Abstract
Since murine cytomegalovirus (MCMV) was first described in 1954, it has been used to model human cytomegalovirus (HCMV) diseases. MCMV is a natural pathogen of mice that is present in wild mice populations and has been associated with diseases such as myocarditis. The species-specific nature of HCMV restricts most research to cell culture-based studies or to the investigation of non-invasive clinical samples, which may not be ideal for the study of disseminated disease. Initial MCMV research used a salivary gland-propagated virus administered via different routes of inoculation into a variety of mouse strains. This revealed that the genetic background of the laboratory mice affected the severity of disease and altered the extent of subsequent pathology. The advent of genetically modified mice and viruses has allowed new aspects of disease to be modeled and the opportunistic nature of HCMV infection to be confirmed. This review describes the different ways that MCMV has been used to model HCMV diseases and explores the continuing difficulty faced by researchers attempting to model HCMV congenital cytomegalovirus disease using the mouse model.
Highlights
It has famously been stated that “mice lie and monkeys exaggerate” [1], but the use of animal models in the study of infectious disease provides strong evidence for the mechanisms underlying the pathogenesis of infections in humans and provides opportunities to study interactions between hosts and pathogens that are not provided by collecting minimally invasive human samples such as blood, feces, saliva and urine
Invariably leads to the predictable loss of genetic regions that does not occur to the same extent with MCMV [24], a recent report has provided evidence that deletions occur as MCMV is propagated from salivary glands in culture [25]
Where MCMV was used as a vaccine vector expressing the mouse ovarian glycoprotein zona pellucida 3 in studies investigating immune-mediated contraception, the specific m157 to Ly49H (NK cell activation receptor) rapid response to infection was broadly associated with vaccine success [51]
Summary
It has famously been stated that “mice lie and monkeys exaggerate” [1], but the use of animal models in the study of infectious disease provides strong evidence for the mechanisms underlying the pathogenesis of infections in humans and provides opportunities to study interactions between hosts and pathogens that are not provided by collecting minimally invasive human samples such as blood, feces, saliva and urine. There are many animal models where laboratory-inoculated animals exhibit symptoms or pathogen replication that mimics human infection, even though infection may not occur in the natural environment These models are useful in carefully evaluated (and disclosed) circumstances (discussed in [6] for SARS-CoV-2) and have provided useful information on infection pathways and the effects of opportunistic infections and potential drug targets [7]. Examples of animal models in non-target species are those developed for influenza and respiratory syncytial virus in ferrets [8] and Ebola virus infection, which have been modeled in suckling (but not adult) immunocompetent mice as well as Syrian golden hamsters [9] These models and others like them have illuminated pathways used by pathogens to travel from the site of infection to organs or other sites of tropism, as well as immune responses, symptom and infection profiles and treatment options. This review will focus on the use of MCMV to model human cytomegalovirus (HCMV) disease
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