evade immune attack and persist lifelong within the host. In a healthy host, CMV causes an asymptomatic infection, but in instances of decreased immune functions, such as in newborns, acquired immunodeficiency syndrome (AIDS) patients and transplant recipients, the infection can result in serious morbidity and mortality. Thus, human CMV (HCMV) is a clinically important pathogen and an understanding of the pathogenesis, mechanisms of immune subversion and, importantly the cascade of immune events that ensue following infection is highly relevant. The studies presented in this thesis have provided useful insight into various aspects of viral immunity and it is hoped that they will assist in the design of more effective therapies against viruses of clinical importance. Genetic variability in humans can greatly influence anti-viral immune responses and the outcome of viral infection. ... Furthermore, these studies provide novel evidence that NK cells are also crucial for the control of virus in some organs of susceptible mice during early acute infection. The data reveals that both NK cells and CD8+ T cells utilise perforin- and IFN-? dependent control of MCMV. Furthermore, these studies provide novel evidence that protection mediated by Ly49H+ NK cells in resistant mice is dependent on perforin. Chapter 3 focuses on the biological relevance of Grz during MCMV infection. These studies found that GrzA and GrzB are essential components of the machinery involved in limiting MCMV during acute infection. These analyses also provide the first evidence suggesting that GrzM plays a role, albeit minor, in controlling MCMV replication. Furthermore, the current studies suggest that Grz can mediate direct antiviral activities independent of the induction of cell death in conjunction with perforin. Interestingly, in the absence of both GrzA and GrzB (GrzAB), mice were as susceptible to MCMV infection as perforin-deficient mice. However, unlike perforin-deficient mice, GrzAB-deficient mice controlled and survived the infection. In Chapter 4 the roles of perforin, GrzA and GrzB in anti-viral immunity and immunopathology during MCMV infection were examined. These studies show that NK cell-derived perforin is required to eliminate infected targets as well as activated effector cells, suggesting that NK cells are crucial not only in defensive immunity but also in limiting the immune activation that follows MCMV infection. In summary, the studies presented in this thesis define the significant role played by specific effector molecules in limiting MCMV replication during different stages of this viral infection. Furthermore, these studies provide novel evidence that perforin, GrzA and GrzB play distinct roles in defensive immunity and limiting immunopathology during MCMV infection.
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Chen, Jianliang, and 陈健良. "The inhibitory effects of human cytomegalovirus on megakaryopoiesis : megekaryocytic cells and bone marrow derived mesenchymal stormal cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193520.

