Role of antibody response in recovery from K-papovavirus infection in mice.
Intraperitoneal inoculation of mouse K papovavirus into infant (2 to 4 days old) Swiss albino mice produced a high-titered viremia which persisted until death due to pneumonitis on day 9 postinfection. Lungs and livers of these mice had virus-specific immunofluorescence and histological lesions. K-virus antibody was undetectable. Three- to four-week-old mice, although as susceptible to infection as infant mice, remained healthy and developed a much lower-titered viremia, a transient lung infection, and K-virus antibody on 4 to 5 days postinfection. Three- to four-week-old mice treated with cyclophosphamide developed a high-titered viremia with death 10 to 17 days postinfection and no detectable antibodies. A single intraperitoneal inoculation of K-virus antibody at 5 h or 1 day postinfection completely protected the infant Swiss albino mice. Partial protection was achieved when antibody was transferred on days 2, 3, and 4 postinoculation. Transfer of antibody to cytoxan-treated Swiss albino mice on days 3 and 6 postinfection completely portected them against K-virus-induced lesions and mortality. Transfer of normal adult BALB/c splenocytes to syngeneic infant mice before K-virus infection did not protect from death but increased survival time. Transfer of 4- to 12-day K-virus-primed adult splenocytes before infection gave a nearly 100% protection. When given before infection, the protection afforded by T-cell-enriched and B-cell-enriched adult primed splenocytes was 0 and 100%, respectively. Transfer of primed B cells on day 1 post-inoculation completely protected the infant mice. This protection decreased to 86, 57, and 56% when the primed B cells were transferred on days 2, 3, and 4 post-inoculation, respectively. These data suggest that the antibody response is of critical importance in the recovery of mice from K-virus infection. Antibody probably acts by aborting viremia, thereby preventing extensive seeding of lungs with virus.
D000375:Aging; D000818:Animals; D000914:Antibodies, Viral / Q000096:biosynthesis*; D001402:B-Lymphocytes / Q000276:immunology; D003520:Cyclophosphamide / Q000494:pharmacology; D007116:Immunization, Passive; D008099:Liver / Q000473:pathology; D008168:Lung / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D027383:Papillomaviridae / Q000276:immunology / Q000472:pathogenicity; D027382:Polyomaviridae; D013154:Spleen / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D014412:Tumor Virus Infections / Q000209:etiology / Q000276:immunology* / Q000401:mortality; D014765:Viral Vaccines / Q000276:immunology; D014766:Viremia / Q000276:immunology
D000914:Antibodies, Viral; D014765:Viral Vaccines; D003520:Cyclophosphamide