Relevant bibliographies by topics / Mice – Viruses

Academic literature on the topic 'Mice – Viruses'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 February 2022

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Journal articles on the topic "Mice – Viruses"

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Hugh, Farida, and K. R. Dumbell. "Virulence of variola viruses for suckling mice." Transactions of the Royal Society of Tropical Medicine and Hygiene 97, no. 1 (January 2003): 97–99. http://dx.doi.org/10.1016/s0035-9203(03)90036-8.

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Joseph, Tomy, Josephine McAuliffe, Bin Lu, Hong Jin, George Kemble, and Kanta Subbarao. "Evaluation of Replication and Pathogenicity of Avian Influenza A H7 Subtype Viruses in a Mouse Model." Journal of Virology 81, no. 19 (July 18, 2007): 10558–66. http://dx.doi.org/10.1128/jvi.00970-07.

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ABSTRACT Avian influenza A H7 subtype viruses pose a significant threat to human health because of their ability to transmit directly from domestic poultry to humans and to cause disease and, sometimes, death. Although it is important to develop vaccines against viruses of this subtype, very limited information is available on the immune response and pathogenesis of H7 viruses in animal models such as mice and ferrets. Ten H7 viruses were selected for possible vaccine development on the basis of their phylogenetic relationships and geographical locations. The virulence of the 10 viruses for mice and the immunogenicity of the viruses in mice and ferrets were evaluated to study the extent of antigenic relatedness and the level of cross-reactivity of antibodies. Most of the viruses showed similar patterns of cross-reactivity with mouse and ferret antisera. The Eurasian viruses elicited broadly cross-reactive antibodies that neutralized viruses from both Eurasian and North American lineages, but the converse was not true. A subset of the viruses was also evaluated for the ability to replicate and cause disease in BALB/c mice following intranasal administration. H7 subtype viruses were able to infect mice without adaptation and manifested different levels of lethality and kinetics of replication. On the basis of phylogenetic data, induction of broadly cross-neutralizing antibodies in mouse and ferret antisera, and their ability to replicate in mice, we have selected A/Netherlands/219/03 (subtype H7N7) and A/chicken/BC/CN-7/04 (subtype H7N3) viruses for vaccine development. The mouse model can be used for the preclinical evaluation of these vaccines against H7 subtype viruses.
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Song, Yafen, Weiqiang Li, Wenbo Wu, Zhiting Liu, Zhuoliang He, Zuxian Chen, Bingbing Zhao, et al. "Phylogeny, Pathogenicity, Transmission, and Host Immune Responses of Four H5N6 Avian Influenza Viruses in Chickens and Mice." Viruses 11, no. 11 (November 10, 2019): 1048. http://dx.doi.org/10.3390/v11111048.

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H5Nx viruses have continuously emerged in the world, causing poultry industry losses and posing a potential public health risk. Here, we studied the phylogeny, pathogenicity, transmission, and immune response of four H5N6 avian influenza viruses in chickens and mice, which were isolated from waterfowl between 2013 and 2014. Their HA genes belong to Clade 2.3.4.4, circulated in China since 2008. Their NA genes fall into N6-like/Eurasian sublineage. Their internal genes originated from different H5N1 viruses. The results suggested that the four H5N6 viruses were reassortants of the H5N1 and H6N6 viruses. They cause lethal infection with high transmission capability in chickens. They also cause mild to severe pathogenicity in mice and can spread to the brain through the blood–brain barrier. During the infection, the viruses result in the up-regulation of PRRs and cytokine in brains and lungs of chickens and mice. Our results suggested that the high viral loads of several organs may result in disease severity in chickens and mice; there were varying levels of cytokines induced by the H5N6 viruses with different pathogenicity in chickens and mice.
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Lu, Xiuhua, Terrence M. Tumpey, Timothy Morken, Sherif R. Zaki, Nancy J. Cox, and Jacqueline M. Katz. "A Mouse Model for the Evaluation of Pathogenesis and Immunity to Influenza A (H5N1) Viruses Isolated from Humans." Journal of Virology 73, no. 7 (July 1, 1999): 5903–11. http://dx.doi.org/10.1128/jvi.73.7.5903-5911.1999.

