Determinants of pegivirus persistence, cross-species infection, and adaptation in the laboratory mouse

PLoS Pathog. 2024 Aug 28;20(8):e1012436. doi: 10.1371/journal.ppat.1012436. eCollection 2024 Aug.

Abstract

Viruses capable of causing persistent infection have developed sophisticated mechanisms for evading host immunity, and understanding these processes can reveal novel features of the host immune system. One such virus, human pegivirus (HPgV), infects ~15% of the global human population, but little is known about its biology beyond the fact that it does not cause overt disease. We passaged a pegivirus isolate of feral brown rats (RPgV) in immunodeficient laboratory mice to develop a mouse-adapted virus (maPgV) that established persistent high-titer infection in a majority of wild-type laboratory mice. maRPgV viremia was detected in the blood of mice for >300 days without apparent disease, closely recapitulating the hallmarks of HPgV infection in humans. We found a pro-viral role for type-I interferon in chronic infection; a lack of PD-1-mediated tolerance to PgV infection; and multiple mechanisms by which PgV immunity can be achieved by an immunocompetent host. These data indicate that the PgV immune evasion strategy has aspects that are both common and unique among persistent viral infections. The creation of maPgV represents the first PgV infection model in wild-type mice, thus opening the entire toolkit of the mouse host to enable further investigation of this persistent RNA virus infections.

MeSH terms

  • Animals
  • Flaviviridae Infections* / immunology
  • Flaviviridae Infections* / virology
  • Flaviviridae* / genetics
  • Flaviviridae* / immunology
  • Humans
  • Immune Evasion
  • Mice
  • Mice, Inbred C57BL
  • Persistent Infection / immunology
  • Persistent Infection / virology
  • Rats

Grants and funding

Startup funds (ALB) via the Department of Pathology and Laboratory Medicine and the School of Medicine and Public Health at the University of Wisconsin–Madison were utilized for study. ASK was supported in part by Open Philanthropy and the Life Sciences Research Foundation. JG is supported by the Wellcome Trust and Royal Society through a Sir Henry Dale Fellowship (107653/Z/15/Z) and through MRC-University of Glasgow Centre for Virus Research core support from the Medical Research Council/UKRI (MC_UU_00034/1). SM was supported by the National Institute of General Medical Sciences of the NIH training grant (T32GM135119). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.