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Thrombocytopenia is one of the most common hematologic presentations of active human cytomegalovirus (HCMV) infection, especially in recipients of allogeneic hematopoietic stem cell transplantations and newborns of congenital HCMV infection. However, mechanisms of HCMV-induced thrombocytopenia have not been well understood. The precursor of circulating platelets – megakaryocyte, is derived from hematopoietic stem/progenitor cell in bone marrow. We postulate that inhibition to megakaryocytic development is the major pathogenesis of HCMV-induced thrombocytopenia. Megakaryocytic cells as well as supportive microenvironment in bone marrow are major targets of HCMV infection. Presented study mainly focused on the impacts of HCMV to megakaryocytic cells and multipotent mesenchymal stromal cells (MSCs) - the precursor of bone marrow stromal cells. Based on a megakaryocytic cell model challenged by HCMV in vitro, inhibited megakaryocytic endomitosis, proliferation, and cellular expression were respectively demonstrated as decreased polyploidy population, decreased colony formation, and reduced c-Mpl (thrombopoietin receptor) expressing cells. Evoked apoptosis of megakaryocytic cells was also evidenced with increased phosphatidylserine exposure on cell surface and intracellular caspase-3 activation after HCMV infection. Involvement of mitochondrial-mediated intrinsic apoptosis was further shown as losing JC-1 fluorescent signal in infected megakaryocytic cells. These results suggest that inhibition induced by HCMV is exerted through multiple processes directly affecting the megakaryopoietic development. Functional failure of bone marrow microenvironment was demonstrated in bone marrow derived MSCs infected by HCMV in vitro. Suppressed cytokine production, impaired cellular migration, and hindered differentiation of HCMV-infected MSCs were respectively demonstrated by lowered level of stromal cell-derived factor 1 in culture medium, decreased number of cells passed through a porous membrane in a transwell culture, and reduced differentiated cells in either adipogenic or osteogenic induction cultures. Alongside with these changes, HCMV-induced programmed cell death further contributed to the supportive failure. Autophagic cell death in infected MSCs was demonstrated as massive accumulation of vacuoles with double membrane structure and LC-3b II molecules followed by viability loss. De novo apoptosis was also observed as another process of programmed cell death, shown as increased phosphatidylserine exposure on cell surface and intracellular caspase-3 activation of infected MSCs. Increased programmed cell death appeared to be associated with extensive HCMV replication in MSCs, which was featured with typical cytopathic morphology, expression of viral tegument protein pp65, and massive accumulation of various viral particles including mature virions. Sustained activation of extracellular signal-regulated kinases likely represented a signal transduction network connecting viral expression or replication with programmed cell death. In a “MSCs-dependent” megakaryopoiesis model, HCMV-infected MSCs failed to support survival and maintenance of megakaryocytic cells. Taken together, these results suggest that active HCMV expression or replication inhibits multiple cellular functions and induces multiple processes of programmed cell death of MSCs. Such inhibition compromises supportive functions of bone marrow microenvironment, and subsequently reduces platelet production in an indirect manner. In summary, HCMV suppresses cellular function and induced apoptosis on both megakaryocytic cells and their supportive cells, MSCs. Therefore, the inhibitory effects of HCMV on megakaryopoiesis are operated via both direct and indirect mechanisms.
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Paediatrics and Adolescent Medicine
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Doctor of Philosophy
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9

Bartlett, Emmalene J. "Efficacy and immunological mechanisms of type 1 interferon gene therapy in murine cytomegalovirus." Thesis, Bartlett, Emmalene J. (2002) Efficacy and immunological mechanisms of type 1 interferon gene therapy in murine cytomegalovirus. PhD thesis, Murdoch University, 2002. https://researchrepository.murdoch.edu.au/id/eprint/214/.

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This thesis presents a comparative analysis of the type I Interferon (IFN) subtypes and an evaluation of their potential as DNA vaccines in a model of murine cytomegalovirus (MCMV) infection and disease. MCMV induces acute and chronic phases of myocarditis, a heart disease characterised by an inflammatory cell infiltrate, in susceptible BALB/c mice. The type I IFNs comprise 14 IFN alpha genes in the human and >10 IFN alpha genes in the mouse with a single IFN beta gene in both species, however, the purpose of their multiplicity has remained unclear to date. An extensive panel of murine type I IFN subtype genes, including IFNA1, A2, A4, A5, A6, A9 and B, were sub-cloned into the mammalian expression vector pkCMVint (Vical, Inc.) for expression in BALB/c mice. These DNA constructs express biologically active IFN both in vitro and in vivo with systemic, low level expression persisting in the mouse for up to 4 weeks. The individual type I IFN subtypes differentially affect the immune response to MCMV challenge. IFNA6 proved most efficacious, reducing viral replication and inflammation in the acute and chronic phase of disease. Data suggests this occurs via induction of a Th1-like cytokine and antibody response. Furthermore, IFNA6 inoculation after the acute phase was shown to protect mice from the onset of chronic myocarditis. Characterisation of the immune cell response in IFN-treated, MCMV-infected mice demonstrated that type I IFN subtypes modulate the type of immune cells infiltrating the myocardium during myocarditis. Notably, reduced CD8+ and CD4+ T cells and B cell numbers in the heart was associated with reduced chronic myocarditis. Finally, coadministration of type I IFNs, in particular, IFNA6 and IFNB, synergistically improved immunotherapy against MCMV infection and myocarditis. The findings detailed here highlight the potential for the type I IFNs as DNA vaccines and most importantly, demonstrate that the type I IFNs have differential antiviral and immunomodulatory efficacies in the MCMV model of infection and myocarditis.
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Bartlett, Emmalene J. "Efficacy and immunological mechanisms of type 1 interferon gene therapy in murine cytomegalovirus." Bartlett, Emmalene J. (2002) Efficacy and immunological mechanisms of type 1 interferon gene therapy in murine cytomegalovirus. PhD thesis, Murdoch University, 2002. http://researchrepository.murdoch.edu.au/214/.

