Susceptibility and Resistance to Viral Leukemogenesis in the Mouse. II. Response to the Virus Relative to Histocompatibility Factors Carried by the Prospective Host2

Publisher Website
Google Scholar
Abstract
Two strains of mice, congenic, with a proved difference at the H-2 locus, manifested a.20 percent difference in susceptibility to viral leukemogenesis when inoculated with the BALB/Tennant-leukemia (B/T-L) virus as sucklings. Crosses were made between females of the BALB/c strain, primary to the virus, and males of each of 8 unrelated "foreign" strains, some of which were resistant and some susceptible to the virus. With one exception (C57BR/cdJ), F1 offspring were 92 to 100 percent susceptible to the virus, regardless of partial or total resistance of the foreign parent; offspring of the (BALB/cJ X C57BR/cd) cross appeared to be totally resistant. F2 subjects of crosses between the BALB/c strain and each of two totally resistant strains (C3HeB/FeJ and C57BR/cdJ) were inoculated as sucklings with virus and serotyped as adults for major H-2 antigens. The first cross yielded 72 percent leukemia induction, the second cross only 39 percent; no correlation was found between the H-2 serotype of the host and its susceptibility or resistance to leukemogenesis by the virus. Backcross individuals of the cross BALB/cJ X C3HeB/FeJ yielded 100 percent leukemia when F1 females were mated to BALB/cJ males, but only 6 percent (within spontaneous incidence bounds) when the males derived from the C3HeB/FeJ strain; again, no correlation was found between H-2 serotype and reactivity of the host to the virus. After one passage through F1, F2, or "foreign" strain mice, virus was returned to the BALB/cJ strain for evidence of alteration of the virus such as might be expected if coating of the virus by protein from the cell membrane had occurred in passage through the intermediate host. No such evidence was found. These results suggest that the H-2 constitution of the host may be a contributing factor to viral leukemogenesis, but is not the predominant factor.