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Data publikacji: 4 czerwca 2021
Data aktualizacji: 11 lutego 2022

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1

Xue, Lumin, i Lumin Xue@csl com au. "Immunological studies of cold-adapted influenza vaccine viruses in mice". RMIT University. Applied Sciences, 2009. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20091027.101804.

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Cold-adapted (ca) live attenuated influenza vaccines (LAIVs) have been introduced as alternatives to existing inactivated influenza vaccines. The influenza A components of the FDA-approved ca LAIVs (Flumist®; Medimmune) have common internal genes derived from the donor strain A/Ann Arbor/6/60 ca and surface genes derived from current wild-type (wt) epidemic strains. The aim of this thesis was to investigate determinants of immunogenicity for reassortants of A/Ann Arbor/6/60 ca, using a range of immunological assays, including recently developed MHC tetramer techniques. From the study, the extent of viral replication in the respiratory tract of mice, the primary site of inoculation, was a key factor in determining ca vaccine immunogenicity. Replication was shown to be influenced by both viral surface Ags and the host MHC. The H3 ca reassortants CR6, CR18, CR29 and CR6-35* exhibited greater replication efficiency (as determined by their PFU:HAU ratios) than the H1 ca reassortants CR35 and CR6-35. The H3 ca reassortant CR6 caused a 3.79% loss in body weight but no losses were observed for the H1 ca reassortant CR35 and the ca H2N2 donor strain A/Ann Arbor/6/60 ca. Higher HI responses were detected after 3 weeks in groups infected with the H3 ca reassortant CR6 (GMT 80) than with the H1 reassortant CR35 (GMT 10) and the H2 ca donor strain A/Ann Arbor/6/60 ca (GMT 13). Recently developed techniques were used to evaluate specific T-cell response to ca LAIVs. Fluorescent-labelled tetramer is the key reagent for use in tetramer-based flow cytometry assays. The NP366-374 peptide of influenza A viruses comprises an immunodominant epitope that is highly conserved between subtypes. Tetramers developed for A/PR/8/34 (H1N1) were able to detect NP-specific cytotoxic T lymphocytes (CTLs) induced by A/Ann Arbor /6/60 ca (H2N2). An attempt to prepare the A/Ann Arbor/6/60 ca-specific-NP-tetramer is described. H-2Db monomers were successfully refolded with the peptide, but only 20% were able to form tetramers through biotin-streptavidin linkage, resulting in a poor capacity to stain. By contrast, an IFN-γ ICC assay developed in parallel demonstrated that peptide NP366-374 was able to restimulate A/Ann Arbor/6/60 NP ca-specific CTLs and secrete IFN-γ when tested in vitro. Specific-B and T cell responses induced in the lungs in response to infection by ca reassortants exhibited great variability that was determined by the growth characteristics of different viruses. Type I (CTL) responses were induced by low yielding ca reassortants, such as CR35 (H1N1). Viruses with enhanced growth characteristics, such as CR6 (H3N2), produced higher Type II (HA-specific Ab) responses. In addition, host factors, such as MHC type, were found to play an important role in responses to the same viruses. Susceptible mouse strains, such as C57BL/6, showed higher CTL but lower serum Ab responses than more resistant strains, such as BALB/c. Throughout this PhD project, a fine balance between the humoral and CMI, local and systemic immune responses induced by ca LAIVs was demonstrated. The need to assess local immune responses, in addition to serum antibody levels, for the evaluation of vaccine efficacy was an important conclusion of the thesis.
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2

Teske, Sabine. "Dioxin-induced deregulation of neutrophil recruitment to the lungs of mice infected with influenza virus". Online access for everyone, 2006. http://www.dissertations.wsu.edu/Dissertations/Spring2006/s%5Fteske%5F012006.pdf.

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3

Qin, Kun. "Role of a distinct PA gene for the pathogenicity and replication properties of avian H5N1 influenza virus in mice". Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43278462.

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4

Repass, John F. "Studies of murine coronavirus cis-acting RNA elements that affect RNA synthesis /". Digital version accessible at:, 2000. http://wwwlib.umi.com/cr/utexas/main.

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5

Pierce, Angela Marie. "Deregulated E2F1 has both oncogenic and tumor suppressive properties in mouse skin /". Digital version accessible at:, 1998. http://wwwlib.umi.com/cr/utexas/main.

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6

Qin, Kun, i 秦堃. "Role of a distinct PA gene for the pathogenicity and replication properties of avian H5N1 influenza virus in mice". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43278462.