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This thesis presents a comparative analysis of the type I Interferon (IFN) subtypes and an evaluation of their potential as DNA vaccines in a model of murine cytomegalovirus (MCMV) infection and disease. MCMV induces acute and chronic phases of myocarditis, a heart disease characterised by an inflammatory cell infiltrate, in susceptible BALB/c mice. The type I IFNs comprise 14 IFN alpha genes in the human and >10 IFN alpha genes in the mouse with a single IFN beta gene in both species, however, the purpose of their multiplicity has remained unclear to date. An extensive panel of murine type I IFN subtype genes, including IFNA1, A2, A4, A5, A6, A9 and B, were sub-cloned into the mammalian expression vector pkCMVint (Vical, Inc.) for expression in BALB/c mice. These DNA constructs express biologically active IFN both in vitro and in vivo with systemic, low level expression persisting in the mouse for up to 4 weeks. The individual type I IFN subtypes differentially affect the immune response to MCMV challenge. IFNA6 proved most efficacious, reducing viral replication and inflammation in the acute and chronic phase of disease. Data suggests this occurs via induction of a Th1-like cytokine and antibody response. Furthermore, IFNA6 inoculation after the acute phase was shown to protect mice from the onset of chronic myocarditis. Characterisation of the immune cell response in IFN-treated, MCMV-infected mice demonstrated that type I IFN subtypes modulate the type of immune cells infiltrating the myocardium during myocarditis. Notably, reduced CD8+ and CD4+ T cells and B cell numbers in the heart was associated with reduced chronic myocarditis. Finally, coadministration of type I IFNs, in particular, IFNA6 and IFNB, synergistically improved immunotherapy against MCMV infection and myocarditis. The findings detailed here highlight the potential for the type I IFNs as DNA vaccines and most importantly, demonstrate that the type I IFNs have differential antiviral and immunomodulatory efficacies in the MCMV model of infection and myocarditis.
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Books on the topic "Cytomegaloviruses"

1

McDougall, James K., ed. Cytomegaloviruses. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74980-3.

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Sinclair, John. Cytomegalovirus protocols. Totowa, N.J: Humana, 2011.

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Yurochko, Andrew D., and William E. Miller, eds. Human Cytomegaloviruses. Totowa, NJ: Humana Press, 2014. http://dx.doi.org/10.1007/978-1-62703-788-4.

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Yurochko, Andrew D., ed. Human Cytomegaloviruses. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1111-1.

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Paolo, Landini Maria, ed. Progress in cytomegalovirus research: Proceedings of the Third International Cytomegalovirus Workshop, Bologna, 11-14 June 1991. Amsterdam: Excerpta Medica, 1991.

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6

Yechiel, Becker, Darai Gholamreza, and Huang E. -S, eds. Molecular aspects of human cytomegalovirus diseases. Berlin: Springer-Verlag, 1993.

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7

Susan, Michelson, and Plotkin Stanley A. 1932-, eds. Multidisciplinary approach to understanding cytomegalovirus disease: Proceedings of the Fourth International Cytomegalovirus Workshop : multidisciplinary approaches to understanding CMV disease, Paris, France, 19-21 April, 1993. Amsterdam: Excerpta Medica, 1993.

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8

D, Sinclair John Ph, ed. Cytomegalovirus protocols. Totowa, N.J: Humana Press, 2000.

