Role of Antibody Response in Recovery from K-Papovavirus Infection in Mice

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Abstract
I.p. inoculation of mouse K papovavirus into infant (2-4 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 4 wk 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 4-5 days postinfection. Three to 4 wk old mice treated with cyclophosphamide developed a high-titered viremia with death 10-17 days postinfection and no detectable antibodies. A single i.p. 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 post-inoculation. Transfer of antibody to cytoxan-treated Swiss albino mice on days 3 and 6 postinfection completely protected 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 O 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. 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.