The murine cytomegalovirus as a model for the study of viral pathogenesis and persistent infections

Jb, Hudson

doi:10.1007/bf01314900

Cited by 159 publications

(119 citation statements)

References 156 publications

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“…Human immunodeficiency virus is frequently also found in brain macrophages from AIDS patients with encephalitis (reviewed by Carne, 1987). Cytomegalovirus may be pathogenic in this setting but we consider it to be unproven at this time, with support only for criterion 4 following intracerebral inoculation of MCMV (Lussier, 1973(Lussier, , 1975Hudson, 1979). Kaposi's sarcoma Fifteen years ago, cultures of cells derived from Kaposi's sarcoma (KS) tissue were found to contain a herpesvirus which resembled CMV (Giraldo, Beth & Haguenau, 1972;.…”

Section: Encephalitismentioning

confidence: 96%

“…Note that not all of the mouse models mirror the human conditions exactly. For example, MCMV causes labyrinthitis in the mouse which is different histologically from the endolymphatic labyrinthitis seen in humans (Davis & Strauss, 1973) and also infects the vascular tissues of the eye rather than the retina and choroid as seen in humans (Hudson, 1979). These discrepancies may be due to differences in the route of infection in the experimental and natural situations and so we have accepted virus infection of the same organ as fulfilment of this criterion.…”

Section: Oncogenicitymentioning

confidence: 98%

“…Cytomegalovirus DNA has been detected in the retina (Kennedy et al 1986), ganciclovir can effectively suppress the disease process (Collaborative Study, 1986) and animal models are available (Hudson, 1979). Criteria 1, 3 and 4 are therefore satisfied.…”

Section: Retinitismentioning

confidence: 99%

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The status of CMV as a human pathogen

Griffiths

Grundy

1988

Epidemiol. Infect.

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Cytomegalovirus (CMV) is a common infectious agent which is well adapted to its host. Following primary infection, which is almost always asymptomatic in people with normal immunity, the virus establishes latency at sites which are unknown. The virus is probably maintained in this latent state by immune surveillance mechanisms since immunosuppression frequently leads to reactivation of virus.Cytomegalovirus has been identified in most anatomical areas of the human body. The aim of this article is to define criteria for pathogenicity so that clinical and experimental data can be reviewed to determine if CMV is likely to cause disease at these various clinical sites. Thus, patients have been shown to die frequentlywithCMV but do they diefromit?

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Section: Encephalitismentioning

confidence: 96%

Section: Oncogenicitymentioning

confidence: 98%

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The status of CMV as a human pathogen

Griffiths

Grundy

1988

Epidemiol. Infect.

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“…Consequently, animal models for CMV depend on studying the CMVs of the respective mammal species. The most widely used model is murine CMV (MCMV), which can address many fundamental questions for biology, pathogenesis and immunology of cytomegalovirus [18,19]. However, the genomes of MCMV and HCMV are quite diVerent and many "non-essential genes", i.e.…”

Section: Introductionmentioning

confidence: 99%

Rhesus CMV: an emerging animal model for human CMV

Powers

Früh

2008

Med Microbiol Immunol

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Human CMV is the predominant infectious cause of congenital birth defects and an opportunistic pathogen in immunosuppressed individuals, including AIDS patients. Most individuals are infected early during their life followed by life-long latent infection. During this latent phase, frequent reactivation and antigen production continue to stimulate the immune system. While the immune response is able to control the virus, it is unable to eradicate it. Moreover, super-infection by diVerent CMV strains has been observed despite a strong immune response. Longterm immune stimulation by CMV has also been implicated in immune senescence and chronic conditions such as atherosclerosis. CMVs are highly species-speciWc and the relatedness of CMV genomes exactly mirrors the relatedness of their hosts. Thus, each CMV species is highly adapted to its respective host species, but is unable to infect other, even closely related hosts. While fascinating from an evolutionary perspective, this host restriction prevents studying HCMV in experimental animals. Exceptions are severely immunocompromised mice, e.g. SCID mice, or SCID/NOD mice, which might allow partial reconstitution of CMV infection in rodents. More practical however, is to study CMVs in their natural host, e.g. murine, rat or guinea pig CMVs. However, while these small animal models have many advantages, such as the availability of inbred animals as well as lower cost, the limited homology of the viral genomes with HCMV limits the functional analysis of homologous gene products. The closest relative to HCMV is chimpanzee CMV (CCMV), but this is not a practical animal model since chimps are a protected species, extremely expensive and of very limited availability. In contrast, rhesus macaques are a more widely used experimental animal species and, while more distant than CCMV, rhesus CMV (RhCMV) contains most of the HCMV gene families thus allowing the study of their role in acute and latent CMV infection. In this review we will discuss the current state of developing RhCMV as a model for HCMV.

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“…The murine cytomegalovirus (MCMV), a betaherpesvirus, has been widely studied as a model of viral infection since many aspects of its biology, replication and pathogenesis resemble those of human cytomegalovirus (HCMV) (Hudson, 1979;Koszinowski et al, 1990;McDougall, 1990;Mocarski, 1991). It has a large DNA genome of 230 kbp encoding over 100 genes, grouped into immediate early (IE), early and late genes (Ebeling et at., 1983;Mercer et al, 1983).…”

Section: Introductionmentioning

confidence: 99%