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7

Choi, Eun-Young Pintel David J. "Determinants that govern alternative splicing of the large intron of minute virus of mice p4-generated PRE-mRNA". Diss., Columbia, Mo. : University of Missouri--Columbia, 2008. http://hdl.handle.net/10355/6696.

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Title from PDF of title page (University of Missouri--Columbia, viewed on Feb 25, 2010). The entire thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file; a non-technical public abstract appears in the public.pdf file. Dissertation advisor: David J. Pintel. Vita. Includes bibliographical references.
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8

Yu, Chun-I. Palucka Karolina Banchereau Jacques. "Humanized mice to test vaccination against influenza virus via dendritic cells". Waco, Tex. : Baylor University, 2008. http://hdl.handle.net/2104/5184.

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Thesis (Ph.D.)--Baylor University, 2008.
In abstract the '2' and '-/-' in NOD-SCID-[beta]2m-/- is superscript. In abstract the '+' after CD34 and CD8 is superscript. In abstract the '-' and '+' in CD45RA-CD27+CD4+ are superscript. Includes bibliographical references (p. 103-123).
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9

Nardiello, Tricia Lynn. "Protease activity in lymphoid organs of BALB/C and C57BL/6 mice following murine leukemia virus /". Connect to online version, 2007. http://ada.mtholyoke.edu/setr/websrc/pdfs/www/2007/214.pdf.

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10

Webster, Marc A. "Mechanisms of polyomavirus transformation of the mouse mammary gland /". *McMaster only, 1996.

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11

Socha, Amanda L. "Differential expression of an endogenous retrovirus in MAIDS susceptible (C57BL/6) versus resistant (BALB/C) mice /". Connect to online version, 2006. http://ada.mtholyoke.edu/setr/websrc/pdfs/www/2006/159.pdf.

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12

Kasumba, Muhandwa Dacquin. "A plant-derived nucleic acid protects mice from respiratory viruses in an IFN-I-dependent and independent manner". Kyoto University, 2017. http://hdl.handle.net/2433/228258.

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13

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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14

Beaumier, Coreen Michele. "Cross-Reactive Memory CD4+ and CD8+ T Cells Alter the Immune Response to Heterologous Secondary Dengue Virus Infections in Mice: A Dissertation". eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/350.

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Dengue virus (DENV) infects 50-100 million people worldwide every year and is the causative agent of dengue fever (DF) and the more severe dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS). There are four genetically and immunologically distinct DENV serotypes (DENV-1, DENV-2, DENV-3, and DENV-4). Evidence suggests that an increased risk for DHF/DSS during secondary infection with a heterologous DENV serotype is due to an immunopathological response mediated by serotype-cross-reactive memory T cells from the primary infection. Furthermore, epidemiological studies have shown that the sequence of infection with different DENV serotypes affects disease severity. Though much has been learned from human studies, there exist uncontrollable variables that are intrinsic in this system such as genetic factors and unknown infection histories. These factors can skew experimental results, making interpretations difficult. Therefore, a murine model to study the immunologic aspects of sequential dengue infections would be an asset to the field of dengue research. To examine the effect of sequential infection with different DENV serotypes on the CD8+ T cell response, we immunized Balb/c mice with a primary DENV infection on day 0 and subsequently challenged with a heterologous secondary DENV infection on day 28. We tested all possible sequences of infection with the four serotypes. We analyzed the T cell response to two previously defined epitopes on the DENV E (Ld-restricted) and NS3 (Kd-restricted) proteins. Using ELISPOT and intracellular cytokine staining, we measured the frequency of T cells secreting IFNγ and TNFα in response to stimulation with these epitopes during three phases: acute primary, acute secondary, and the memory phase after primary infection. We found that the T cell response in heterologous secondary infections was higher in magnitude than the response in acute primary infection or during the memory phase. We also found that the hierarchy of epitope specific responses, as measured by IFNγ secretion, was influenced by the sequence of infections. The adoptive transfer of immune serum or immune splenocytes suggested that memory T cells from the primary infection responded to antigens from the secondary infection. In vitroexperiments with T cell lines generated from mice with primary and secondary DENV infections suggested the preferential expansion of crossreactive memory T cells. In testing all of the different possible sequences of infection, we observed that two different sequences of infection (e.g., DENV-2 followed by DENV-1 versus DENV-2 followed by DENV-3) resulted in differential CD8+ T cell responses to the NS3 peptide even though both secondary infection serotypes contain the identical peptide sequence. To investigate this phenomenon, we examined the role of CD4+ T cell help on the memory CD8+ T cell response. We found that CD4+ T cell cytokine responses differ depending on the sequence of infection. In addition, it was also shown that crossreactivities of the CD4+ T cell response are also sequence-dependent. Moreover, denguespecific memory CD4+ T cells can augment the secondary CD8+ T cell response. Taken together, we demonstrated that this serotype sequence-dependent phenomenon is the result of differential help provided by cross-reactive memory CD4+T cells. The findings in this novel mouse model support the hypothesis that both CD4+ and CD8+ serotype-cross-reactive memory T cells from a primary dengue virus infection alter the immune response during a heterologous secondary dengue virus infection. These data further elucidate potential mechanisms whereby the specific sequence of infection with different dengue virus serotypes influences disease outcomes in humans.
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15

