Survivin: A key apoptosis inhibitor in COVID-19 infection and its implication for treatment protocol
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View abstract on PubMed
Summary
This summary is machine-generated.COVID-19 patients show increased white blood cell apoptosis and proliferation. Strategies to prevent this apoptosis may help mitigate severe COVID-19 outcomes and lymphopenia.
Area Of Science
- Immunology
- Virology
- Cell Biology
Background
- The impact of Coronavirus disease (COVID-19) on cellular apoptosis and proliferation is not well understood.
- Viruses can manipulate host cell processes like apoptosis and proliferation to influence infection outcomes.
- Understanding these cellular changes is crucial for comprehending COVID-19 pathogenesis.
Purpose Of The Study
- To evaluate apoptosis and proliferation rates in peripheral blood cells of COVID-19 patients.
- To compare these rates in patients before and after vaccination against healthy controls.
- To explore the role of specific immune markers in COVID-19-associated cellular changes.
Main Methods
- Analysis of peripheral blood cells (lymphocytes and granulocytes) from newly diagnosed COVID-19 patients and healthy controls.
- Assessment of apoptosis and proliferation levels.
- Measurement of soluble Fas ligand (FaSL) and Interleukin-38 (IL-38) levels.
Main Results
- Significant increases in proliferation and apoptosis were observed in lymphocytes and granulocytes of COVID-19 patients compared to controls.
- Elevated levels of soluble Fas ligand (FaSL) and IL-38 were detected in COVID-19 patients.
- Individuals vaccinated or recovered from COVID-19 showed higher survivin rates, indicating potential lung damage mitigation.
Conclusions
- White blood cell (WBC) apoptosis plays a critical role in COVID-19 pathogenesis and pathogenicity.
- Immune dysregulation, indicated by elevated FaSL and IL-38, is associated with COVID-19.
- Targeting WBC apoptosis presents a potential therapeutic strategy to prevent lymphopenia and severe COVID-19 outcomes.
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