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A, Spector Stephen, ed. Ganciclovir therapy for cytomegalovirus infection. New York: M. Dekker, 1991.

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Guibert, Hervé. Cytomegalovirus: A hospitalization diary. New York: Fordham University Press, 2016.

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Book chapters on the topic "Cytomegaloviruses"

1

Ho, Monto. "Nonhuman Cytomegaloviruses." In Cytomegalovirus, 319–26. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4757-9942-2_15.

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Trivizki, Omer, and Zohar Habot-Wilner. "Cytomegaloviruses, Retinitis." In Encyclopedia of Ophthalmology, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-35951-4_1120-1.

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Trivizki, Omer, and Zohar Habot-Wilner. "Cytomegaloviruses, Retinitis." In Encyclopedia of Ophthalmology, 570–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-540-69000-9_1120.

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Beisser, P. S., H. Lavreysen, C. A. Bruggeman, and C. Vink. "Chemokines and Chemokine Receptors Encoded by Cytomegaloviruses." In Current Topics in Microbiology and Immunology, 221–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-77349-8_13.

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Stinski, Mark F. "History of the Molecular Biology of Cytomegaloviruses." In Methods in Molecular Biology, 1–14. Totowa, NJ: Humana Press, 2014. http://dx.doi.org/10.1007/978-1-62703-788-4_1.

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Bauer, Dagmar, Frank Momburg, and Hartmut Hengel. "Manipulation of MHC-encoded proteins by cytomegaloviruses." In Major Histocompatibility Complex, 305–19. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-65868-9_23.

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Spector, D. H. "Molecular Studies on the Cytomegaloviruses of Mice and Men." In Genetic Engineering: Principles and Methods, 199–234. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4973-0_10.

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Ho, Monto. "History of Cytomegalovirus." In Cytomegalovirus, 1–6. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4757-9942-2_1.

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Ho, Monto. "Pathology of Cytomegalovirus Infection." In Cytomegalovirus, 189–204. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4757-9942-2_10.

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Ho, Monto. "Congenital and Perinatal Human Cytomegalovirus Infections." In Cytomegalovirus, 205–27. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4757-9942-2_11.

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Conference papers on the topic "Cytomegaloviruses"

1

Grama, Alina, Claudia Sirbe, Madalina Grigore, Adriana Bungardi, and Tudor L. Pop. "P334 Congenital cytomegalovirus infection." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.683.

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Belyaeva, E. D., and D. R. Fayzullina. "CYTOMEGALOVIRUS MICRORNAS INHIBIT AUTOPHAGY." In OpenBio-2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-231.

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Cytomegalovirus persistence correlates with the aggressiveness of some human cancers. We have shown that the viral microRNA UL70-3P suppresses autophagy in glioblastoma cells. Regulatory molecules both act constitutively and are secreted as part of exosomes to influence the cell microenvironment.
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Andrievskaya, Irina, Nataliya Ishutina, Inna Dovzhikova, and Nikolay Prihod'ko. "METHOD FOR ASSESSMENT THE IMPAIRMENT OF EMBRYO IMPLANTATION DURING PREGNANCY COMPLICATED BY CYTOMEGALOVIRAL INFECTION BY DETERMINING CYCLOOXYGENASE-2 IN HOMOGENATE OF VILLOUS CHORION." In XIV International Scientific Conference "System Analysis in Medicine". Far Eastern Scientific Center of Physiology and Pathology of Respiration, 2020. http://dx.doi.org/10.12737/conferencearticle_5fe01d9c086109.30801383.

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A method for assessing the impairment of embryo implantation during pregnancy complicated by cytomegalovirus infection, based on the detection of cyclooxygenase 2 in the villous chorionic homogenate, is proposed
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Ishutina, Nataliya, Irina Andrievskaya, Inna Dovzhikova, and Nikolay Dorofienko. "METHOD FOR PREDICTION OF ANEMIA IN PREGNANT WOMEN WITH CYTOMEGALOVIRAL INFECTION." In XIV International Scientific Conference "System Analysis in Medicine". Far Eastern Scientific Center of Physiology and Pathology of Respiration, 2020. http://dx.doi.org/10.12737/conferencearticle_5fe01d9c14faa1.78766579.

