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Updated: Jun 24, 2025

In Silico Identification and Characterization of circRNAs During Host-Pathogen Interactions
Published on: October 21, 2022
Illuminating the pathogenic role of SARS-CoV-2: Insights into competing endogenous RNAs (ceRNAs) regulatory networks
1Deputy of Research and Technology, Babol University of Medical Sciences, Babol, Iran.
Abstract:
The appearance of SARS-CoV-2 in 2019 triggered a significant economic and health crisis worldwide, with heterogeneous molecular mechanisms that contribute to its development are not yet fully understood. Although substantial progress has been made in elucidating the mechanisms behind SARS-CoV-2 infection and therapy, it continues to rank among the top three global causes of mortality due to infectious illnesses. Non-coding RNAs (ncRNAs), being integral components across nearly all biological processes, demonstrate effective importance in viral pathogenesis. Regarding viral infections, ncRNAs have demonstrated their ability to modulate host reactions, viral replication, and host-pathogen interactions. However, the complex interactions of different types of ncRNAs in the progression of COVID-19 remains understudied. In recent years, a novel mechanism of post-transcriptional gene regulation known as "competing endogenous RNA (ceRNA)" has been proposed. Long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), and viral ncRNAs function as ceRNAs, influencing the expression of associated genes by sequestering shared microRNAs. Recent research on SARS-CoV-2 has revealed that disruptions in specific ceRNA regulatory networks (ceRNETs) contribute to the abnormal expression of key infection-related genes and the establishment of distinctive infection characteristics. These findings present new opportunities to delve deeper into the underlying mechanisms of SARS-CoV-2 pathogenesis, offering potential biomarkers and therapeutic targets. This progress paves the way for a more comprehensive understanding of ceRNETs, shedding light on the intricate mechanisms involved. Further exploration of these mechanisms holds promise for enhancing our ability to prevent viral infections and develop effective antiviral treatments.
Insights
Non-coding RNAs (ncRNAs) play a crucial role in COVID-19 pathogenesis. Disruptions in competing endogenous RNA regulatory networks (ceRNETs) are linked to SARS-CoV-2 infection mechanisms, offering potential therapeutic targets.
Area of Science:
- Molecular Biology
- Virology
- Genetics
Background:
- SARS-CoV-2 caused a global health crisis with incompletely understood molecular mechanisms.
- Non-coding RNAs (ncRNAs) are vital in biological processes and viral pathogenesis, modulating host responses and viral replication.
- The intricate roles of various ncRNAs in COVID-19 progression are not fully elucidated.
Purpose of the Study:
- To explore the role of competing endogenous RNA regulatory networks (ceRNETs) in SARS-CoV-2 pathogenesis.
- To investigate how ncRNAs, including long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), and viral ncRNAs, function as ceRNAs in COVID-19.
- To identify potential biomarkers and therapeutic targets related to ceRNET disruptions in SARS-CoV-2 infection.
Main Methods:
- Review and analysis of recent research on ncRNA interactions and ceRNA mechanisms in SARS-CoV-2.
- Investigation of how disruptions in ceRNETs affect gene expression related to viral infection.
- Exploration of the implications of these findings for understanding COVID-19 progression.
Main Results:
- Disruptions in specific ceRNETs are associated with abnormal expression of key infection-related genes in SARS-CoV-2.
- These disruptions contribute to the unique characteristics of COVID-19 infection.
- ncRNAs, acting as ceRNAs, significantly influence host-pathogen interactions and viral pathogenesis.
Conclusions:
- ceRNETs represent a critical layer of gene regulation in SARS-CoV-2 infection.
- Understanding ceRNETs provides new insights into COVID-19 pathogenesis.
- Targeting ceRNETs offers promising avenues for developing novel biomarkers and antiviral therapies.
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