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ABSTRACT During 1997 in Hong Kong, 18 human cases of respiratory illness, including 6 fatalities, were caused by highly pathogenic avian influenza A (H5N1) viruses. Since H5 viruses had previously been isolated only from avian species, the outbreak raised questions about the ability of these viruses to cause severe disease and death in humans. To better understand the pathogenesis and immunity to these viruses, we have used the BALB/c mouse model. Four H5N1 viruses replicated equally well in the lungs of mice without prior adaptation but differed in lethality for mice. H5N1 viruses that were highly lethal for mice were detected in multiple organs, including the brain. This is the first demonstration of an influenza A virus that replicates systemically in a mammalian species and is neurotropic without prior adaptation. The mouse model was also used to evaluate a strategy of vaccination against the highly pathogenic avian H5N1 viruses, using an inactivated vaccine prepared from nonpathogenic A/Duck/Singapore-Q/F119-3/97 (H5N3) virus that was antigenically related to the human H5N1 viruses. Mice administered vaccine intramuscularly, with or without alum, were completely protected from lethal challenge with H5N1 virus. Protection from infection was also observed in 70% of animals administered vaccine alone and 100% of mice administered vaccine with alum. The protective effect of vaccination correlated with the level of virus-specific serum antibody. These results suggests a strategy of vaccine preparedness for rapid intervention in future influenza pandemics that uses antigenically related nonpathogenic viruses as vaccine candidates.
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Williams, Simon H., Xiaoyu Che, Joel A. Garcia, John D. Klena, Bohyun Lee, Dorothy Muller, Werner Ulrich, et al. "Viral Diversity of House Mice in New York City." mBio 9, no. 2 (April 17, 2018): e01354-17. http://dx.doi.org/10.1128/mbio.01354-17.

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ABSTRACTThe microbiome of wildMus musculus(house mouse), a globally distributed invasive pest that resides in close contact with humans in urban centers, is largely unexplored. Here, we report analysis of the fecal virome of house mice in residential buildings in New York City, NY. Mice were collected at seven sites in Manhattan, Queens, Brooklyn, and the Bronx over a period of 1 year. Unbiased high-throughput sequencing of feces revealed 36 viruses from 18 families and 21 genera, including at least 6 novel viruses and 3 novel genera. A representative screen of 15 viruses by PCR confirmed the presence of 13 of these viruses in liver. We identified an uneven distribution of diversity, with several viruses being associated with specific locations. Higher mouse weight was associated with an increase in the number of viruses detected per mouse, after adjusting for site, sex, and length. We found neither genetic footprints to known human viral pathogens nor antibodies to lymphocytic choriomeningitis virus.IMPORTANCEMice carry a wide range of infectious agents with zoonotic potential. Their proximity to humans in the built environment is therefore a concern for public health. Laboratory mice are also the most common experimental model for investigating the pathobiology of infectious diseases. In this survey of mice trapped in multiple locations within New York City over a period of 1 year, we found a diverse collection of viruses that includes some previously not associated with house mice and others that appear to be novel. Although we found no known human pathogens, our findings provide insights into viral ecology and may yield models that have utility for clinical microbiology.
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Beck, Melinda A. "Selenium and host defence towards viruses." Proceedings of the Nutrition Society 58, no. 3 (August 1999): 707–11. http://dx.doi.org/10.1017/s0029665199000920.

