The Visceral Lesions Produced in Mice by the Salivary Gland Virus of Mice

McCordock, Howard A.; Smith, Marvin E.

doi:10.1084/jem.63.3.303

Cited by 69 publications

(32 citation statements)

References 3 publications

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“…Variation in susceptibility to MCMV among strains of mice was first noted in 1936 (McCordock & Smith, 1936) and recent studies have established that genes within the H-2 complex as well as non-H-2 genes regulate resistance to infection [Chalmer et al, 1977;Grundy (Chalmer) et al, 1981]. Host resistance genes influence the growth of MCMV in target cells in vitro (Harnett & Shellam, 1982) and the effectiveness of the interferon response (Harnett & Shellam, 1985), although their effect is thought to be largely on early mechanisms which are nonimmunological (Shellam et al, 1983).…”

confidence: 99%

Delayed-type Hypersensitivity Responses to Murine Cytomegalovirus in Genetically Resistant and Susceptible Strains of Mice

Lawson

Grundy

Shellam

1987

Journal of General Virology

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SUMMARYThe delayed-type hypersensitivity (DTH) response in mice infected with murine cytomegalovirus (MCMV) was measured by ear swelling following a challenge with heat-treated MCMV. DTH was dose-dependent and could be detected as early as 3 days post-infection with peak responses occurring between days 15 and 21 postinfection. The DTH response was found to be specific for MCMV since it could not be elicited by either herpes simplex virus type 1 or influenza A virus in MCMV-primed mice. The elicited DTH response was greater in mice primed with attenuated compared with virulent MCMV. The DTH response was shown to correlate positively with the genetically determined resistance status of mouse strains to this virus.

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confidence: 99%

Delayed-type Hypersensitivity Responses to Murine Cytomegalovirus in Genetically Resistant and Susceptible Strains of Mice

Lawson

Grundy

Shellam

1987

Journal of General Virology

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“…Depending on the dose of virus, experimental infection of mice with murine cytomegalovirus (MCMV) can result in a fatal disease with widespread and extensive visceral lesions or a chronic infection of various organs with virus persisting especially in the salivary glands (McCordock & Smith, 1936;Smith, 1954;Brodsky & Rowe, 1958;Mannini & Medearis, 1961 ;Medearis, 1964;Henson et al, 1966;Henson & Neapolitan, 1970;Henson & Strano, 1972;Lussier et al, 1974;Larson, 1976;Olding et al, 1976;Smith & Wehner, 1980;Grundy et al, 1981 ;. The liver, spleen, lymphoid tissues, heart, kidney, bone marrow as well as the salivary glands are usually invaded by MCMV in the course of the disease.…”

Section: Introductionmentioning

confidence: 99%

An Ultrastructural Investigation of Cytomegalovirus Replication in Murine Hepatocytes

Papadimitriou¹,

Shellam

Robertson³

1984

Journal of General Virology

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SUMMARYThe morphological characteristics of murine cytomegalovirus replication in murine hepatocytes were investigated by electron microscopy and structural evidence of an unusual mode of virus maturation was detected. Nucleocapsids form in the nucleus; those with electron-dense cores bud into the perinuclear cisternae and acquire an outer envelope from the inner membrane of the nuclear envelope. Viral envelopes fuse with the outer membrane of the nuclear envelope releasing nucleocapsids in the paranuclear zone where they aggregate and form cytoplasmic inclusions. These inclusions are invariably surrounded by lamellae and vesicles of the Golgi complex into which nucleocapsids again bud. Virions, now covered with a new membrane envelope, are transported within secondary lysosomes and released by emiocytosis into the extraceUular space.

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“…Virus isolated from salivary glands is more virulent than virus propagated in cell culture or isolated from other organs (68). For this reason, and because natural viral transmission is mediated by saliva, pathogenesis studies have relied on salivary gland-derived virus (20,23,40,49,50,65,69). The Smith strain of MCMV was subjected to serial propagation through sal-ivary glands of Swiss-Webster mice (51), resulting in the isolation of strain K181.…”

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confidence: 99%

Antiviral T Cell Response Triggers Cytomegalovirus Hepatitis in Mice

Livingston-Rosanoff

Daley‐Bauer

García

et al. 2012

J Virol

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e One common sign of human cytomegalovirus infection is altered liver function. Murine cytomegalovirus strain v70 induces a rapid and severe hepatitis in immunocompetent mice that requires the presence of T cells in order to develop. v70 exhibits approximately 10-fold-greater virulence than the commonly used strain K181, resulting in a more severe, sustained, and lethal hepatitis but not dramatically higher viral replication levels. Hepatitis and death are markedly delayed in immunodeficient SCID compared to immunocompetent BALB/c mice. Transfer of BALB/c splenocytes to SCID mice conferred rapid disease following infection, and depletion of either CD4 or CD8 T cells in BALB/c mice reduced virus-induced hepatitis. The frequency of CD8 T cells producing gamma interferon and tumor necrosis factor in response to viral antigen was higher in settings where more severe disease occurred. Thus, virus-specific effector CD8 T cells appear to contribute to lethal virus-induced hepatitis, contrasting their protective role during sublethal infection. This study reveals how protection and disease during cytomegalovirus infection depend on viral strain and dose, as well as the quality of the T cell response.

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The Visceral Lesions Produced in Mice by the Salivary Gland Virus of Mice

Cited by 69 publications

References 3 publications

Delayed-type Hypersensitivity Responses to Murine Cytomegalovirus in Genetically Resistant and Susceptible Strains of Mice

Delayed-type Hypersensitivity Responses to Murine Cytomegalovirus in Genetically Resistant and Susceptible Strains of Mice

An Ultrastructural Investigation of Cytomegalovirus Replication in Murine Hepatocytes

Antiviral T Cell Response Triggers Cytomegalovirus Hepatitis in Mice

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