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[Apoptosis as a mechanism for the cytopathic action of tick-borne encephalitis virus]
Abstract:
The ability of tick-borne encephalitis (TBE) virus to cause programmed cell death (apoptosis) in viral infection of newborn mice and of two cell cultures is studied. The time course of virus antigen accumulation detected by enzyme immunoassay and of endonuclease fragmentation of nuclear DNA detected by agarose gel electrophoresis is compared. All three TBE strains differing by the source of isolation and biological characteristics can cause oligonucleosomal fragmentation of DNA of brain cells of two-day white mice and of SPEV cells in acute infection. In VERO-E6 cells the same three strains caused a latent infection; accumulation of virus antigen was not associated with endonuclease fragmentation of DNA or any other signs of cytopathic destruction. These data indicate that TBE virus can cause programmed cell death both in vitro and in vivo, which is apparently one mechanism of the cytopathic effect of the virus.
Insights
Tick-borne encephalitis (TBE) virus induces programmed cell death (apoptosis) in mouse brain cells and SPEV cells during acute infection. However, in VERO-E6 cells, TBE virus causes a latent infection without inducing apoptosis.
Area of Science:
- Virology
- Cell Biology
- Neuroscience
Background:
- Tick-borne encephalitis (TBE) virus is a significant human pathogen.
- Understanding the mechanisms of TBE virus pathogenesis, including its interaction with host cells, is crucial.
- Programmed cell death, or apoptosis, is a key cellular process implicated in viral infections.
Purpose of the Study:
- To investigate the capacity of TBE virus to induce apoptosis in vivo (newborn mice) and in vitro (cell cultures).
- To compare the kinetics of viral antigen accumulation with DNA fragmentation during TBE virus infection.
Main Methods:
- Enzyme immunoassay was used to detect virus antigen accumulation.
- Agarose gel electrophoresis was employed to detect endonuclease fragmentation of nuclear DNA.
- Studies were conducted in newborn mice, SPEV cells, and VERO-E6 cells.
Main Results:
- All three tested TBE virus strains induced oligonucleosomal DNA fragmentation in brain cells of newborn mice and in SPEV cells during acute infection.
- In VERO-E6 cells, the same TBE virus strains resulted in a latent infection.
- Viral antigen accumulation in VERO-E6 cells did not correlate with DNA fragmentation or cytopathic effects.
Conclusions:
- TBE virus can induce programmed cell death (apoptosis) in susceptible cells both in vivo and in vitro.
- Apoptosis appears to be a mechanism contributing to the cytopathic effect of TBE virus.
- Cell-type-specific responses to TBE virus infection, including the induction of apoptosis, were observed.