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The association between viral disease and nutrition has long been thought to be due to effects on the host immune system. This theory suggests that when a host is malnourished, the immune system is compromised, and thus increased susceptibility to viral infection will occur. However, the virus itself may also be affected by the nutritional status of the host. We have demonstrated that a normally-benign strain of coxsackievirus B3 (CVB3/0) becomes virulent in either Se-deficient or vitamin E-deficient mice. Although the deficient animals are immunosuppressed, the virus itself is also altered. Six nucleotide changes were found in the virus that replicated in the deficient mice, and once these mutations occurred, even mice with normal nutrition became susceptible to disease. Thus, the nutritional status of the host was able to transform an avirulent virus into a virulent one due to genomic changes in the virus. We believe that a common mechanism of oxidative stress is the underlying cause of the genetic changes. Both vitamin E and Se act as antioxidants, and benign virus inoculated into GSH peroxidase (EC 1.11.1.9)-knockout mice will also convert to virulence due to genomic changes. Our work points to the importance of host nutrition during a viral disease, not only from the perspective of the host, but from the perspective of the viral pathogen as well.
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Ilyushina, Natalia A., Alexey M. Khalenkov, Jon P. Seiler, Heather L. Forrest, Nicolai V. Bovin, Henju Marjuki, Subrata Barman, Robert G. Webster, and Richard J. Webby. "Adaptation of Pandemic H1N1 Influenza Viruses in Mice." Journal of Virology 84, no. 17 (June 30, 2010): 8607–16. http://dx.doi.org/10.1128/jvi.00159-10.

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ABSTRACT The molecular mechanism by which pandemic 2009 influenza A viruses were able to sufficiently adapt to humans is largely unknown. Subsequent human infections with novel H1N1 influenza viruses prompted an investigation of the molecular determinants of the host range and pathogenicity of pandemic influenza viruses in mammals. To address this problem, we assessed the genetic basis for increased virulence of A/CA/04/09 (H1N1) and A/TN/1-560/09 (H1N1) isolates, which are not lethal for mice, in a new mammalian host by promoting their mouse adaptation. The resulting mouse lung-adapted variants showed significantly enhanced growth characteristics in eggs, extended extrapulmonary tissue tropism, and pathogenicity in mice. All mouse-adapted viruses except A/TN/1-560/09-MA2 grew faster and to higher titers in cells than the original strains. We found that 10 amino acid changes in the ribonucleoprotein (RNP) complex (PB2 E158G/A, PA L295P, NP D101G, and NP H289Y) and hemagglutinin (HA) glycoprotein (K119N, G155E, S183P, R221K, and D222G) controlled enhanced mouse virulence of pandemic isolates. HA mutations acquired during adaptation affected viral receptor specificity by enhancing binding to α2,3 together with decreasing binding to α2,6 sialyl receptors. PB2 E158G/A and PA L295P amino acid substitutions were responsible for the significant enhancement of transcription and replication activity of the mouse-adapted H1N1 variants. Taken together, our findings suggest that changes optimizing receptor specificity and interaction of viral polymerase components with host cellular factors are the major mechanisms that contribute to the optimal competitive advantage of pandemic influenza viruses in mice. These modulators of virulence, therefore, may have been the driving components of early evolution, which paved the way for novel 2009 viruses in mammals.
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Bocharov, E. F., Yu P. Shorin, I. A. Solodovnikova, L. S. Kazaryan, V. G. Selyatitskaya, and N. A. Pal'chikova. "Experimental diabetes in mice infected with coxsackie viruses." Bulletin of Experimental Biology and Medicine 103, no. 2 (February 1987): 182–86. http://dx.doi.org/10.1007/bf00840326.

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Tan, Mingming, Wenkui Sun, Chunlai Feng, Di Xia, Xiaoyue Shen, Yuan Ding, Zhicheng Liu, Zheng Xing, Xin Su, and Yi Shi. "The microRNA-let-7b-mediated attenuated strain of influenza A (H1N1) virus in a mouse model." Journal of Infection in Developing Countries 10, no. 09 (September 30, 2016): 973–81. http://dx.doi.org/10.3855/jidc.6861.

