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Neutrophil apoptosis induction by tick-borne encephalitis virus
N G Plekhova1, L M Somova, I N Lyapun
1Laboratory of Pathomorphology and Electron Microscopy, Institute of Epidemiology and Microbiology, Siberian Division of Russian Academy of Medical Sciences, Vladivostok, Russia. pl_nat@hotmail.com
Bulletin of Experimental Biology and Medicine
|July 19, 2012
Summary
Tick-borne encephalitis virus infects neutrophils, leading to cell death. This is indicated by changes in cellular energy production and enzyme activity within the infected neutrophils.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Tick-borne encephalitis virus (TBEV) is a significant human pathogen.
- Neutrophils are critical immune cells involved in the early response to viral infections.
Purpose of the Study:
- To investigate the impact of TBEV infection on neutrophil function.
- To determine if TBEV induces apoptosis in neutrophils.
Main Methods:
- Infection of human neutrophils with TBEV.
- Measurement of succinate dehydrogenase activity.
- Measurement of lactate dehydrogenase activity.
Main Results:
- TBEV infection of neutrophils was confirmed.
- A moderate increase in succinate dehydrogenase activity was observed.
- A trend towards anaerobic energy production, indicated by increased lactate dehydrogenase activity, was noted in infected neutrophils.
Conclusions:
- TBEV infection induces apoptosis in neutrophils.
- Altered cellular metabolism, including a shift towards anaerobic energy production, is a hallmark of TBEV-induced neutrophil apoptosis.
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