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. 2010 Dec;84(24):12841-9.
doi: 10.1128/JVI.01863-10. Epub 2010 Oct 13.

Common inbred strains of the laboratory mouse that are susceptible to infection by mouse xenotropic gammaretroviruses and the human-derived retrovirus XMRV

Surendranath Baliji  1 , Qingping Liu, Christine A Kozak
Affiliations

Common inbred strains of the laboratory mouse that are susceptible to infection by mouse xenotropic gammaretroviruses and the human-derived retrovirus XMRV

Surendranath Baliji et al. J Virol. 2010 Dec.

Abstract

Laboratory mouse strains carry endogenous copies of the xenotropic mouse leukemia viruses (X-MLVs), named for their inability to infect cells of the laboratory mouse. This resistance to exogenous infection is due to a nonpermissive variant of the XPR1 gammaretrovirus receptor, a resistance that also limits in vivo expression of germ line X-MLV proviruses capable of producing infectious virus. Because laboratory mice vary widely in their proviral contents and in their virus expression patterns, we screened inbred strains for sequence and functional variants of the XPR1 receptor. We also typed inbred strains and wild mouse species for an endogenous provirus, Bxv1, that is capable of producing infectious X-MLV and that also contributes to the generation of pathogenic recombinant MLVs. We identified the active Bxv1 provirus in many common inbred strains and in some Japanese Mus molossinus mice but in none of the other wild mouse species that carry X-MLVs. Our screening for Xpr1 variants identified the permissive Xpr1(sxv) allele in 7 strains of laboratory mice, including a Bxv1-positive strain, F/St, which is characterized by lifelong X-MLV viremia. Cells from three strains carrying Xpr1(sxv), namely, SWR, SJL, and SIM.R, were shown to be infectable by X-MLV and XMRV; these strains carry different alleles at Fv1 and vary in their sensitivities to specific X/P-MLV isolates and XMRV. Several strains with Xpr1(sxv) lack the active Bxv1 provirus or other endogenous X-MLVs and may provide a useful model system to evaluate the in vivo spread of these gammaretroviruses and their disease potential in their natural host.

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Figures

FIG. 1.
FIG. 1.
Analysis of the Bxv1 provirus in common strains of laboratory mice and wild-derived mouse strains. (Top) Bxv1 provirus integration site and the empty locus on Chr 1 with PCR primers used to amplify these locus alternatives. For clarity, the Bxv1 provirus is diagrammed in the forward orientation, as opposed to its reverse orientation in GenBank accession no. AC115959. (Bottom left) PCR screening of mouse DNAs previously shown to carry Bxv1 (C57BL, BALB/c) or to lack this provirus (NFS, NIH 3T3) and a hamster/mouse somatic cell hybrid, BE7-2, that carries a Chr 1 fragment containing Bxv1. (Bottom right) PCR results for representative common inbred strains and wild-derived mice.
FIG. 2.
FIG. 2.
Distribution of allelic variants of Bxv1, Fv1, and Xpr1 in inbred strains of the laboratory mouse. The organization of strains into groups based on their related breeding histories is derived from the analysis done by Beck and associates (3). The Bxv1 provirus insertion is identified by + and the empty locus by −; numbers identify strains previously typed for Bxv1 as a Chr 1-linked induction locus (superscript “1”) (18, 19, 51) or by Southern blotting (superscript “2”) (8). Fv1 typing identified the presence of the “n” or “b” restriction fragments that distinguish Fv1n and Fv1nr from Fv1b (45). Identical results were obtained for strain sublines SJL/BmJ and SJL/J, for AKR/N and AKR/J, and for C57BL/6 and C57BL/10. Xpr1 variants confirmed by sequencing are indicated with asterisks; all others were typed by PCR. SAMR1 and SAMP8 are hybrids of AKR and an unknown mouse. NOR was derived from a cross between NOD and C57BLKS/J. NZB was derived from NZO; NZM is a hybrid of NZB and NZW. NZL was developed from NZO with contributions from NZB, C57BL, and 129.
FIG. 3.
FIG. 3.
Distribution of Bxv1 in wild mouse species and wild-derived inbred strains. DNAs were screened by PCR for the Bxv1 insertion (+) or for the empty locus (−). A total of four wild-trapped California mice, along with California mouse-derived SC-1 cells, were tested.
FIG. 4.
FIG. 4.
Xpr1 variants in laboratory mouse strains. The exon structure of the Xpr1 gene is indicated at the top. Exon 13 contains the receptor determining the putative ECL4 loop and contains the indicated deletions or substitutions that distinguish the 4 house mouse alleles of Xpr1. aa, amino acids. At the bottom are shown PCR products using exon 13 primers, Ex13F and Ex13R. The first 4 lanes contain DNAs from mice carrying the 4 indicated alleles. The remaining 6 lanes contain DNAs of the indicated strains mixed with DNAs from mice carrying Xprsxv. Doublets are indicative of mice carrying the Xpr1n deletion.
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References

    1. Aaronson, S. A., G. J. Todaro, and E. M. Scolnick. 1971. Induction of murine C-type viruses from clonal lines of virus-free BALB/3T3 cells. Science 174:157-159. - PubMed
    1. Battini, J.-L., J. E. J. Rasko, and A. D. Miller. 1999. A human cell-surface receptor for xenotropic and polytropic murine leukemia viruses: possible role in G protein-coupled signal transduction. Proc. Natl. Acad. Sci. U. S. A. 96:1385-1390. - PMC - PubMed
    1. Beck, J. A., S. Lloyd, M. Hafezparast, M. Lennon-Pierce, J. T. Eppig, M. F. W. Festing, and E. M. C. Fisher. 2000. Genealogies of mouse inbred strains. Nat. Genet. 24:23-25. - PubMed
    1. Chattopadhyay, S. K., M. R. Lander, S. Gupta, E. Rands, and D. R. Lowy. 1981. Origin of mink cytopathic focus-forming (MCF) viruses: comparison with ecotropic and xenotropic murine leukemia virus genomes. Virology 113:465-483. - PubMed
    1. Cloyd, M. W., M. M. Thompson, and J. W. Hartley. 1985. Host range of mink cell focus-inducing viruses. Virology 140:239-248. - PubMed

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