Activation of Immune System May Cause Pathophysiological Changes in the Myocardium of SARS-CoV-2 Infected Monkey Model

Rabbani, Maryam; Rappaport, Jay; Gupta, Manish Kumar

doi:10.3390/cells11040611

Cited by 3 publications

(1 citation statement)

References 39 publications

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“…Consequently, the impact of respiratory infections on immune cells may exacerbate the progression of HF. Research indicates that myocardial samples from SARS-CoV-2 infection models show a significant increase in T lymphocytes and macrophages, suggesting that SARS-CoV-2 infection induces an excessive inflammatory response, leading to myocardial remodeling and subsequent fibrosis, thereby worsening HF [47]. Additionally, severe COVID-19 patients exhibit dysregulated immune responses, particularly cytokine storms that result in systemic inflammation and multi-organ failure [48].…”

Section: Discussionmentioning

confidence: 99%

Integrating Bioinformatics and Machine Learning to Investigate the Mechanisms by Which Three Major Respiratory Infectious Diseases Exacerbate Heart Failure

Yu,

Zhang,

Shi

et al. 2024

Preprint

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BackgroundHeart failure (HF) is a severe cardiovascular disease often worsened by respiratory infections like influenza, COVID-19, and community-acquired pneumonia (CAP). This study aims to uncover the molecular commonalities among these respiratory diseases and their impact on HF, identifying key mediating genes.MethodsDatasets from the GEO database were analyzed for differential expression to find common molecular features of the three respiratory diseases. Weighted Gene Co-expression Network Analysis (WGCNA) was used to identify gene modules associated with HF. GO and KEGG enrichment analyses determined the biological processes and pathways involved in HF exacerbation by respiratory diseases. Key genes were screened using LASSO, RF, and SVM-RFE machine learning algorithms, with accuracy validated by ROC curves. Single-sample GSEA (ssGSEA) was performed, and the Drug Signature Database (DSigDB) was used for drug prediction. Immune infiltration analysis was conducted using CIBERSORT.ResultsWe identified 51 characteristic genes of respiratory diseases and 10 potential genes exacerbating HF, primarily involved in innate immune response, inflammation, and coagulation pathways. Machine learning algorithms identified RSAD2 and IFI44L as key genes with high accuracy (AUC > 0.7). ssGSEA indicated RSAD2’s involvement in complement and coagulation cascades, while IFI44L is associated with myocardial contraction in HF progression. DSigDB predicted six potential therapeutic drugs. Immune infiltration analysis revealed significant differences in eight immune cell types between HF patients and healthy controls.ConclusionOur findings enhance the understanding of molecular interactions between respiratory diseases and heart failure, paving the way for future research and therapeutic strategies.

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Section: Discussionmentioning

confidence: 99%

Integrating Bioinformatics and Machine Learning to Investigate the Mechanisms by Which Three Major Respiratory Infectious Diseases Exacerbate Heart Failure

Yu,

Zhang,

Shi

et al. 2024

Preprint

View full text Add to dashboard Cite

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Possible mechanisms of SARS-CoV-2-associated myocardial fibrosis: reflections in the post-pandemic era

Wang,

Li,

Yang

et al. 2024

Front. Microbiol.

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Since December 2019, coronavirus disease 2019 (COVID-19) has been spreading worldwide with devastating immediate or long-term effects on people’s health. Although the lungs are the primary organ affected by COVID-19, individuals infected with SARS-CoV-2 also develop systemic lesions involving multiple organs throughout the body, such as the cardiovascular system. Emerging evidence reveals that COVID-19 could generate myocardial fibrosis, termed “COVID-19-associated myocardial fibrosis.” It can result from the activation of fibroblasts via the renin-angiotensin-aldosterone system (RAAS), transforming growth factor-β1 (TGF-β1), microRNAs, and other pathways, and can also occur in other cellular interactions with SARS-CoV-2, such as immunocytes, endothelial cells. Nonetheless, to gain a more profound insight into the natural progression of COVID-19-related myocardial fibrosis, additional investigations are necessary. This review delves into the underlying mechanisms contributing to COVID-19-associated myocardial fibrosis while also examining the antifibrotic potential of current COVID-19 treatments, thereby offering guidance for future clinical trials of these medications. Ultimately, we propose future research directions for COVID-19-associated myocardial fibrosis in the post-COVID-19 era, such as artificial intelligence (AI) telemedicine. We also recommend that relevant tests be added to the follow-up of COVID-19 patients to detect myocardial fibrosis promptly.

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HIV Protein Nef Induces Cardiomyopathy Through Induction of Bcl2 and p21

Kondrachuck,

Ciccone,

Ford

et al. 2024

IJMS

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HIV-associated cardiovascular diseases remain a leading cause of death in people living with HIV/AIDS (PLWHA). Although antiretroviral drugs suppress the viral load, they fail to remove the virus entirely. HIV-1 Nef protein is known to play a role in viral virulence and HIV latency. Expression of Nef protein can be detected in different organs, including cardiac tissue. Despite the established role of Nef protein in HIV-1 replication, its impact on organ function inside the human body is not clear. To understand the effect of Nef at the organ level, we created a new Nef-transgenic (Nef-TG) mouse that expresses Nef protein in the heart. Our study found that Nef expression caused inhibition of cardiac function and pathological changes in the heart with increased fibrosis, leading to heart failure and early mortality. Further, we found that cellular autophagy is significantly inhibited in the cardiac tissue of Nef-TG mice. Mechanistically, we found that Nef protein causes the accumulation of Bcl2 and Beclin-1 proteins in the tissue, which may affect the cellular autophagy system. Additionally, we found Nef expression causes upregulation of the cellular senescence marker p21 and senescence-associated β-galactosidase expression. Our findings suggest that the Nef-mediated inhibition of autophagy and induction of senescence markers may promote aging in PLWHA. Our mouse model could help us to understand the effect of Nef protein on organ function during latent HIV infection.

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Activation of Immune System May Cause Pathophysiological Changes in the Myocardium of SARS-CoV-2 Infected Monkey Model

Cited by 3 publications

References 39 publications

Integrating Bioinformatics and Machine Learning to Investigate the Mechanisms by Which Three Major Respiratory Infectious Diseases Exacerbate Heart Failure

Integrating Bioinformatics and Machine Learning to Investigate the Mechanisms by Which Three Major Respiratory Infectious Diseases Exacerbate Heart Failure

Possible mechanisms of SARS-CoV-2-associated myocardial fibrosis: reflections in the post-pandemic era

HIV Protein Nef Induces Cardiomyopathy Through Induction of Bcl2 and p21

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