Enterotropic coronavirus (mouse hepatitis virus) in mice: influence of host age and strain on infection and disease
Barthold, S.W.; Beck, D.S.; Smith, A.L.
Laboratory Animal Science 43(4): 276-284
1993
ISSN/ISBN: 0023-6764 PMID: 8231082 Document Number: 412477
The course of enterotropic mouse hepatitis virus (MHV) infection was examined in genetically susceptible (BALB) and resistant (SJL) mice of different ages at inoculation (1, 3, and 12 weeks) and at sequential intervals (1, 2, 3, 5, 10, 20 and 30 days) after oral inoculation with the Y strain of MHV (MHV-Y). Virus was quantified in stomach, upper and lower segments of small intestine, caecum, upper and lower segments of colon, Peyer's patches, mesenteric lymph nodes, and faeces, and tissues were examined microscopically. An infant mouse bioassay was used to quantify virus in all tissues of 3-week-old BALB mice and ascending colons of other mouse groups. MHV-specific serum IgG antibody titres were measured with an enzyme immunoassay, using MHV-S-infected 17 Cl 1 cells as antigen. Lesions were first detected at 2 days and were severest in 1-week-old mice and more severe in BALB mice than in SJL mice. Additional day old BALB mice developed severe enterocolitis whereas SJL mice of the same age developed lesions equivalent to those in 1-week-old BALB mice. Virus was first detectable at 2 days and virus titres were highest at 2, 3, and 5 days, then diminished on days 10, 20, and 30. Lesions were severest and virus titres highest in the ascending colon. In spite of age- and genotype-related lesion severity, peak MHV titres in the ascending colon were equivalent in all age groups and in both mouse strains, except in 1-week-old BALB mice, which had the highest virus titres. Seroconversion occurred between days 10 and 20, with higher titres among younger mouse groups. The relative median MHV-Y infectious dose was identical among BALB mice inoculated at 1,3, or 12 weeks of age and SJL mice inoculated at 3 and 12 weeks of age. It is suggested that the significant age- and genotype-related differences in disease severity may be a reflexion of tissue susceptibility to virus damage, rather than differences in virus replicative activity or susceptibility to infection.