BREAKING! SARS-CoV-2 Upregulates Endogenous Retroviruses That Play A Role In COVID-19 Pathogenesis!
Nikhil Prasad Fact checked by:Thailand Medical News Team Apr 06, 2024 3 weeks, 2 days, 12 hours, 24 minutes ago
COVID-19 News: The ongoing COVID-19 pandemic has spurred intensive research into the molecular mechanisms underlying SARS-CoV-2 infection. Among these investigations, a recent study that is covered in this
COVID-19 News report, conducted by the Institute of Systems Biomedicine, Department of Immunology, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Systems Biology, Peking University Health Science Center in China, has shed new light on the potential role of endogenous retroviruses (ERVs) in the pathogenesis of COVID-19.
SARS-CoV-2 Upregulates Endogenous Retroviruses And Plays A Role In COVID-19
The most upregulated transposable elements (TEs) were subfamilies of endogenous retroviruses in COVID-19 patients. (A) Compositions of upregulated TEs in COVID-19 patients. (B) Distributions of long terminal repeats (LTRs) in the mild and severe groups. (C) The scatter plotting represents the correlation of TEs between the mild and severe patients. (D) Compositions of upregulated TEs in the monkeys and mice infected by SARS-CoV-2. (E) Distributions of LTRs in the monkeys and the mice group, respectively. (F) The scatter plotting represents the correlation of TEs between the mice and monkeys. (G, H) GREAT prediction analysis of upregulated TEs from the mild and severe patients, respectively. (I, J) GREAT prediction analysis of upregulated TEs from the monkeys and mice, respectively.
Thailand
Medical News had in our past articles had covered studies showing the reactivation of various endogenous retroviruses during infection and also their contribution to certain aspects of COVID-19.
https://www.thailandmedical.news/news/covid-19-news-researchers-discover-that-sars-cov-2-infection-activates-endogenous-retroviruses-of-the-ltr69-subfamily
https://www.thailandmedical.news/news/breaking-covid-19-news-study-discovers-that-sars-cov-2-modulates-human-endogenous-retrovirus-herv-transcriptome-during-infection
https://www.thailandmedical.news/news/breaking-sars-cov-2-infection-induces-human-endogenous-retrovirus-type-w-envelope-protein-expression-in-blood-lymphocytes-and-tissues
disease,-mis-c-and-even-covid-19-severity">https://www.thailandmedical.news/news/covid-19-news-sars-cov-2-reactivation-of-human-endogenous-retroviruses-contributes-to-kawasaki-disease,-mis-c-and-even-covid-19-severity
https://www.thailandmedical.news/news/study-finds-that-sars-cov-2-activates-ancient-retroviral-genes-and-inflammatory-herv-w-envelope-protein-in-covid-19-patients
Endogenous Retroviruses(ERVs)
ERVs are remnants of ancient viral infections that have become integrated into the human genome over evolutionary time. Despite constituting a substantial portion of our genetic material (approximately 8% of the genome), the specific functions of ERVs, particularly in the context of viral infections like COVID-19, have been poorly understood. This study aimed to comprehensively investigate the expression patterns and potential implications of ERVs following SARS-CoV-2 infection across human, monkey, and mouse models.
Identification and Characterization of ERVs in COVID-19
The study utilized advanced genome-wide analysis techniques to identify and characterize ERVs in human peripheral blood mononuclear cells (hPBMCs), primary lung epithelial cells from monkeys, and mice infected or uninfected with SARS-CoV-2. The analysis revealed a significant upregulation of ERVs following SARS-CoV-2 infection across these species, indicating a potential correlation between viral infection and ERV activation.
Specifically, the study identified ERVs such as HERV1_I-int: ERV1:LTR and LTR7Y: ERV1:LTR that were significantly upregulated in severe COVID-19 cases compared to mild cases or healthy controls. These ERVs belong to the ERV1 subfamily and were found to be closely associated with genes involved in immune responses and epigenetic modifications, suggesting their potential role as biomarkers for predicting COVID-19 severity.
Functional Insights and Validation Studies
To gain further insights into the functional implications of upregulated ERVs, the researchers conducted additional experiments using mouse bone marrow-derived macrophages (BMDMs) infected with vesicular stomatitis virus (VSV) and herpes simplex virus 1 (HSV-1). These experiments validated the initial findings, demonstrating consistent upregulation of ERVs and their interactions with host genes involved in antiviral immunity.
For example, the study identified ERVB2_1-I_MM-int:ERVK : LTR as one of the most upregulated ERVs in response to viral infection, particularly VSV and HSV-1. This ERV was found to interact with interferon-stimulated genes (ISGs) such as Ifi208 and Ifi213, highlighting its potential role in modulating the host's innate immune responses.
Implications for Diagnosis and Therapy
The identification of ERVs as potential biomarkers for COVID-19 severity opens up new avenues for diagnostic and therapeutic strategies. By monitoring the expression levels of specific ERVs like HERV1_I-int: ERV1:LTR and LTR7Y: ERV1:LTR, clinicians may be able to predict the likelihood of severe disease progression in COVID-19 patients, allowing for early intervention and personalized treatment approaches.
Moreover, understanding the functional roles of ERVs in the host's immune responses could lead to the development of targeted therapies aimed at modulating ERV activity and enhancing antiviral defenses. By leveraging the intricate interplay between ERVs and host genes, researchers may uncover novel therapeutic targets for combating COVID-19 and other viral infections.
Future Directions and Concluding Remarks
While this study represents a significant step forward in our understanding of ERVs' involvement in COVID-19 pathogenesis, several questions and avenues for future research remain. Further investigations into the mechanisms by which ERVs modulate immune responses, interact with viral pathogens, and contribute to disease severity are warranted.
Additionally, exploring the potential of ERVs as therapeutic targets and developing strategies to manipulate ERV activity in a controlled manner could revolutionize antiviral therapy. Continued collaboration between virologists, immunologists, and genomic researchers will be essential in unraveling the complex roles of ERVs in viral infections and advancing our capabilities in combating emerging infectious diseases like COVID-19.
In conclusion, the study underscores the intricate interplay between viral infections, host genomic elements like ERVs, and immune responses. By elucidating these relationships, researchers are paving the way for more precise diagnostics, targeted therapeutics, and a deeper understanding of COVID-19's pathogenesis at the molecular level.
The study findings were published in the peer reviewed journal: Frontiers in Immunology.
https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1294020/full
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