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Updated: Nov 4, 2025

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
Published on: October 28, 2019
Therapeutic Potential of Exploiting Autophagy Cascade Against Coronavirus Infection
1School of Biotechnology, Presidency University, Kolkata, India.
Abstract:
Since its emergence in December 2019 in Wuhan, China, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) created a worldwide pandemic of coronavirus disease (COVID-19) with nearly 136 million cases and approximately 3 million deaths. Recent studies indicate that like other coronaviruses, SARS-CoV-2 also hijacks or usurps various host cell machineries including autophagy for its replication and disease pathogenesis. Double membrane vesicles generated during initiation of autophagy cascade act as a scaffold for the assembly of viral replication complexes and facilitate RNA synthesis. The use of autophagy inhibitors - chloroquine and hydroxychloroquine initially appeared to be as a potential treatment strategy of COVID-19 patients but later remained at the center of debate due to high cytotoxic effects. In the absence of a specific drug or vaccine, there is an urgent need for a safe, potent as well as affordable drug to control the disease spread. Given the intricate connection between autophagy machinery and viral pathogenesis, the question arises whether targeting autophagy pathway might show a path to fight against SARS-CoV-2 infection. In this review we will discuss about our current knowledge linking autophagy to coronaviruses and how that is being utilized to repurpose autophagy modulators as potential COVID-19 treatment.
Insights
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) hijacks host cell autophagy for replication. Targeting this pathway with autophagy modulators may offer a potential treatment strategy for coronavirus disease (COVID-19).
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused a global pandemic, leading to millions of cases and deaths.
- Coronaviruses, including SARS-CoV-2, exploit host cell autophagy for viral replication and pathogenesis.
- Autophagy, a cellular degradation process, involves double-membrane vesicles crucial for viral replication complex assembly.
Purpose of the Study:
- To review the current understanding of the link between autophagy and coronaviruses.
- To explore the potential of repurposing autophagy modulators as therapeutic agents for COVID-19.
- To address the urgent need for safe and effective treatments against SARS-CoV-2 infection.
Main Methods:
- Literature review of studies on autophagy and coronavirus interactions.
- Analysis of existing research on autophagy inhibitors (e.g., chloroquine) for COVID-19 treatment.
- Discussion of the role of autophagy modulation in combating SARS-CoV-2.
Main Results:
- Autophagy plays a critical role in the replication cycle of SARS-CoV-2.
- Initial therapeutic strategies using autophagy inhibitors like chloroquine showed promise but were limited by cytotoxicity.
- Targeting the autophagy pathway presents a viable avenue for developing novel COVID-19 treatments.
Conclusions:
- The intricate relationship between autophagy and viral pathogenesis highlights its significance in COVID-19.
- Repurposing autophagy modulators offers a promising strategy for developing safe and affordable treatments.
- Further research into autophagy modulation is crucial for effective COVID-19 therapeutic development.
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