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Published on: October 28, 2019
Autophagy Modulation in Lymphocytes From COVID-19 Patients: New Therapeutic Target in SARS-COV-2 Infection
Marta Vomero1, Cristiana Barbati1, Tania Colasanti1
1Rheumatology Unit, Department of Clinical, Internal, Anesthesiological and Cardiovascular Sciences, Sapienza University of Rome, Rome, Italy.
Abstract:
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is the novel coronavirus, causing coronavirus disease 2019 (COVID-19). During virus infection, several pro-inflammatory cytokines are produced, leading to the "cytokine storm." Among these, interleukin (IL)-6, tumor necrosis factor-α (TNF-α), and IL-1β seem to have a central role in the progression and exacerbation of the disease, leading to the recruitment of immune cells to infection sites. Autophagy is an evolutionarily conserved lysosomal degradation pathway involved in different aspects of lymphocytes functionality. The involvement of IL-6, TNF-α, and IL-1β in autophagy modulation has recently been demonstrated. Moreover, preliminary studies showed that SARS-CoV-2 could infect lymphocytes, playing a role in the modulation of autophagy. Several anti-rheumatic drugs, now proposed for the treatment of COVID-19, could modulate autophagy in lymphocytes, highlighting the therapeutic potential of targeting autophagy in SARS-CoV-2 infection.
Insights
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection triggers a cytokine storm, impacting lymphocyte autophagy. Targeting this pathway with anti-rheumatic drugs shows therapeutic potential for COVID-19 treatment.
Area of Science:
- Immunology
- Cell Biology
- Virology
Background:
- Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) causes COVID-19, characterized by a pro-inflammatory "cytokine storm."
- Key cytokines like Interleukin-6 (IL-6), Tumor Necrosis Factor-alpha (TNF-α), and IL-1β are implicated in disease severity and immune cell recruitment.
- Autophagy, a cellular degradation process, is crucial for lymphocyte function and its modulation by these cytokines is increasingly recognized.
Purpose of the Study:
- To investigate the role of SARS-CoV-2 in modulating lymphocyte autophagy.
- To explore the potential of targeting autophagy in lymphocytes as a therapeutic strategy for COVID-19.
Main Methods:
- Review of existing literature on SARS-CoV-2, cytokine storm, autophagy, and lymphocyte function.
- Analysis of preliminary studies examining SARS-CoV-2 infection in lymphocytes and its effect on autophagy.
- Examination of the impact of anti-rheumatic drugs on autophagy in lymphocytes.
Main Results:
- SARS-CoV-2 infection may directly impact and modulate autophagy within lymphocytes.
- Pro-inflammatory cytokines (IL-6, TNF-α, IL-1β) play a role in modulating autophagy.
- Certain anti-rheumatic drugs, considered for COVID-19 treatment, demonstrate the ability to modulate autophagy in lymphocytes.
Conclusions:
- Autophagy modulation in lymphocytes represents a potential therapeutic target for managing SARS-CoV-2 infection.
- The interplay between SARS-CoV-2, cytokines, and autophagy in lymphocytes warrants further investigation for novel treatment strategies.
- Anti-rheumatic drugs targeting autophagy may offer a promising avenue for COVID-19 treatment.
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