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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16

Mire, Chad Edward. "Investigation of the vesicular stomatitis virus matrix protein uncoating and assembly /". View the abstract Download the full-text PDF version, 2008. http://etd.utmem.edu/abstracts/2008-035-Mire-index.html.

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Thesis (Ph.D.)--University of Tennessee Health Science Center, 2008.
Title from title page screen (viewed on September 9, 2008). Research advisor: Michael A. Whitt, Ph.D. Document formatted into pages (xi, 119 p. : ill.). Vita. Abstract. Includes bibliographical references (p. 104-119).
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17

Mouw, Matthew B. "Gene regulation in two parvoviruses : minute virus of mice and adeno-associated virus /". free to MU campus, to others for purchase, 2000. http://wwwlib.umi.com/cr/mo/fullcit?p9974668.

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18

Schiavi, Susan C. "MYC and E1A Oncogenes Alter the Response of PC12 Cells to Nerve Growth Factor and Block Differentiation: A Thesis". eScholarship@UMMS, 1988. https://escholarship.umassmed.edu/gsbs_diss/259.

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PC12 rat pheochromocytoma cells respond to nerve growth factor (NGF) by neuronal differentiation and partial growth arrest. Mouse c-myc and adenovirus E1A genes were introduced into PC12 cells to study the influence of these nuclear oncogenes on neuronal differentiation. Expression of myc and E1A blocked morphological differentiation and caused NGF to stimulate rather than inhibit cell proliferation. NGF binding to cell surface receptors, activation of ribosomal S6 kinase, and ornithine decarboxylase induction were similar in myc and E1A expressing clones compared with wild-type PC12 cells, suggesting that changes in the cellular response to NGF were at a post-receptor level. The ability of myc and E1A expression to block the transcription-dependent induction of microtubule associated proteins by NGF further suggested that these genes may inhibit differentiation by interfering with NGP's ability to regulate transcription. These results illustrate that NGF can promote either growth or differentiation of PC12 cells, and that myc or E1A alter the phenotypic responses to growth factors.
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19

Hindersson, Maria. "Coxsackie B virus pathogenesis in mice /". Stockholm : Karolinska institutet, 2006. http://diss.kib.ki.se/2006/20060608hind/.

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20

Janus, Lydia Maria. "Transmission of minute virus of mice in mouse populations international PhD program "infection biology"". Giessen DVG-Service, 2009. http://d-nb.info/995700702/04.

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21

Leyva-Grado, Victor Hugo. "Neuropathogenesis of the acute phase response to influenza virus in mice". Online access for everyone, 2008. http://www.dissertations.wsu.edu/Dissertations/Summer2008/V_Leyva-Grado_071808.pdf.

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22

Thorpe, Linsay Clare. "Molecular studies on pneumonia virus of mice". Thesis, University of Warwick, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269067.

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23

Cook, Pamela Mary. "Pathogenesis and persistance of pneumonia virus of mice". Thesis, University of Warwick, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263839.

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Huffman, John Henry. "Studies on Encephalomyocarditis Virus-Induced Diabetes in Mice". DigitalCommons@USU, 1988. https://digitalcommons.usu.edu/etd/4046.

