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Mouse Scarb2 Modulates EV-A71 Pathogenicity in Neonatal Mice.
Wakako Miwatashi1, Minori Ishida1, Ayako Takashino1
1Neurovirology Project, Department of Disease and Infection, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Journal of Virology
|July 22, 2022
Summary
Enterovirus A71 (EV-A71) uses mouse Scarb2 (mScarb2) to infect neonatal mice. mScarb2 expression levels influence disease severity and susceptibility duration in this model.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- Enterovirus A71 (EV-A71) causes hand, foot, and mouth disease, potentially leading to severe neurological complications.
- EV-A71 utilizes human scavenger receptor B2 (hSCARB2) for human infection and can infect neonatal mice experimentally.
- The mechanisms regulating EV-A71 host range, tropism, and the transient susceptibility of neonatal mice remain unclear.
Purpose of the Study:
- To investigate the role of mouse scavenger receptor B2 (mScarb2) in mediating EV-A71 infection in neonatal mice.
- To determine how mScarb2 expression levels affect viral tropism, disease severity, and susceptibility duration.
- To elucidate the factors contributing to the age-dependent loss of susceptibility in the mouse model.
Main Methods:
- Preparation of rhabdomyosarcoma (RD) cells expressing mScarb2 for in vitro infection studies.
- Infection of wild-type (WT) and mouse-adapted (MA) EV-A71 strains in mScarb2-expressing cells.
- In vivo infection experiments using Scarb2-/- and Scarb2+/- mice, alongside age-matched controls.
- Correlation of Scarb2 expression levels in muscle tissue with age and susceptibility to EV-A71 infection.
Main Results:
- Both WT and MA EV-A71 strains infected mScarb2-expressing cells, with MA strains showing higher efficiency.
- In vivo infection by both WT and MA strains was completely abolished in Scarb2-/- mice.
- Scarb2+/- mice exhibited milder pathology compared to Scarb2+/+ mice after WT EV-A71 infection.
- Decreased Scarb2 expression in muscle tissue with aging correlated with reduced susceptibility in older mice.
Conclusions:
- EV-A71 infection in neonatal mice is mediated by mScarb2.
- mScarb2 expression levels are critical in modulating EV-A71 disease severity, viral spread, and the period of susceptibility.
- These findings highlight the importance of the viral receptor in determining host range and disease characteristics in the EV-A71 neonatal mouse model.