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Introduction: Evaluating the attenuation of influenza viruses in animal studies is important in developing safe and effective vaccines. This study aimed to demonstrate that the microRNA (miRNA)-let-7b-mediated attenuated influenza viruses (miRT-H1N1) are sufficiently attenuated and safe in mice. Methodology: The pathogenicity of the miRT-H1N1virus was investigated in a mouse model, evaluated with median lethal dose (LD50). The replicative dynamics of the miRT-H1N1, wild type (wt)-H1N1, and scramble (scbl)-H1N1 viruses in the lungs of infected mice were compared. The degrees of lesions and the expression levels of IL-6, TNF-α, and IFN-β in the lungs of mice infected with different viruses were also analyzed. Results: In miRT-H1N1 virus-infected mice, 100% of mice survived, and a lower pathogenicity was characterized with non-significant weight loss when compared to mice infected with the control wt virus. The miRT-H1N1 virus was not fatal for mice, even at the highest dose administered. The viral load in the lungs of miRT-H1N1-infected mice was significantly lower than that of the wild-type virus-infected mice. Fewer pulmonary lesions and lower levels of selected pro-inflammatory cytokines in the lungs of the mice infected with the miRT-H1N1 virus were also observed. The virulence of the miRT-H1N1 virus reduced significantly, suggesting that the miRT-H1N1 virus was safe for mice. Conclusions: Our study demonstrated that the miRNA-mediated gene silencing is an alternative approach to attenuating the pathogenicity of wt influenza viruses that have potential in the development of influenza vaccines.
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Gillim-Ross, Laura, Celia Santos, Zhongying Chen, Amy Aspelund, Chin-Fen Yang, Dan Ye, Hong Jin, George Kemble, and Kanta Subbarao. "Avian Influenza H6 Viruses Productively Infect and Cause Illness in Mice and Ferrets." Journal of Virology 82, no. 21 (August 20, 2008): 10854–63. http://dx.doi.org/10.1128/jvi.01206-08.

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ABSTRACT Influenza pandemic preparedness has focused on influenza virus H5 and H7 subtypes. However, it is not possible to predict with certainty which subtype of avian influenza virus will cause the next pandemic, and it is prudent to include other avian influenza virus subtypes in pandemic preparedness efforts. An H6 influenza virus was identified as a potential progenitor of the H5N1 viruses that emerged in Hong Kong in 1997. This virus continues to circulate in the bird population in Asia, and other H6 viruses are prevalent in birds in North America and Asia. The high rate of reassortment observed in influenza viruses and the prevalence of H6 viruses in birds suggest that this subtype may pose a pandemic risk. Very little is known about the replicative capacity, immunogenicity, and correlates of protective immunity for low-pathogenicity H6 influenza viruses in mammals. We evaluated the antigenic and genetic relatedness of 14 H6 influenza viruses and their abilities to replicate and induce a cross-reactive immune response in two animal models: mice and ferrets. The different H6 viruses replicated to different levels in the respiratory tracts of mice and ferrets, causing varied degrees of morbidity and mortality in these two models. H6 virus infection induced similar patterns of neutralizing antibody responses in mice and ferrets; however, species-specific differences in the cross-reactivity of the antibody responses were observed. Overall, cross-reactivity of neutralizing antibodies in H6 virus-infected mice did not correlate well with protection against heterologous wild-type H6 viruses. However, we have identified an H6 virus that induces protective immunity against viruses in the North American and Eurasian lineages.
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Dissertations / Theses on the topic "Mice – Viruses"

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Xue, Lumin, and 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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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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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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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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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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Qin, Kun, and 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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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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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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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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Webster, Marc A. "Mechanisms of polyomavirus transformation of the mouse mammary gland /." *McMaster only, 1996.

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Books on the topic "Mice – Viruses"

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Interaction of polycyclic aromatic hydrocarbons and tumourigenic DNA viruses in nude mouse fibroblast transformation assay. Kuopio: Dept. of Clinical Microbiology, University of Kuopio, 1989.

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Cook, Pamela Mary. Pathogenesis and persistence of pneumonia virus of mice. [s.l.]: typescript, 1996.

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Morgan, David John. Dejective interfering influenza virus reverses the immunopathological effects of standard influenza virus in mice. [s.l.]: typescript, 1992.

