Relevant bibliographies by topics / Cytomegaloviruses – Animal models

Academic literature on the topic 'Cytomegaloviruses – Animal models'

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Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Cytomegaloviruses – Animal models"

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Roark, Hunter K., Jennifer A. Jenks, Sallie R. Permar, and Mark R. Schleiss. "Animal Models of Congenital Cytomegalovirus Transmission: Implications for Vaccine Development." Journal of Infectious Diseases 221, Supplement_1 (March 5, 2020): S60—S73. http://dx.doi.org/10.1093/infdis/jiz484.

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Abstract Although cytomegaloviruses (CMVs) are species-specific, the study of nonhuman CMVs in animal models can help to inform and direct research aimed at developing a human CMV (HCMV) vaccine. Because the driving force behind the development of HCMV vaccines is to prevent congenital infection, the animal model in question must be one in which vertical transmission of virus occurs to the fetus. Fortunately, two such animal models—the rhesus macaque CMV and guinea pig CMV—are characterized by congenital infection. Hence, each model can be evaluated in “proof-of-concept” studies of preconception vaccination aimed at blocking transplacental transmission. This review focuses on similarities and differences in the respective model systems, and it discusses key insights from each model germane to the study of HCMV vaccines.
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Moulden, Jerome, Cathy Yea Won Sung, Ilija Brizic, Stipan Jonjic, and William Britt. "Murine Models of Central Nervous System Disease following Congenital Human Cytomegalovirus Infections." Pathogens 10, no. 8 (August 21, 2021): 1062. http://dx.doi.org/10.3390/pathogens10081062.

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Human cytomegalovirus infection of the developing fetus is a leading cause of neurodevelopmental disorders in infants and children, leading to long-term neurological sequela in a significant number of infected children. Current understanding of the neuropathogenesis of this intrauterine infection is limited because of the complexity of this infection, which includes maternal immunological responses that are overlaid on virus replication in the CNS during neurodevelopment. Furthermore, available data from human cases are observational, and tissues from autopsy studies have been derived from only the most severe infections. Animal models of this human infection are also limited by the strict species specificity of cytomegaloviruses. However, informative models including non-human primates and small animal models have been developed. These include several different murine models of congenital HCMV infection for the study of CMV neuropathogenesis. Although individual murine models do not completely recapitulate all aspects of the human infection, each model has provided significant information that has extended current understanding of the neuropathogenesis of this human infection. This review will compare and contrast different murine models in the context of available information from human studies of CNS disease following congenital HCMV infections.
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Kern, Earl R., Deborah J. Bidanset, Caroll B. Hartline, Zhaohua Yan, Jiri Zemlicka, and Debra C. Quenelle. "Oral Activity of a Methylenecyclopropane Analog, Cyclopropavir, in Animal Models for Cytomegalovirus Infections." Antimicrobial Agents and Chemotherapy 48, no. 12 (December 2004): 4745–53. http://dx.doi.org/10.1128/aac.48.12.4745-4753.2004.

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ABSTRACT We reported previously that purine 2-(hydroxymethyl)methylenecyclopropane analogs have good activity against cytomegalovirus infection. A second-generation analog, (Z)-9-{[2,2-bis-(hydroxymethyl)cyclopropylidene]methyl}guanine (ZSM-I-62, cyclopropavir [CPV]), has particularly good activity against murine and human cytomegaloviruses (MCMV and HCMV) in vitro. To determine the oral activity of this compound in vivo, BALB/c or severe combined immunodeficient (SCID) mice infected with MCMV and two models using SCID mice implanted with human fetal tissue and subsequently infected with HCMV were used. In MCMV-infected normal mice, CPV at 10 mg/kg of body weight was highly effective in preventing mortality when administered at 24, 48, or 72 h post-viral inoculation and reduced titers of virus in tissues of SCID mice by 2 to 5 log10. In one HCMV model, human fetal retinal tissue was implanted into the anterior chamber of the mouse eye and inoculated with the Toledo strain of HCMV, and in the second, human fetal thymus and liver tissues were implanted under the kidney capsule of mice and then inoculated with HCMV. In general, replication of HCMV in both types of implant tissue increased from 7 through 21 to 28 days and then gradually decreased to undetectable levels by 8 weeks postinfection. Oral treatment with 45 or 15 mg of CPV/kg initiated 24 h after infection was highly effective in reducing replication to undetectable levels in both models and was generally more effective than ganciclovir. These data indicate that the methylenecyclopropane analog, CPV, was highly efficacious in these four animal models and should be evaluated for use in HCMV infections in humans.
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Taher, Husam, Eisa Mahyari, Craig Kreklywich, Luke S. Uebelhoer, Matthew R. McArdle, Matilda J. Moström, Amruta Bhusari, et al. "In vitro and in vivo characterization of a recombinant rhesus cytomegalovirus containing a complete genome." PLOS Pathogens 16, no. 11 (November 24, 2020): e1008666. http://dx.doi.org/10.1371/journal.ppat.1008666.