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A method is proposed for predicting anemia in pregnant women with cytomegalovirus infection, based on the determination of arachidonic acid, TBA-active products, and total hemoglobin in peripheral blood erythrocytes.
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Py, S., A. Guitton, F. Lardet-Vieudrin, N. Marthouret, L. Pazart, A. Coaquette, W. Boireau, G. Thiriez, G. Herbein, and B. Wacogne. "Dynamic Detection of Cytomegalovirus in Breastmilk." In 11th International Conference on Biomedical Electronics and Devices. SCITEPRESS - Science and Technology Publications, 2018. http://dx.doi.org/10.5220/0006634602000205.

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Saeed, M., M. Khan, A. Khan, D. M. U. R. Safi, J. Margapuri, M. Radulovic, J. Stoeckel, et al. "Cytomegalovirus Pneumonia in an Immunocompetent Patient." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5210.

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Kingkosol, P., P. Pooprasert, P. Choopong, B. Hunchangsith, V. Laksanaphuk, and C. Tantibundhit. "Automated Cytomegalovirus Retinitis Screening in Fundus Images." In 2020 42nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC) in conjunction with the 43rd Annual Conference of the Canadian Medical and Biological Engineering Society. IEEE, 2020. http://dx.doi.org/10.1109/embc44109.2020.9175461.

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Shibanov, Alexey, Vladimir Stakhanov, and Natalia Karazhas. "Cytomegalovirus infection in patients with lung tuberculosis." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa2715.

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Gorikov, Igor, and Irina Andrievskaya. "RELATIONSHIP OF IMMUNO-HISTOMETRIC INDICATORS OF THE PLACEENTA IN EXACERBATION OF CYTOMEGALOVIRAL INFECTION IN THE SECOND TRIMESTER OF PREGNANCY." In XIV International Scientific Conference "System Analysis in Medicine". Far Eastern Scientific Center of Physiology and Pathology of Respiration, 2020. http://dx.doi.org/10.12737/conferencearticle_5fe01d9c510d54.83584889.

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The relationship between the concentration of tumor necrosis factor-alpha (TNF-α) in the placenta homogenate and its histometric parameters in women during physiological pregnancy and during pregnancy complicated by an exacerbation of cytomegalovirus infection in the second trimester of gestation, leading to the development of chronic compensated placental insufficiency, was studied.
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Andrievskaya, Irina, A. Milovanov, Igor Gorikov, Inna Dovzhikova, and Nataliya Ishutina. "RELATIONSHIP OF INTERLEUKIN-6 AND BLOOD FLOW IN THE UMBILICAL ARTERY DURING EXCERVATION OF MONO- AND MIXT-CYTOMEGALOVIRAL INFECTION IN THE SECOND TRIMESTER OF PREGNANCY." In XIV International Scientific Conference "System Analysis in Medicine". Far Eastern Scientific Center of Physiology and Pathology of Respiration, 2020. http://dx.doi.org/10.12737/conferencearticle_5fe01d9c664388.47461710.

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In order to determine the role of a cytokine in the regulation of blood supply to the placenta, the relationship between interleukin-6 (IL-6) in serum and blood flow in the umbilical artery in healthy pregnant women and during pregnancy complicated by exacerbation of mono- and mixed cytomegalovirus infection in the second trimester was studied
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Reports on the topic "Cytomegaloviruses"

1

Smith, Kendall O. The Role of Cytomegalovirus in the Development of ARC-AIDS. Fort Belvoir, VA: Defense Technical Information Center, August 1991. http://dx.doi.org/10.21236/ada241733.

