Genetic Determinants of Virus Susceptibility: Epidemiologic Implications of Murine Models

Host Genetic Control of Mouse Hepatitis Virus Type 4 (JHM Strain) Replication. I. Restriction of Virus Amplification and Spread in Macrophages from Resistant Mice

“…The limitation of infection during the first cycle and subsequent restriction of virus amplification in the second cycle of infection in SJL/J macrophages may reflect a genetically controlled processing defect of the E-2 glycoprotein by resistant SJL/J cells. Lack of an active proteolytic enzyme, necessary for cleavage of the E-2 glycoprotein and fusion (Sturman & Holmes, 1984), or another processing molecule are potential mechanisms of genetic resistance to virus infection (Brinton & Nathanson, 1981;Brinton et al, 1983).…”

“…The resistance of mice to infection by a particular virus may be a manifestation of lack of a receptor for virus attachment, inappropriate intracellular processing and replication, or failure of virus assembly or release, and may reflect genetically controlled responses (for reviews, see Brinton & Nathanson, 1981;Brinton et al, 1983). Furthermore, lymphokines, such as interferon, influence the replication of numerous viruses (De Maeyer & De Maeyer-Guignard, 1979;Hailer et al, 1981), including a strain of murine coronavirus (Virelizier, 1981).…”

Replication of Flaviviruses

“…Since virus infections often induce permanent impair-ment or death in their hosts, it is not unreasonable to expect that they could exert a selective pressure for the maintenance of host alleles that fortuitously confer a reduced susceptibility to viral diseases in host populations (Brinton and Nathanson, 1981;Brinton et al, 1984). To date, murine genes that can specifically influence the outcome of infections with members of three families of DNA viruses and five families of RNA viruses have been identified (Brinton et al, 1984).…”

Adaptation of Borna Disease Virus to the Mouse

“…Only two reports described transmission of virus with expressed disease (Nicolau & Galloway, 1927, 1928. Since a mouse model may facilitate study of persistent infection or slow progressing diseases in many ways (Brinton & Nathanson, 1981 ;Buchmeier et al, 1980;Kimberlin, 1981 ;Lehmann-Grube et al, 1983;Mahy et al, 1982;Pearson & Mims, 1983;Wege et al, 1982), renewed efforts were made to infect this small animal following our induction of a persistent, tolerant or subacute infection in the rat (Hirano et al, 1983).…”