Genetically determined resistance to lethal XXXX infection is mediated by interferon-dependent and -independent restriction of virus replication.

@entity19 @entity21215 @entity281 @entity2020 @entity20589
Susceptibility of 4-week-old @entity19 of different strains to lethal @entity21215 ) infection was studied. Strains homozygous for H-2k and C57BL strains were resistant to greater than or equal to 10(5.5) PFU. @entity2020 .BR @entity19 congenic for C57BL background genes and H-2k were about 10-fold more resistant than either C3H/HeN or C57BL strains. BALB/c @entity19 (H-2d) were susceptible (50% lethal dose, 10(5.05) PFU). This susceptibility was dominant over resistance associated with H-2k but not that associated with C57BL background genes. The dominant susceptibility trait segregated in backcross @entity19 as if carried by a single gene. Virus replication in spleen cells in vivo correlated with susceptibility to @entity281 . A similar trend was found in tests of salivary glands. Replication of @entity20589 in vitro in cultures of adherent spleen cells and primary @entity19 embryo cells correlated with replication in vivo. Neutralization of interferon (IFN) in cultures of adherent spleen cells reversed H-2k-linked restriction of viral replication but had minor effects on cells of other strains. Natural killer cell responses to infection were often higher in more resistant strains, but @entity2020 .BR @entity19 developed minimal natural killer cell responses. Specific antibody and cytotoxic T cell responses in @entity2020 .BR @entity19 were similar or lower than in other strains. Thus, resistance to lethal @entity20589 infection was not immunologically mediated, was dependent on and reflected by the capacity of cells from a given @entity19 to support replication in vivo and in vitro, and was IFN dependent and recessive if linked to H-2k but IFN independent when associated with C57BL background genes.
