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Blocking of in vitro and in vivo susceptibility to mouse hepatitis virus
Abstract:
By pretreatment with concanavalin A (Con A) both in vivo and in vitro genetically susceptible mice and their cultured macrophages have been converted to animals and cells which are phenotypically resistant to mouse hepatitus virus (MHV). Con A at 1.0 mg/mouse decreased the mortality from 100% to less than 40% by inducing a prominent inflammatory response, increasing the number of macrophages in the virus inoculation site, and producing a population of macrophages not uniformly susceptible to the virus. In addition, mediators derived from Con A-treated spleen cells conferred resistance to normally susceptible syngeneic macrophages to 100 TCID50 of MHV.
Insights
Pretreatment with concanavalin A (Con A) confers resistance to mouse hepatitis virus (MHV) in mice and macrophages. This study demonstrates Con A
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Mouse hepatitis virus (MHV) infection poses a significant threat to susceptible mouse populations.
- Understanding host-pathogen interactions is crucial for developing effective antiviral strategies.
Purpose of the Study:
- To investigate the potential of concanavalin A (Con A) as a prophylactic agent against MHV infection.
- To elucidate the mechanisms by which Con A confers resistance to MHV.
Main Methods:
- Mice and cultured macrophages were pretreated with concanavalin A (Con A) in vivo and in vitro.
- Mice were infected with MHV, and mortality rates were assessed.
- Macrophage populations were analyzed for susceptibility to MHV infection.
- Mediators from Con A-treated spleen cells were used to assess resistance transfer.
Main Results:
- Con A pretreatment significantly reduced mortality in MHV-infected mice from 100% to less than 40%.
- Con A induced an inflammatory response and increased macrophage recruitment to the inoculation site.
- Con A-treated macrophages exhibited reduced susceptibility to MHV infection.
- Mediators from Con A-treated spleen cells conferred resistance to normally susceptible macrophages.
Conclusions:
- Concanavalin A pretreatment can convert genetically susceptible mice and macrophages to a phenotypically resistant state against MHV.
- The protective effect of Con A involves inducing inflammation, increasing macrophage numbers, and altering macrophage susceptibility.
- Con A-derived mediators offer a potential therapeutic avenue for conferring antiviral resistance.