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The D-variant of encephalomyocarditis (EMC-D) virus was given to SJUJ mice by the artificial, intraperitoneal (ip) route of infection , or by the natural routes of infection per os (po) or intranasal (i.n .), in comparable concentrations. The po route of infection was found to be ineffective. Mice given virus by either the ip or i.n. routes of infection became diabetic. Mice were more resistant to the infectious and diabetogenic properties of the virus when given by the i.n. than when given by the ip route. Glycosuria in mice given virus i.n. usually lagged one day behind that in mice given virus ip. Measurement of glucose in mouse urine by use of Diastix® reagent strips was found to be a reliable indicator of diabetes. This test was easily and quickly accomplished without harm or pain to the mice. Crude virus preparations were compared to purified virus preparations for their diabetogenic and infectious properties in mice. No statistically significant differences in either parameter were observed. Virus prepared by a single passage in BHK-21 cells was fully diabetogenic, contrary to a previously published report. Male SJUJ mice were infected with a diabetogenic dose of EMC-D virus by the i.n. route. Relative times of development of virus infection and mouse resistance parameters were compared to the time of development of signs of diabetes in the mice. A rapid decrease of plasma interferon titer corresponded to the time of development of signs of diabetes in the infected mice. Whether this was coincidental or has some significance in development of diabetes is unknown. Tissue sections from pancreas, spleen , kidney, liver, lung , heart, and thymus were studied by immunohistochemical staining techniques for the presence of virus antigen, insulin, and the three types of mouse interferon (α, β, and γ). Glucose was excreted in the saliva of mice with glycosuria. Previous reports of this excretion in diabetic mice have not been found in the literature. Mice without glycosuria did not excrete measurable (by Clinistix® or Diastix®) glucose in saliva. Some mice were able to control the polyuria, polydipsia, and polyphagia normally seen in diabetes mellitus. These mice eventually reverted from having signs of diabetes to a normal state of plasma glucose and urine devoid of glucose. The mechanisms by which the mice were able to do this are unknown at this time.
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25

Cohen, Sarah. "Nuclear entry of the parvovirus minute virus of mice". Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/30414.

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In order to promote infection, viruses must target their genomes to specific compartments within the host cell. I have used the parvovirus minute virus of mice (MVM) as a model to study the trafficking of non-enveloped viruses. Parvoviruses are single-stranded DNA viruses which replicate in the nucleus of the cell. Most viruses that replicate in the nucleus transport their genomes through nuclear pore complexes, large protein assemblies that mediate nucleocytoplasmic transport. However, previous studies have shown that MVM can induce disruption of the nuclear membranes, called the nuclear envelope (NE). This led to the hypothesis that MVM enters the nucleus by an unusual mechanism: disruption of the NE and entry through the resulting breaks. The objectives of this thesis were to: (1) characterize the effect of MVM on the NE, (2) define the molecular mechanism used by MVM to induce NE disruption, (3) determine the role of NE disruption in the MVM replication cycle, and (4) identify host proteins involved in MVM infection. I found that MVM causes small, transient disruptions of the NE early during infection. I tested the hypothesis that viral enzymatic activity is necessary for MVM-induced NE disruption and found that this was not the case. Next I tested the hypothesis that MVM hijacks a cellular program for NE breakdown, and found that MVM utilizes apoptotic proteases called caspases to facilitate these disruptions. Caspase inhibition prevents NE disruption in MVM-infected cells, reduces viral gene expression, and prevents entry of MVM capsids into the nucleus. I propose that NE disruption involving caspases facilitates parvovirus genome delivery into the nucleus. NE disruption also alters the compartmentalization of host proteins, which may be favorable for the virus. I have shown that MVM uses a novel nuclear entry strategy, unlike those previously described for any virus or cellular protein. It will be of great interest to determine whether this strategy is shared by other viruses. Parvoviruses are not considered a serious threat as human pathogens. However, they may prove useful as vectors for gene therapy. An understanding of the basic biology of parvoviruses could help in the development of parvovirus-based therapeutics.
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26

Garcin, Pierre. "Study of the minute virus of mice cell entry". Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/50245.