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Randhawa, J. S. Molecular characterisation of the pneumonia virus of mice glycoprotein genes. [s.l.]: typescript, 1993.

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Barr, John. The nucleotide sequence of the gene encoding the nucleocapsid protein of pneumonia virus of mice. [s.l.]: typescript, 1989.

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Barr, John Nicholas. Expression of the nucleoprotein and phosphoprotein genes of pneumonia virus of mice and specific interactions ofthe gene products. [s.l.]: typescript, 1993.

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Pollwein, Peter. Spezifische Bindungsstellen von SV40 T-Antigen im zellulären Mausgenom. Konstanz: Hartung-Gorre, 1987.

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Sapo. Corvallis, Ore: Ecopress, 1996.

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Junji, Yodoi, ed. Adult T cell leukemia and related diseases. New York: Springer, 1995.

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Howard, Colin R. Arenaviruses. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0032.

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There are few groups of viral zoonoses that have attracted such widespread publicity as the arenaviruses, particularly during the 1960’s and 1970’s when Lassa emerged as a major cause of haemorrhagic disease in West Africa. More than any other zoonoses, members of the family are used extensively for the study of virus-host relationships. Thus the study of this unique group of enveloped, single-stranded RNA viruses has been pursued for two quite separate reasons. First, lymphocytic choriomeningitis virus (LCM) has been used as a model of persistent virus infections for over half a century; its study has contributed, and continues to contribute, a number of cardinal concepts to our present understanding of immunology. LCM virus remains the prototype of the Arenaviridae and is a common infection of laboratory mice, rats and hamsters. Once thought rare in humans there is now increasing evidence of LCM virus being implicated in renal disease and as a complication in organ transplantation. Second, certain arenaviruses cause severe haemorrhagic diseases in man, notably Lassa fever in Africa, Argentine and Bolivian haemorrhagic fevers in South America, Guaranito infection in Venezuela and Chaparé virus in Bolivia. The latter is a prime example for the need of ever-continuing vigilance for the emergence of new viral diseases; over the past few years several new arenaviruses have been reported as implicated with severe human disease and indeed the number of new arenaviruses discovered since the last edition of this book have increased the size of this virus family significantly.In common with LCM, the natural reservoir of these infections is a limited number of rodent species (Howard, 1986). Although the initial isolates from South America were at first erroneously designated as newly defined arboviruses, there is no evidence to implicate arthropod transmission for any arenavirus. However, similar methods of isolation and the necessity of trapping small animals have meant that the majority of arenaviruses have been isolated by workers in the arbovirus field. A good example of this is Guaranito virus that emerged during investigation of a dengue virus outbreak in Venezuela (Salas et al. 1991).There is an interesting spectrum of pathological processes among these viruses. All the evidence so far available suggests that the morbidity of Lassa fever and South American haemorrhagic fevers due to arenavirus infection results from the direct cytopathic action of these agents. This is in sharp contrast to the immunopathological basis of ‘classic’ lymphocytic choriomeningitis disease seen in adult mice infected with LCM virus and the use of this system for elucidating the phenomenon of H2-restriction of the host cytotoxic T cell response (Zinkernagel and Doherty 1979). Despite the utility of this experimental model for dissecting the nature of the immune response to virus infection and the growing interest in arenaviruses of rodents, there remains much to be done to elucidate the pathogenesis of these infections in humans.
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Book chapters on the topic "Mice – Viruses"

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Gaudilliere, Jean-Paul. "Circulating Mice and Viruses." In The Practices of Human Genetics, 89–124. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4718-7_4.

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Bendinelli, Mauro, Donatella Matteucci, and Antonio Toniolo. "Retrovirus-Induced Immunodeficiency in Mice." In Viruses, Immunity, and Immunodeficiency, 129–40. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2185-9_13.

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Müllbacher, A., and R. V. Blanden. "T-Cell-Mediated Control of Poxvirus Infection in Mice." In Viruses and Apoptosis, 39–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-540-74264-7_3.

