Factors influencing susceptibility of laboratory rodents to infection with mouse adenovirus strains K87 and FL

Smith, Abigail L.; Barthold, Stephen W.

doi:10.1007/bf01311342

Cited by 13 publications

(2 citation statements)

References 10 publications

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“…The results of previous studies showing sensitivity to disseminated MAV-1 disease in all of the murine strains tested when infected prior to 3 weeks of age strengthens the argument that immunologic differences can be the basis for strain differences (16,17,37,42). This is based on the fact that the development of resistance to MAV-1 clinical disease correlates with the maturation of the murine immune system (8,12,40).…”

Section: Discussionsupporting

confidence: 53%

Mouse adenovirus type 1 causes a fatal hemorrhagic encephalomyelitis in adult C57BL/6 but not BALB/c mice

Guida

Fejér

Pirofski

et al. 1995

J Virol

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Mouse adenovirus type 1 (MAV-1) produces a lethal disease in newborn or suckling mice characterized by infectious virus and viral lesions in multiple organs. Previous reports of MAV-1 infection of adult mice generally described serologic evidence of infection without morbidity or mortality. However, our current results demonstrate that MAV-1 causes a fatal illness in adult C57BL/6 (B6) mice (50% lethal dose, [LD 50 ], 10 3.0 PFU) but not in adult BALB/c mice at all of the doses tested (LD 50 , >10 5.0 PFU). Adult (BALB/c ؋ B6)F 1 mice were intermediately susceptible (LD 50 , 10 4.5 PFU). Clinically, the sensitive B6 mice showed symptoms of acute central nervous system (CNS) disease, including tremors, seizures, ataxia, and paralysis. Light microscopic examination of CNS tissue from the B6 animals revealed petechial hemorrhages, edema, neovascularization, and mild inflammation in the brain and spinal cord. Analysis by electron microscopy showed evidence of inflammation, such as activated microglia, as well as swollen astrocytic endfeet and perivascular lipid deposition indicative of blood-brain barrier dysfunction. Outside of the CNS, the only significant pathological findings were foci of cytolysis in the splenic white pulp. Assessment of viral replication from multiple tissues was performed by using RNase protection assays with an antisense MAV-1 early region 1a probe. The greatest amounts of viral mRNA in MAV-1-infected B6 animals were located in the brain and spinal cord. Less viral message was detected in the spleen, lungs, and heart. No viral mRNA was detected in BALB/c mouse tissue, with the exception of low levels in the heart. Viral titers of organ tissues were also determined and were concordant with RNase protection findings on the brain and spinal cord but failed to demonstrate significant infectious virus in additional organs. Our experiments demonstrate that MAV-1 has a striking tropism for the CNS that is strain dependent, and this provides an informative in vivo model for the study of adenoviral pathogenesis.

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Section: Discussionsupporting

confidence: 53%

Mouse adenovirus type 1 causes a fatal hemorrhagic encephalomyelitis in adult C57BL/6 but not BALB/c mice

Guida

Fejér

Pirofski

et al. 1995

J Virol

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“…More recently, virome profiling studies have added more insights and provided evidence for new rodent adenoviruses . The ‘murine’ adenoviruses that have been characterized to date do not infect infant rats , and thus this review covers only mouse adenoviruses.…”

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confidence: 99%

Murine adenoviruses: tools for studying adenovirus pathogenesis in a natural host

Hemmi

Spindler

2019

FEBS Letters

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Small laboratory animals are powerful models for investigating in vivo viral pathogenesis of a number of viruses. For adenoviruses (AdVs), however, species-specificity poses limitations to studying human adenoviruses (HAdVs) in mice and other small laboratory animals. Thus, this review covers work on naturally occurring mouse AdVs, primarily mouse adenovirus type 1 (MAdV-1), a member of the species Murine mastadenovirus A. Molecular genetics, virus life cycle, cell and tissue tropism, interactions with the host immune response, persistence, and host genetics of susceptibility are described. A brief discussion of MAdV-2 (member of species Murine mastadenovirus B) and MAdV-3 (member of species Murine mastadenovirus C) is included. We report the use of MAdVs in the development of vectors and vaccines.

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Mouse

Percy¹,

Barthold

2007

Pathology of Laboratory Rodents and Rabbits

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The laboratory mouse is an artificial creation, and there is no true "wildtype" laboratory mouse. Furthermore, there is no such thing as "normal" microflora, since laboratory mice are maintained in microbially pristine environments devoid of pathogens and opportunistic pathogens, as well as other commensal flora/fauna. House mice, from which laboratory mice originated, are represented by several species and subspecies native to the Old World. Laboratory mice are largely derived from domesticated "fancy mice" that arose from many years of trading of mouse variants among fanciers in Europe, Asia, North America, and Australia. The laboratory mouse genome, including its retroelements, is a mosaic derived from different subspecies of the Mus musculus complex, including M.m. domesticus, M.m. musculus, M.m. castaneus, M.m. molossinus (a natural hybrid of M.m. musculus and M.m. castaneus), and M. bactrianus.The genome of M.m. domesticus is the predominant contributor to most strains of mice, but many inbred strains share a common "Eve" with a mitochondrial genome of M.m. musculus origin, and a common "Adam" that contributed their Y chromosome from Asian mice. In addition, there is evidence that other Mus species, outside of the M. musculus complex, may have contributed to the genome of some laboratory mouse strains. The C57BL mouse genome contains a contribution from M. spretus. The 1st inbred mouse (DBA), and other strains with DBA genetic contributions, was partially derived from Japanese waltzing mice with M. bactrianus parentage. Perhaps the only laboratory mouse that is derived from a single species (subspecies), M.m. domesticus, is the "Swiss" mouse, but there is a high likelihood that several Swiss stocks and strains have been genetically corrupted.There are over 450 inbred strains of laboratory mice that have arisen during the last century, and these strains, which were selectively inbred to pan-genomic homozygosity for purposes entirely unrelated to modern research, are the foundation upon which literally thousands of spontaneous mutants and GEMs have been built. Additional inbred strains have been developed from wild mice (M.m. castaneus, M. spretus, etc.). Furthermore, "outbred" mice (mostly Swiss mice) are highly homozygous and nearly inbred. There is no such thing as an outbred laboratory mouse with a fully heterozygous genome representative of wildtype M. musculus, and there is no wild mouse genetic counterpart of the laboratory mouse. When working with mice, the pathologist must also become facile with hybrids,

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Factors influencing susceptibility of laboratory rodents to infection with mouse adenovirus strains K87 and FL

Cited by 13 publications

References 10 publications

Mouse adenovirus type 1 causes a fatal hemorrhagic encephalomyelitis in adult C57BL/6 but not BALB/c mice

Mouse adenovirus type 1 causes a fatal hemorrhagic encephalomyelitis in adult C57BL/6 but not BALB/c mice

Murine adenoviruses: tools for studying adenovirus pathogenesis in a natural host

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