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The minute virus of mice prototype (MVMp) is a non-enveloped single stranded DNA virus of the family Parvoviridae. MVMp is one of the smallest viruses and shows intriguing abilities to preferentially infect and kill cancer cells (oncotropism/oncolytism), suggesting a potential for MVMp as an anti-cancer agent. Unfortunately, there is a lack of knowledge of the early events of MVMp infection cycle, such as binding to the cell surface and subsequent endocytosis. In an attempt to identify cellular partners of MVMp infection, our lab performed a mass spectrometry analysis of MVMp potential binding partners. Following this analysis, the galactose-binding lectin (galectin) 3 (Gal-3) was identified as binding partner for MVMp. Given the involvement of this extra-cellular matrix protein in the clustering and endocytosis of cell surface receptors, and its up-regulation in various aggressive tumor cells, I hypothesized that Gal-3 could play a role in MVMp cell entry, and potentially in its oncotropism. Using siRNA knockdown of Gal-3 in different cells followed by immunofluorescence microscopy analysis, I found that Gal-3 is necessary for an efficient MVMp cell entry and infection in different cells. Moreover, I discovered that the Golgi enzyme β1,6-acetylglucosaminyltransferase 5 (Mgat5), whose role is the addition of complex N-glycosylation to various cell surface receptors for Gal-3 binding, is required for MVMp infection. I also found that cancer cells with higher Gal-3 expression are more susceptible to MVMp infection than cells with lower Gal-3 levels. Next I used a combination of flow cytometry, immuno-fluorescence and transmission electron microscopy to characterize the early events of MVMp infection in various tissue-culture cell lines. My results show that many crucial parameters of the mesenchymal cell migration process regulate MVMp cellular entry and infection. I found that MVMp relies on cell protrusions to cluster at the leading edge of migrating cells rapidly after binding to the plasma membrane, from where it is subsequently endocytosed. Moreover, transmission electron microscopy analysis revealed that MVMp uses various endocytic pathways, which was confirmed using drug inhibitors of endocytosis. Finally, I found that epithelial-mesenchymal transition, an inducer of cancer cell migration, triggers MVMp infection in highly dividing non-permissive cancer cells.
Science, Faculty of
Zoology, Department of
Graduate
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27

Chan, Wan-yi. "Influenza A virus replication and cytokine responses in murine macrophages in vitro". Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B33829937.

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28

Hayes, Peter John. "The role of macrophages in respiratory syncytial virus infection of mice". Thesis, University of Newcastle Upon Tyne, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.358972.

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29

Randhawa, J. S. "Molecular characterisation of the pneumonia virus of mice glycoprotein genes". Thesis, University of Warwick, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387336.

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Oliver, Kevin Russell. "Consequences of neurotropic virus infections of developing and adult mice". Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.389959.

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31

Morgan, David John. "Defective interfering influenza virus reverses the immunopathological effects of standard influenza virus in mice". Thesis, University of Bristol, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.332491.

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32

Geldmacher, Astrid. "Immunogenicity of hantavirus Dobrava nucleocapsid protein derivatives in mice". Doctoral thesis, [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=977995550.

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33

Yirrell, D. L. "Double infections with HSV in the mouse". Thesis, University of Bristol, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234887.

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34

Guadarrama, F. R. E. "Specificity and function of Th-cells in influenza A virus infection in a mouse model". Thesis, Brunel University, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384057.

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35

Cambouropoulos, Peter. "Studies on the induction and prevention of delayed type hypersensitivity to herpes simplex virus". Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336550.

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36

Chan, Wan-yi, i 陳韻怡. "Influenza A virus replication and cytokine responses in murine macrophages in vitro". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B33829937.

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37

Brunstein, John. "Analysis of the internal replication sequence of minute virus of mice". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ27113.pdf.

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38

Usherwood, Edward John. "The role of CD4+ T cells in Theiler's virus infected mice". Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339479.

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39

Dibben, Oliver Edwin. "Development of a reverse genetics system for Pneumonia virus of mice". Thesis, University of Warwick, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.479230.

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40

Nobiron, Isabelle. "DNA vaccination against bovine viral diarrhoea virus in mice and cattle". Thesis, Royal Veterinary College (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271012.

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41

Wolk, Kendra E. "Influenza A Virus Inhibits Alveolar Fluid Clearance in BALB/c Mice". The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1337791191.

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42

Han, Yi. "Identification of the SV40 large T antigen integration site in TRAMP mice /". Free to MU Campus, others may purchase, 2004. http://wwwlib.umi.com/cr/mo/fullcit?p1422928.

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43

Krishna, Kaja Murali. "Cytotoxic T lymphocyte Responses Against Japanese Encephalitis Virus In Mice: Specificity And Immunotherapeutic Value". Thesis, Indian Institute of Science, 1994. http://hdl.handle.net/2005/152.