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Christen, Urs, and Matthias G. von Herrath. "Virus-Induced Models for Type 1 Diabetes in Mice." In Diabetes and Viruses, 259–69. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4051-2_25.

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Racaniello, V. R., and R. Ren. "Transgenic mice and the pathogenesis of poliomyelitis." In Positive-Strand RNA Viruses, 79–86. Vienna: Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-9326-6_9.

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Wade, W. F., C. Dees, T. L. German, and R. F. Marsh. "Scrapie Infection in Athymic and Germ-Free Mice." In Viruses, Immunity, and Immunodeficiency, 245–49. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2185-9_23.

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Forrest, James Craig, Laurie T. Krug, and Samuel H. Speck. "Murine Gammaherpesvirus 68 Infection of Mice: A Small Animal Model for Characterizing Basic Aspects of Gammaherpesvirus Pathogenesis." In DNA Tumor Viruses, 735–75. New York, NY: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-68945-6_28.

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Gould, Cheryl L., Karyle G. McMannama, Nancy J. Bigley, and David J. Giron. "Exacerbation of the Pathogenesis of the Diabetogenic Variant of Encephalomyocarditis Virus in Mice by Interferon." In Viruses, Immunity, and Immunodeficiency, 307–11. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2185-9_29.

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Efrat, S., and D. Hanahan. "Evidence for Threshold Effects in Transformation of Pancreatic β Cells by SV40 T Antigen in Transgenic Mice." In Transforming Proteins of DNA Tumor Viruses, 89–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74578-2_11.

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Sweet, C., and D. M. Coates. "Studies of the pathogenesis of Dugbe virus in normal and in immunosuppressed mice." In Hemorrhagic Fever with Renal Syndrome, Tick- and Mosquito-Borne Viruses, 181–95. Vienna: Springer Vienna, 1990. http://dx.doi.org/10.1007/978-3-7091-9091-3_21.

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Conference papers on the topic "Mice – Viruses"

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Bochkov, Y. A. "POLYVALENT INACTIVATED RHINOVIRUS C VACCINE INDUCES BROAD NEUTRALIZING ANTIBODY RESPONSES IN MICE." In Viruses: Discovering Big in Small. TORUS PRESS, 2019. http://dx.doi.org/10.30826/viruses-2019-08.

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Li, Yan, Ying Chi, Qian Bian, Tian Wen, and Wenshuai Zhang. "Mesenchymal Stem Cells Therapy for H9N2 Avian Influenza Viruses Induced Acute Lung Injury in Mice." In 2012 International Conference on Biomedical Engineering and Biotechnology (iCBEB). IEEE, 2012. http://dx.doi.org/10.1109/icbeb.2012.271.

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Hawkins, Gabrielle M., Amber N. McCoy, Wenchuan Sun, Temitope Keku, Chunxiao Zhou, Wendy R. Brewster, and Victoria L. Bae-Jump. "Abstract B29: Impact of obesity on the uterine microbiome in pre- and postmenopausal mice with endometrial cancer." In Abstracts: AACR Special Conference on the Microbiome, Viruses, and Cancer; February 21-24, 2020; Orlando, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.mvc2020-b29.

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Di Minno, G., A. Fusco, G. Portella, A. H. Cerbone, C. Iride, G. Tajana, O. Russo, and P. L. Mattioli. "MYELOPROLIFERATIVE DISEASE CHARACTERIZED BY THROMBOSIS, BLEEDING AND PLATELET DYSFUNCTION IN MICE INJECTED WITH THE POLYOMA MURINE LEUKEMIA VIRUS (PyMLV)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643580.