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Cytomegaloviruses (CMVs) are highly adapted to their host species resulting in strict species specificity. Hence, in vivo examination of all aspects of CMV biology employs animal models using host-specific CMVs. Infection of rhesus macaques (RM) with rhesus CMV (RhCMV) has been established as a representative model for infection of humans with HCMV due to the close evolutionary relationships of both host and virus. However, the only available RhCMV clone that permits genetic modifications is based on the 68–1 strain which has been passaged in fibroblasts for decades resulting in multiple genomic changes due to tissue culture adaptations. As a result, 68–1 displays reduced viremia in RhCMV-naïve animals and limited shedding compared to non-clonal, low passage isolates. To overcome this limitation, we used sequence information from primary RhCMV isolates to construct a full-length (FL) RhCMV by repairing all mutations affecting open reading frames (ORFs) in the 68–1 bacterial artificial chromosome (BAC). Inoculation of adult, immunocompetent, RhCMV-naïve RM with the reconstituted virus resulted in significant viremia in the blood similar to primary isolates of RhCMV and furthermore led to high viral genome copy numbers in many tissues at day 14 post infection. In contrast, viral dissemination was greatly reduced upon deletion of genes also lacking in 68–1. Transcriptome analysis of infected tissues further revealed that chemokine-like genes deleted in 68–1 are among the most highly expressed viral transcripts both in vitro and in vivo consistent with an important immunomodulatory function of the respective proteins. We conclude that FL-RhCMV displays in vitro and in vivo characteristics of a wildtype virus while being amenable to genetic modifications through BAC recombineering techniques.
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Farrell, Helen. "Animal models of human cytomegalovirus congenital infection." Microbiology Australia 36, no. 4 (2015): 196. http://dx.doi.org/10.1071/ma15068.

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Human cytomegalovirus (HCMV) infection is highly species-specific, which means that it is unable to productively infect laboratory animals. Despite this caveat, studies of animal CMV counterparts in their natural hosts have revealed significant correlations with observed neuropathological effects of congenital HCMV infection and have improved our understanding of host responses to vaccination. The biological relatedness between human and animal CMVs has been confirmed by phylogenetic analyses; the conservation of ‘core' genes that are essential for virus replication as well as genes that contribute similar mechanisms for virus persistence in their respective host species. The common animal models of HCMV congenital infection include Rhesus CMV (RhCMV), guinea-pig CMV (GPCMV) and mouse CMV (MCMV). Whilst animal models of CMV do not fully recapitulate HCMV infection, they each offer specific advantages in understanding HCMV congenital/perinatal infection (summarised in Table 1).
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McGregor, Alistair, and K. Yeon Choi. "Cytomegalovirus antivirals and development of improved animal models." Expert Opinion on Drug Metabolism & Toxicology 7, no. 10 (September 2011): 1245–65. http://dx.doi.org/10.1517/17425255.2011.613824.

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Imperiale, Michael J., and Mengxi Jiang. "What DNA Viral Genomic Rearrangements Tell Us about Persistence." Journal of Virology 89, no. 4 (December 3, 2014): 1948–50. http://dx.doi.org/10.1128/jvi.01227-14.