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Cytotoxic T Lymphocytes (CTL) are known to play an important role in clearing infectious virus from infected hosts in a variety of viral infections. Depending on the type of virus and mode of virus entry both class I and class II restricted CTL can contribute to protection from virus-induced disease. Although CD8 positive CTL are associated with virus elimination and control in many viral infections, elimination of neurotropic viruses from the Central Nervous system (CNS) is more complex due to the lowered expression of MHC antigens on neuronal cells. This failure to constitutively express high levels of MHC antigens by neurons could serve as an advantage to avoid damage to this differentiated and non-renewable tissue. However, abnormal induction of MHC antigens in the CNS mediated by CD4 positive lymphocytes or by astrocytes have also been shown to cause destructive inflammation in the CNS. The present study deals with CTL responses against one such neurotropic virus called Japanese Encephalitis Virus (JEV). JEV is a positive-stranded RNA virus that belongs to the flavivirus group, a group that is among the most important agents causing human encephalitis worldwide. Although passive transfer of monoclonal antibodies against this virus has been shown to confer protection of mice from lethal challenge with virus, neither the presence of CTL against this virus nor its role in conferring protection has been reported so far. Understanding the CTL responses against these viruses acquired importance in light of recent reports that neurovirulence of JEV and yellow fever viruses can be enhanced by the administration of virus specific antibodies. Hence this study was undertaken to examine the possibility of raising CTL specific to JEV. The specificity of the CTL raised, their therapeutic value and the ability of different lymphocyte subsets to mediate protection in vivo are dealt with in this study. Generation of CTL against JEV The generation of CTL against JEV in BALB/c mice, requires MHC defined cell lines that not only support virus infection but are also histocompatible. Several cell lines were initially examined for their ability to support JEV infection as a prc-rcquisitc before their utilization in in vivo and in vitro stimulation protocols aimed at generating JEV-specific CTL. Virus infection was monitored by immunofluorescence using JEV envelope-specific monoclonal antibodies as well as by titration of virus produced from infected cells by plaque assays. These different cell lines that were characterised for their ability to support JEV infection were then utilised to generate and monitor antiviral CTL. Several in vivo immunisation protocols were examined initially find out which of these infected cells prime BALB/c mice efficiently for generation of virus-specific CTL upon secondary stimulation in vitro with infected syngeneic cells. Immunisation of mice with infected cells per se was preferred over free virus since this was thought to facilitate priming against some viral non-structural proteins preferentially found on infected cells in addition to other viral structural proteins. It was observed that not only infected syngeneic and allogeneic cells but also infected xenogeneic cells prime BALB/c mice for the generation of JEV- specific CTL upon secondary restimulation in vitro. An optimal protocol was standardised for the generation of CTL against JEV. This included primary in vivo immunisation of mice followed by secondary in vitro restimulation of splenocytes with infected syngeneic cells. Either immunisation alone or in vitro stimulation of naive splenocytes alone was unsuccessful. The effector cells generated specifically lysed JEV-infccted P388D1 targets but not uninfected P388D1 or YAC-1 targets suggesting that the lysis on infected targets is not mediated by Natural Killer activity. Specificity and MHC restriction of anti JEV Effectors Cell depletion studies using complement mediated lysis were performed to examine the phenotype of the cells mediating virus specific lysis of infected targets. Depletion of Lyt 2.2+ or Thy 1+ but not L3T4+ sub-populations of effector cells inhibited lysis of infected targets showing that the effectors mediating virus-specific lysis were Lyt-2+ T cells. Examination of target specificities and MHC restriction of the antiviral CTL generated showed that although infected xenogeneic cells were used for immunisation, the effector cells recognised only infected syngeneic (P388D1, Sp2/0) and semisyngeneic (Neuro 2a, YAC-1) cells. Virus-specific recognition was found to be class I Kd and class I Dd restricted. These effector cells were also found to recognise cells infected with a closely related flavivirus, West Nile Virus (WNV) suggesting that they were crossreactive to some degree. Based on the consensus motif that has been established for H-2Kd associated peptides, several nonamers were predicted as possible CTL epitopes by scanning the deduced amino acid sequences of three strains of JEV and WNV. Among several predicted nonamers, three peptides were examined for their ability to reconstitute lysis of uninfected targets by polyclonal anti JEV CTL populations. Results demonstrate that peptides derived from NS1 and NS3 but not NS5 protein of JEV were able to partially reconstitute lysis of uninfected targets by effectors when pulsed with the appropriate peptide. Protective ability of the CTL raised against JEV To examine whether anti-JEV effectors raised in vitro could confer protection from intracerebral challenge with JEV, these effectors were adoptively transferred into adult BALB/c mice intracerebrally along with 10 x LDJ0 dose of JEV. More than 55% of these animals were protected from death and survived beyond 100 days after JEV challenge demonstrating that adoptively transferred anti-JEV effectors could indeed confer protection from lethal challenge with JEV. However, adoptive transfer of effectors by either intravenous or intraperitoneal routes did not protect adult mice from the lethal effects of intracerebral challenge with JEV. In contrast to adult mice, newborn mice were not protected from death by the adoptively transferred effector cells. This was also supported by experiments where a correlation was observed with the increasing age of mice and the success of protection conferred by the adoptively transferred effector cells. To establish the identity of cell subsets responsible for protection, Lyt 2, L3T4 or Thy 1 positive cells were specifically depleted from the polyclonal CTL by multiple cycles of complement mediated lysis and the remaining cells were adoptively transferred intracerebrally along with 10 x LD of JEV. These results demonstrate that both Lyt 2 and L3T4 positive T cells present in the effector population were necessary to confer protection of adult mice. Examination of virus-specific neutralising antibodies in the sera of protected and unprotected mice revealed that presence of L3T4 positive cells in the adoptively transferred population increases virus-specific neutralising antibodies. However presence of neutralising antibodies alone was not sufficient to confer protection. The protection required both Lyt-2 and L3T4 positive cells together. These studies could in the long term throw some light on similar observations about age dependant susceptibility to JEV in humans.
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44

