Virus-Specific Immunity in Neonatal and Adult Mouse Rotavirus Infection

Abstract

Mouse rotavirus (epizootic diarrhea of infant mice) was used as a model to study the role of virus-specific immunity in infection and diarrheal disease. The distribution of viral antigen in intestinal tissues was determined by immunofluorescent staining with anti-simian rotavirus (SA-11) serum. The location and proportion of antigen-positive cells appeared to vary as a function of time postinfection and age of the animal at the time of infection. In animals infected at 1 and 7 days of age, antigen-positive cells (5 to 25%) were first detected (1 day postinfection) in the proximal segment of the small intestine, and infection progressed to the middle and distal segments. At 10 days postinfection, virusinfected cells were no longer observed in the proximal segment. In animals infected at 21 days of age (disease-free), a significantly lower proportion of cells were antigen positive (2 to 5%), and they were restricted to the middle and distal segments of the small intestine. Infection, defined according to the presence of virus and viral antigens in intestinal tissues and by seroconversion in the immunoglobulin M (IgM) isotype as determined by enzyme-linked immunosorbent assay with SA-11 antigen, was observed for all age groups (neonatal to adult), even in the presence of virus-specific serum or intestinal immunoglobulins. On the other hand, diarrheal disease was not detected in neonatal mice (1 to 3 days old) positive for passively acquired virus-specific intestinal IgG. The presence of virus-specific IgA in the intestinal tract at the time of infection did not protect from subsequent diarrheal disease. Virus-specific, cell-mediated immunity, determined by a delayed-type hypersensitivity response, did not develop in neonatal mice infected at 5 and 12 days of age. Reinfection of adult mice was associated with suppression of virus-specific delayed-type hypersensitivity and a significant decrease in the titers of the virus-specific serum IgG and IgA. 917 on July 16, 2020 by guest

Development of nasal, fecal and serum isotype-specific antibodies in calves challenged with bovine coronavirus or rotavirus

“…Patterns of serum and fecal antibody responses in calves were similar to those noted following infection of children (Sonza, 1980;Riepenhoff-Talty et al, 1981;Stals et al, 1984), pigs (Corthier and Vannier, 1983) and mice (Sheridan et al, 1983) with rotavirus. Rotavirus antibody isotype-specific responses detected using ELISA, and VN tests on sera from calves #148 (upper panel) and #151 (lower panel) inoculated with coronavirus.…”

Rotaviruses: Immunological Determinants of Protection Against Infection and Disease

“…The humoral immune response, using animals infected with homologous host rotavirus strains, has been the primary focus of a number of studies. Studies of calves, rabbits, and pigs orally inoculated with cell culture-adapted strains (Conner et al, 1991;Corthier and Vannier, 1983;Saif, 1987;Saif et al, 1992;Vonderfecht and Osburn, 1982) and mice with murine strains poorly adapted to growth in cell culture (Sheridan et al, 1983) have produced important information on the site of rotavirus-specific antibody-bearing cells (i.e., B cells and plasma cells) and the isotype and neutralization capacity of these antibodies. Within 10 days of infection, rotavirus-specific binding and neutralizing antibodies of all isotypes are detected both in the serum and in small intestinal fluids; in both sites the appearance of rotavirusspecific IgM precedes the appearance of virus-specific IgA and IgG.…”

Natural killer cell activity of chicken intraepithelial leukocytes against rotavirus-infected target cells

“…Most of these studies have examined antibody-mediated responses. In mammals, rotavirusspecific intestinal antibodies clearly mediate passive immunity (Offit and Clark, 1985;Archambault et al, 1988), and are thought to be important in the active immune response to primary (Sheridan et al, 1983;Van Zaane et al, 1986 ) and secondary (Bishop et al, 1986 ) rotavirus infections. However, there is evidence to suggest that mechanisms besides rotavirus-specific intestinal antibodies may participate in recovery and resistance.…”