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Wang, Li Fang, Yan Ting Cao, Tegeleqi Bu, Lin Fu, Jun Li Liu, and Jing Zhao. Do We Receive Cytomegalovirus Vaccination Before Solid Organ Transplant: a Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0143.

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Review question / Objective: We compared cytomegalovirus (CMV) vaccination for solid organ transplantation recipients ( SOTs) with placebo treatment, to investigate the efficacy and safety for the prevention of CMV infection in SOTs. Condition being studied: Patients after solid organ transplantation subsequently become immunosuppressed, and cytomegalovirus (CMV) is the most common opportunistic pathogen to this population. The prevalence of CMV infection can reach 50% in the general population, and further up to 64-72% in solid organ transplant recipients (SOTs). CMV seropositive donors (CMV D+) puts even more pressure of CMV infection for SOTs. Post-transplant CMV infection can lead to neutropenia, lymphopenia, thrombocytopenia, tissue/end-organ invasive CMV disease (gastroenteritis, pneumonia, hepatitis, encephalitis), other infectious diseases, graft dysfunction, and multiple organ failure. CMV can disturb immune cell function, thus is one of the major risk factors that increase mortality within 6 months after transplantation. However, practical, effective method to prevent postoperative CMV infection for SOTs remains unresolved. Vaccination of CMV is only at clinical trials stage. To date, there is a lack of guidelines or consensus for preventing CMV disease for SOTs. Given the increasing clinical trials of CMV vaccination, it is important to clarify the evidence-based benefits and risks of CMV vaccination for SOTs, and to provide the best CMV disease prevention measurements.
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Smith, Kendall O., and Joah M. Ratner. The Role of Cytomegalovirus as a Cofactor in the Development of ARC-AIDS. Fort Belvoir, VA: Defense Technical Information Center, December 1988. http://dx.doi.org/10.21236/ada203448.

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Wood, Lisa J. Cytokine Response to Subclinical Cytomegalovirus Reactivation as a Cause of Severe Fatigue in Women Undergoing Chemotherapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada574866.

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Hill, Ann. Cytokine Response to Subclinical Cytomegalovirus Reactivation as a Cause of Severe Fatigue in Women Undergoing Chemotherapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada586600.

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Wood, Lisa. Cytokine Response to Subclinical Cytomegalovirus Reactivation as a Cause of Severe Fatigue in Women Undergoing Chemotherapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada599299.

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Hill, Ann. Cytokine Response to Subclinical Cytomegalovirus Reactivation as a Cause of Severe Fatigue in Women Undergoing Chemotherapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada599305.

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Oh, Ju Hyun, Aimee Martinez, Huaixuan Cao, Garrett George, Jared Cobb, Poonam Sharma, Lauren Fassero, et al. Radio frequency heating of washable conductive textiles for bacteria and virus inactivation. Engineer Research and Development Center (U.S.), January 2024. http://dx.doi.org/10.21079/11681/48060.

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The ongoing COVID-19 pandemic has increased the use of single-use medical fabrics such as surgical masks, respirators, and other personal protective equipment (PPE), which have faced worldwide supply chain shortages. Reusable PPE is desirable in light of such shortages; however, the use of reusable PPE is largely restricted by the difficulty of rapid sterilization. In this work, we demonstrate successful bacterial and viral inactivation through remote and rapid radio frequency (RF) heating of conductive textiles. The RF heating behavior of conductive polymer-coated fabrics was measured for several different fabrics and coating compositions. Next, to determine the robustness and repeatability of this heating response, we investigated the textile’s RF heating response after multiple detergent washes. Finally, we show a rapid reduction of bacteria and virus by RF heating our conductive fabric. 99.9% of methicillin-resistant Staphylococcus aureus (MRSA) was removed from our conductive fabrics after only 10 min of RF heating; human cytomegalovirus (HCMV) was completely sterilized after 5 min of RF heating. These results demonstrate that RF heating conductive polymercoated fabrics offer new opportunities for applications of conductive textiles in the medical and/or electronic fields.
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