Teepe, Annette. "Relationship of Estrous Cycle to Herpes Simplex Virus Type 2 Susceptibility in Female Mice". Thesis, North Texas State University, 1987. https://digital.library.unt.edu/ark:/67531/metadc500408/.

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In CBA/NJ mice, splenic natural killer (NK) cell activity varies with stages of estrous. Susceptibility of ICR mice to intravaginal inoculation of herpes simplex virus type 2 (HSV-2) decreases with age. Susceptibility of female ICR and CBA/NJ mice to HSV-2 inoculated intravaginally and intraperitoneally was examined during the estrous cycle. In cycling ICR mice, greatest susceptibility to intravaginal inoculation was observed during diestrous and the least during metestrous. CBA/NJ mice were most susceptible to intravaginal inoculation of HSV-2 during diestrous. ICR mice were ovariectomized to mimic diestrous and found to be highly susceptible to intravaginal inoculation at all virus doses. No difference in susceptibility among phases of the estrous cycle was seen following intraperitoneal inoculation.
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45

Jin, Zeming. "Effects of soy isoflavones on breast tumorigensis in MMTV-NEU transgenic mice /". free to MU campus, to others for purchase, 2003. http://wwwlib.umi.com/cr/mo/fullcit?p3101026.

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46

Slobedman, Barry. "Molecular analysis of herpes simplex virus type 1 latency in experimentally infected mice /". Title page, contents and abstract only, 1994. http://web4.library.adelaide.edu.au/theses/09PH/09phs634.pdf.

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Thesis (Ph. D.)--University of Adelaide, Dept. of Microbiology and Immunology, 1995?
Copies of author's previously published articles inserted inside back cover. Includes bibliographical references (leaves 137-179).
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47

Sadigh, Yashar Mohammadzadeh. "A reverse genetics approach to study the pathogenesis of pneumonia virus of mice". Thesis, University of Warwick, 2011. http://wrap.warwick.ac.uk/38417/.

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Human and bovine respiratory syncytial viruses (HRSV and BRSV), along with pneumonia virus of mice (PVM) are the members of the genus Pneumovirus in the subfamily Pneumovirinae of the family Paramyxoviridae. Although both HRSV and BRSV have been associated with important diseases in human and livestock, there is no clearcut description of the molecular aspects of their pathogenesis. For HRSV, the lack of a suitable study model is one of the main reasons hampering the study of aspects of pathogenesis of the virus. HRSV infects a wide range of animal models, however most of the common laboratory animal models are not sufficiently permissive to study the infectivity of the virus. PVM naturally infects mice and causes a disease indistinguishable from that of HRSV in humans. Two strains of PVM have been described: strain 15 (Warwick) which is not pathogenic and strain J3666 which is highly pathogenic. The main difference between these two strains lies in the organisation of the gene encoding the attachment (G) glycoprotein. The G gene in strain J3666 has two ORFs. The larger second ORF codes for the G glycoprotein and is located downstream of the first ORF which has no known function. The strain 15 G gene also contains two ORFs but in this case both the first and main ORFs overlap each other. The aim of the project was to investigate the molecular basis for pathogenesis of PVM as a model for pneumoviruses. As a first step, the pathogenesis of PVM strain J3666 was revaluated and the effect of consecutive tissue culture passages on the pathogenicity of the virus was examined. It was shown that consecutive passages of PVM strain J3666 caused attenuation of the virus. To investigate the possible mutations causing the attenuation the majority of the virus genome was sequenced from three passage stocks where the transition from pathogenic to non-pathogenic occurred. No differences in the genome sequences for the three passage stocks were found. However, sequence analysis of individual clones of the SH and G genes of the viruses showed evidence that the stocks contained a mixed population of sequences. A robust reverse genetics system was established to rescue recombinant PVM from cDNA using co-transfection of plasmids coding for the ribonucleoprotein complex of the virus (N, L, M2-1 and P proteins) and a cDNA copy of the virus genome cloned under the control of the bacteriophage T7 RNA polymerase. Using this system, four viruses differing in their G gene organisation were generated and used to infect mice to study the effect of mutations on pathogenicity. It was shown that the viruses with the G gene of strain 15 (Warwick) lacking the first ORF manifest a modest increase in their pathogenicity compared to the non-pathogenic PVM strain 15(Warwick) parent. The recombinant viruses containing the G gene organisation of strain J3666 showed the highest level of pathogenicity. The reverse genetics system was used to study the role of the first ORF in G glycoprotein expression. Using a dicistronic minigenome construct, the effect of the presence or absence of the first ORF in both the strain 15 and strain J3666 G gene organisation was studied. It was shown that the presence of the first ORF of the G gene in the strain 15 (Warwick) suppressed the expression of the G protein, while the first ORF in the strain J3666 did not have any significant effect on G protein expression.
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48