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Understanding the life cycle and pathogenesis of animal viruses requires that we have systems in which the viruses can replicate and cause disease. For the latter, we rely upon animal models or information that we can obtain from studying natural infections of humans and other animals. For the former, however, we are largely dependent on the availability of cell culture systems in which viruses can be propagated to investigate the molecular mechanisms of viral replication. For many years, it was assumed that replication in culture provided an accurate description of the life cycle of the organism. In this Gem, we will discuss two viruses, polyomavirus and cytomegalovirus, in which cell culture systems have accidentally provided unique potential insights into viral replication and persistence in their hosts.
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Tsutsui, Yoshihiro. "Developmental disorders of the mouse brain induced by murine cytomegalovirus: Animal models for congenital cytomegalovirus infection." Pathology International 45, no. 2 (February 1995): 91–102. http://dx.doi.org/10.1111/j.1440-1827.1995.tb03428.x.

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Kaul, Artur, Uwe Schönmann, and Stefan Pöhlmann. "Seroprevalence of viral infections in captive rhesus and cynomolgus macaques." Primate Biology 6, no. 1 (March 26, 2019): 1–6. http://dx.doi.org/10.5194/pb-6-1-2019.

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Abstract. Macaques serve as important animal models for biomedical research. Viral infection of macaques can compromise animal health as well as the results of biomedical research, and infected animals constitute an occupational health risk. Therefore, monitoring macaque colonies for viral infection is an important task. We used a commercial chip-based assay to analyze sera of 231 macaques for the presence of antibody responses against nine animal and human viruses. We report high seroprevalence of cytomegalovirus (CMV), lymphocryptovirus (LCV), rhesus rhadinovirus (RRV) and simian foamy virus (SFV) antibodies in all age groups. In contrast, antibodies against simian retrovirus type D (SRV/D) and simian T cell leukemia virus (STLV) were detected only in 5 % and 10 % of animals, respectively, and were only found in adult or aged animals. Moreover, none of the animals had antibodies against herpes B virus (BV), in keeping with the results of in-house tests previously used for screening. Finally, an increased seroprevalence of measles virus antibodies in animals with extensive exposure to multiple humans for extended periods of time was observed. However, most of these animals were obtained from external sources, and a lack of information on the measles antibody status of the animals at the time of arrival precluded drawing reliable conclusions from the data. In sum, we show, that in the colony studied, CMV, LCV, RRV and SFV infection was ubiquitous and likely acquired early in life while SRV/D and STLV infection was rare and likely acquired during adulthood.
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Kanai, Kyosuke, Souichi Yamada, Yumiko Yamamoto, Yoshiko Fukui, Ichiro Kurane, and Naoki Inoue. "Re-evaluation of the genome sequence of guinea pig cytomegalovirus." Journal of General Virology 92, no. 5 (May 1, 2011): 1005–20. http://dx.doi.org/10.1099/vir.0.027789-0.

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Congenital infection by human cytomegalovirus (HCMV) is a major cause of birth defects and developmental abnormalities. Since guinea pig cytomegalovirus (GPCMV) crosses the placenta and causes infection in utero, GPCMV models are useful for studies of the mechanisms of transplacental transmission. During our characterization of a genomic locus required for GPCMV dissemination in animals, we found that the nucleotide sequence in and around the nearby immediate–early genes in our lineage of GPCMV strain 22122 [designated GPCMV (ATCC-P5)] showed clear differences from that reported previously for the same strain [designated GPCMV (UMN)] passaged extensively in vitro. Since in vitro passaging of HCMV is known to result in genetic alterations, especially in the UL128–UL131A locus, and loss of growth ability in particular cell types, in this study we determined the complete genome sequence of GPCMV (ATCC-P5), which grows efficiently in animals. A total of 359 differences were identified between the genome sequences of GPCMV (UMN) and GPCMV (ATCC-P5), and these resulted in structural differences in 29 protein-encoding regions. In addition, some genes predicted from our analysis but not from GPCMV (UMN) are well conserved among cytomegaloviruses. An additional 18 passages of GPCMV (ATCC-P5) in vitro generated no further marked alterations in these genes or in the locus corresponding to the HCMV UL128–UL131A. Our analyses indicate that the published sequence of GPCMV (UMN) contains a substantial number of sequencing errors and, possibly, some mutations resulting from a long history of passaging in vitro. Our re-evaluation of the genetic content of GPCMV will provide a solid foundation for future studies.
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Dissertations / Theses on the topic "Cytomegaloviruses – Animal models"

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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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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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Koontz, Thadeus B. "MCMV induced cerebellar maldevelopment." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2007p/koontz.pdf.

