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Host cell resistance to mouse hepatitis virus type 3 is expressed in vitro in macrophages and lymphocytes
L Lamontagne1, D Decarie, J M Dupuy
1Departement des Sciences Biologiques, Université du Québec à Montréal, Canada.
Abstract:
Phenotypic expression of in vivo sensitivity to mouse hepatitis virus type 3 (MHV3) was studied in vitro in macrophages and lymphocytes. MHV3 infections were induced in peritoneal exudate (PE), nonadherent spleen (NAS) and thymus (THY) cells from resistant A/J, susceptible C57BL/6 or semisusceptible (C57BL/6xA/J)F1 mice. Differences in cytopathic effect, cell viability and virus titers were found only at 48 hrs postinfection (p.i.). "Carrier state" infections were performed at 48 hrs p.i. by transfer of supernatants of infected cells to newly collected cells originating from the same strain of mice. A passage-dependent restriction of viral replication was detected in vitro and was expressed in PE, NAS and THY cells as a recessive phenotype. No defective-interfering viral particles were involved in the restriction of viral replication. Results obtained with crossed infections and determination of the number of productively infected cells demonstrated that restriction of viral replication in macrophages and lymphoid cells from resistant A/J mice is controlled by a genetically-determined intrinsic cellular mechanism acting principally on the level of production of infectious viral particles by the infected cell.
Insights
Genetic factors control mouse hepatitis virus type 3 (MHV3) replication in immune cells. Resistant A/J mice exhibit an intrinsic cellular mechanism restricting viral particle production, a recessive trait independent of defective-interfering particles.
Area of Science:
- Immunology
- Virology
- Genetics
Background:
- Mouse hepatitis virus type 3 (MHV3) sensitivity varies among mouse strains.
- Understanding the genetic basis of viral resistance is crucial for disease control.
Purpose of the Study:
- To investigate the in vitro phenotypic expression of MHV3 sensitivity in macrophages and lymphocytes.
- To elucidate the cellular mechanisms underlying MHV3 resistance in genetically distinct mouse models.
Main Methods:
- Infection of peritoneal exudate, spleen, and thymus cells from A/J, C57BL/6, and (C57BL/6xA/J)F1 mice with MHV3.
- Assessment of cytopathic effect, cell viability, and virus titers at 48 hours post-infection.
- Carrier state infections and crossed infections to determine viral replication restriction mechanisms.
Main Results:
- A passage-dependent restriction of MHV3 replication was observed in vitro, acting as a recessive phenotype.
- This restriction was present in macrophages, spleen, and thymus cells from resistant A/J mice.
- No defective-interfering viral particles were implicated in the observed viral replication restriction.
Conclusions:
- MHV3 replication restriction in resistant A/J mice is controlled by an intrinsic, genetically determined cellular mechanism.
- This mechanism primarily affects the production of infectious viral particles within infected macrophages and lymphoid cells.
- The findings highlight a cell-intrinsic resistance factor to MHV3 infection in specific mouse genotypes.