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H-2-linked regulation of xenotropic murine leukemia virus expression

Insights

The F/St mouse strain exhibits a high-virus phenotype, producing infectious xenotropic murine leukemia virus (X-MuLV). This trait is controlled by the Cxv-1 gene interacting with a chromosome 1 V locus, indicating a complex genetic basis for viral production.

Area of Science:

  • Virology
  • Immunogenetics
  • Mouse Models

Background:

  • F/St mice lymphocytes produce infectious xenotropic murine leukemia virus (X-MuLV).
  • These cells express high levels of cell surface antigens (XenCSA) linked to X-MuLV.
  • Understanding the genetic control of X-MuLV production is crucial for viral pathogenesis research.

Purpose of the Study:

  • To investigate the genetic basis of the high-virus phenotype in F/St mice.
  • To identify the specific genetic loci controlling X-MuLV production and XenCSA expression.
  • To elucidate the interaction between different genetic factors influencing viral replication.

Main Methods:

  • Genetic crosses between F/St and AKR mouse strains.
  • Analysis of viral production and XenCSA expression in hybrid mice.
  • Congeneic mouse strain analysis (B10.F and C57BL/10) to map genetic loci.
  • Segregation analysis of chromosome 1 loci in hybrid mice.

Main Results:

  • The high-virus phenotype in F/St mice is recessive and controlled by a single locus, Cxv-1.
  • Cxv-1 is located less than 2 centimorgans from the H-2K region, indicating linkage to the H-2 complex.
  • Congeneic B10.F mice, carrying the F/St H-2 region, showed high X-MuLV and XenCSA levels, unlike C57BL/10 mice.
  • The high-virus phenotype depends on the interaction between Cxv-1 and a chromosome 1 X-MuLV induction locus (V locus).

Conclusions:

  • The genetic control of X-MuLV production in F/St mice involves at least two loci: Cxv-1 near H-2K and a V locus on chromosome 1.
  • The interaction between Cxv-1 and the V locus is essential for the high-virus phenotype.
  • This study provides insights into the complex genetic regulation of retroviral replication in mice.

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