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After i.p. injection of PyMLV, NIH/OLAC mice showed thrombi in tail veins, ears, muscles and nesenterium together with thrombi and hematomas of subcutaneous tissues. This was followed by infarctions of lungs, brain and heart, that caused death of the animals. Laboratory evaluations of the infected mice showed normochromic anemia, mild thrombocytosis and marked defects in the aggregation and in the secretion of ATP from platelets exposed to AJP, collagen, thrombin or A23137. About 10% of cells present in the bone marrow was formed by blasts; 20% by multinucleated cells identified as megakariocytes (M) by peroxidase and acethyl-cholinesterase staining, and the vast majority of the other cells by entities belonging to all stages of maturation of the myeloid lineage. Hybridization experiments showed that the blasts present in the bone marrow were the only cells in which viral replication takes place. Maturation of M in the bone marrow was completely normal, and as for M from non-infected mice, proliferation and maturation in vitro was dependent on the presence of interleukin 3. Finally, studies in other strains of mice showed that the Fv-2 locus is involved in the pathogenicity of PyMLV in NIH/OLAC mice. Ne conclude that, in addition to its obvious pathophysiological significance, the myeloproliferative disease that occurs in mice after i.p. injection of PyMLV, can serve as an important probe for understanding basic events leading to bleeding and thrombosis.
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Scorgie, B., Prakash Veeraraghavan, and Somnath Ghosh. "Early virus detection for Windows Mobile." In 2009 IEEE 9th Malaysia International Conference on Communications (MICC). IEEE, 2009. http://dx.doi.org/10.1109/micc.2009.5431517.

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Maruoka, Shuichiro, Sotaro Shikano, Yasuhiro Gon, Kazumichi Kuroda, Kaori Soda, Eriko Tsuboi, Ikuko Takeshita, Kazufumi Shimizu, and Shu Hashimoto. "Carbocisteine attenuates influenza virus A replication in the bronchoalveolar lavage fluids of virus-infected mice." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.oa489.

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Lomakina, N. F., T. A. Timofeeva, I. A. Rudneva, A. V. Lyashko, O. L. Voronina, E. I. Aksenova, N. N. Ryzhova, M. S. Kunda, A. A. Treshchalina, and A. S. Gambaryan. "INCREASING VIRULENCE OF NONPATHOGENIC INFLUENZA VIRUS H5N3 DURING ADAPTATION FOR MICE." In Molecular Diagnostics and Biosafety. Federal Budget Institute of Science 'Central Research Institute for Epidemiology', 2020. http://dx.doi.org/10.36233/978-5-9900432-9-9-235.

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Caulk, Alexander W., and Rudolph L. Gleason. "Treatment With Non-Nucleoside Reverse Transcriptase Inhibitor Efavirenz Leads to Increase of Carotid Intima-Media Thickness in Mice." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14744.

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Since the advent of highly active antiretroviral therapy (HAART), patients infected with human immunodeficiency virus-1 (HIV-1) are living longer lives. However, HIV-1-positive (HIV-1+) patients are now experiencing many non-AIDS related comorbidities including myocardial infarction, atherosclerotic lesions, and other preclinical markers of atherosclerosis including increased carotid intima-media thickness (cIMT), arterial stiffness, and impaired flow-mediated dilation (FMD). Studies have implicated the virus, the treatment, or both in the progression of these co-morbidities, causing the exact mechanisms of cardiovascular disease progression to remain unclear.
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Khalaf, Luaay Kahtan. "Assessment of wheat curl mite virulence to wheat genotypes and distribution of mite-vectored viruses in the north central United States." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.112966.

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Tsai, Kuen-Nan. "A mechanical transmission of dengue virus infection in mice by mosquitoAedes aegypti." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.115700.

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Reports on the topic "Mice – Viruses"

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Schurig, Gerhardt G. Expression of Brucella Antigens in Vaccinia Virus to Prevent Brucellosis in Humans: Protection Studies in Mice. Fort Belvoir, VA: Defense Technical Information Center, August 2000. http://dx.doi.org/10.21236/ada382850.

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Stanton, G. J., and T. K. Hughes. The Effects of Orally Applied and Systemic Interferon and Cytokines on Hormonal and Host Defense Mechanisms of Virus-Infected Mice. Fort Belvoir, VA: Defense Technical Information Center, March 1995. http://dx.doi.org/10.21236/ada292762.

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