Williams, J. H. (June Heather). "Pathology of west nile virus lineages 1 and 2 in mice and horses". Diss., University of Pretoria, 2014. http://hdl.handle.net/2263/40816.

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West Nile virus (WNV) is a widespread emerging zoonotic neurotropic flavivirus cycling naturally between mosquitos and birds. WNV causes disease in 20% of infections in the most susceptible incidental hosts which are horses and humans. Up to 40% of affected horses and 1- to approximately 50% of affected humans develop neurological signs and/or flaccid paralysis, in some cases fatal or severely debilitating, due to variable encephalitis, meningitis and poliomyelitis. Two predominant genetic lineages exist, 1 and 2, with neurovirulent lineage 1 strains recorded in the northern and western hemispheres, the milder lineage 1 Kunjin strain in Australia, and the lineage 2 strain endemic to southern Africa and Madagascar and considered, until recently, to have mainly mildly pathogenic strains. Since 2002 investigations into South African lineage 2 WNV strains showed that they resulted in severe neurological disease in horses and humans. From 2004 lineage 2 strains were recorded for the first time in southern Europe as a cause of neurological signs and death in birds, and increasingly, in horses and humans. In 2011 the mild lineage 1 Kunjin strain mutated to an equine neurovirulent strain in New South Wales, Australia, and in 2010 the first South African case of lineage 1 WNV was reported from the western Cape in a mare which showed severe neurological signs, abortion and death. Laboratory strains of mice are extremely susceptible to WNV and have been mostly used in experimental studies since the 1937 discovery of the virus in Uganda. In the early 2000s studies in mice showed that field strains of lineage 1 and 2 WNV ranged from mildly pathogenic to highly neurovirulent, however, the associated pathology of the lineage 2 infections was not studied. In the current study, the macroscopic and microscopic pathology of a South African human-neurovirulent field strain of lineage 2 WNV (SPU93/01) and the neurovirulent lineage 1 (NY99/385) strain were investigated and compared in mice used as controls in 2 WNV vaccine studies. The clinical signs, CNS and extra-CNS pathology were indistinguishable between the lineages and some lesions were comparable to those previously reported. Lineage 1 WNV equine pathology has been well described but that of lineage 2 only briefly previously described. The pathology in 6 naturally-occurring fatal lineage 2 WNV-infected horses with severe neurological signs, was investigated and compared with that of the single South African lineage 1 WNV field infection. Diagnoses were confirmed by real-time RT-PCR. Similarities and some slight differences in lesions were found in both mouse and horse studies when compared with lineage 1 pathology cases and with previous reports, and the neurovirulence of the lineage 2 field strains was confirmed. WNV immunohistochemistry (IHC) of all mouse tissues allowed speculation as to pathogenesis of intestinal lesions, but in equine CNS lesions was mostly negative. Ultrastructure of IHC positive cells showed rare WNV particles. In the horse cases rabies, equine herpes virus, and other arboviral co-infections were excluded and similarities and implications of gross lesions of African horsesickness to those often seen in WNV infections were discussed.
Dissertation (MSc)--University of Pretoria, 2014.
gm2014
Medical Virology
unrestricted
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49

Curran, John Andrew. "The oncogenic activity of the latent membrane protein of EBV in transgenic mice". Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388552.

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50

Loiacono, Christina Marie. "Mechanism of herpes simplex virus type 1 latency in transgenic mouse models". MU has, 2002. http://wwwlib.umi.com/cr/mo/fullcit?p3052194.

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