Difference of two new LCMV strains in lethality and viral genome load in tissues

Toshikazu Takagi1,2, Makiko Ohsawa3, Hitoki Yamanaka3

  • 1Division of Comparative Medicine, Center for Frontier Life Sciences, Nagasaki University Graduate School of Biomedical Sciences, 1-12-4 Sakamoto, Nagasaki, Nagasaki 852-8523, Japan.

Experimental Animals
|March 7, 2017
PubMed

Insights

Two new lymphocytic choriomeningitis virus (LCMV) strains showed varied pathogenicity in mice. Viral genome load and specific viral sequences, not just host genetics, influence LCMV disease.

Area of Science:

  • Virology
  • Immunology
  • Genetics

Background:

  • Lymphocytic choriomeningitis virus (LCMV) strains vary in pathogenicity.
  • Host genetics, specifically major histocompatibility complex (MHC) class I molecules, influence LCMV disease outcomes.

Purpose of the Study:

  • To investigate the pathogenicity, clinical signs, and lethality of two novel LCMV strains (BRC and OQ28).
  • To analyze viral genome load and sequence variations in relation to host genetic background.

Main Methods:

  • Infection of three inbred mouse strains with different H-2D haplotypes using LCMV strains BRC and OQ28.
  • Assessment of clinical signs and lethality.
  • Quantification of viral genome load using real-time RT-PCR.
  • Sequence comparison of LCMV epitope peptide regions.

Main Results:

  • LCMV strain OQ28 caused clinical signs and lethality, while strain BRC did not.
  • C57BL/6 mice infected with OQ28 showed higher viral genome loads in all tissues compared to BRC.
  • Viral genome load remained highest in lungs at 28 days post-infection for both strains.
  • Sequence analysis revealed distinct amino acid differences in epitope regions between OQ28 and BRC.

Conclusions:

  • LCMV strain pathogenicity and viral genome load are influenced by factors beyond host MHC class I molecules.
  • Specific viral sequence variations contribute to differential pathogenicity observed between LCMV strains.