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Book chapters on the topic "Cytomegaloviruses – Animal models"

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Podlech, Jürgen, Rafaela Holtappels, Natascha K. A. Grzimek, and Matthias J. Reddehase. "Animal models: Murine cytomegalovirus." In Immunology of Infection, 493—IN11. Elsevier, 2002. http://dx.doi.org/10.1016/s0580-9517(02)32103-2.

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Bernstein, D. I., and N. Bourne. "Animal Models for Cytomegalovirus Infection." In Handbook of Animal Models of Infection, 935–41. Elsevier, 1999. http://dx.doi.org/10.1016/b978-012775390-4/50251-7.

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Stals, F. S. "Animal Models for Cytomegalovirus Infection." In Handbook of Animal Models of Infection, 943–50. Elsevier, 1999. http://dx.doi.org/10.1016/b978-012775390-4/50252-9.

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Kern, E. R. "Animal Models for Cytomegalovirus Infection." In Handbook of Animal Models of Infection, 927–34. Elsevier, 1999. http://dx.doi.org/10.1016/b978-012775390-4/50250-5.

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Kemble, G. W., G. M. Duke, and E. S. Mocarski. "Human Cytomegalovirus Infection of the SCID-hu (thy/liv) Mouse." In Handbook of Animal Models of Infection, 951–56. Elsevier, 1999. http://dx.doi.org/10.1016/b978-012775390-4/50253-0.

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Bidanset, D. J., O. M. Faye-Petersen, E. R. Kern, M. del Cerro, and E. S. Lazar. "Animal Model for Ocular Human Cytomegalovirus Infections in SCID-hu Mice." In Handbook of Animal Models of Infection, 957–62. Elsevier, 1999. http://dx.doi.org/10.1016/b978-012775390-4/50254-2.

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Yamashita, Yushiro. "Congenital Infections." In Cognitive and Behavioral Abnormalities of Pediatric Diseases. Oxford University Press, 2010. http://dx.doi.org/10.1093/oso/9780195342680.003.0037.

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Congenital infections are designated frequently by the term ‘‘TORCH syndrome’’ (toxoplasmosis, other infections/pathogens [i.e., syphilis and human immunodeficiency virus], rubella, cytomegalovirus [CMV], and herpes simplex). Most of the patients are asymptomatic in the neonatal period, although the neonatal neurological symptoms that do occur are quite dramatic. Infants with congenital infections are at high risk for developmental disabilities (Stagno and Britt 2006; Volpe 2000). The infection may not be apparent immediately after birth, but may manifest with signs of disease weeks, months, or years later, such as seen in chorioretinitis of Toxoplasma gondii. Because of this increased neurodevelopmental risk, these infections require comprehensive, longitudinal follow-up that should begin in the neonatal period and continue through adolescence (Willamson 1994). In this chapter, I review the pathophysiology, neurological manifestations, and imaging of congenital infections by CMV, rubella virus, and Toxoplasma gondii briefly followed by their cognitive and behavioral manifestations. Cytomegalovirus is the leading cause of congenital infection in the United States and northwestern Europe (Istas et al. 1995). Neonatal signs of intrauterine CMV infection include hepatosplenomegaly, petechial rash (usually related to thrombocytopenia), small-for-gestational-age infant, hyperbilirubinemia, microcephaly, and chorioretinitis. Ten to 15% of neonates with asymptomatic congenital CMV infection and almost all neonates with symptomatic infection develop persistent problems, most commonly neurological impairment. Cytomegalovirus can be transmitted from mother to fetus anytime during gestation through the placenta. It is most likely to cause serious harm to the fetus when the mother has a primary CMV infection during pregnancy. Primary CMV infections are reported in 1%–4% of seronegative women during pregnancy, and the risk for viral transmission to the fetus is 30%–40%. Reactivation of the infection during pregnancy is reported in 10%–30% of seropositive women, and the risk of transmitting the virus is about 1%–3% (Stagno and Britt 2006). The pathogenesis of central nervous system (CNS) infection by CMV in the developing fetus remains poorly understood because of the lack of autopsy cases and well-developed animal models.
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