Bioinformatics and systems biology approaches to identify molecular targeting mechanism influenced by COVID-19 on heart failure

Abstract

Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has emerged as a contemporary hazard to people. It has been known that COVID-19 can both induce heart failure (HF) and raise the risk of patient mortality. However, the mechanism underlying the association between COVID-19 and HF remains unclear. The common molecular pathways between COVID-19 and HF were identified using bioinformatic and systems biology techniques. Transcriptome analysis was performed to identify differentially expressed genes (DEGs). To identify gene ontology terms and Kyoto Encyclopedia of Genes and Genomes pathways, common DEGs were used for enrichment analysis. The results showed that COVID-19 and HF have several common immune mechanisms, including differentiation of T helper (Th) 1, Th 2, Th 17 cells; activation of lymphocytes; and binding of major histocompatibility complex class I and II protein complexes. Furthermore, a protein-protein interaction network was constructed to identify hub genes, and immune cell infiltration analysis was performed. Six hub genes (FCGR3A, CD69, IFNG, CCR7, CCL5, and CCL4) were closely associated with COVID-19 and HF. These targets were associated with immune cells (central memory CD8 T cells, T follicular helper cells, regulatory T cells, myeloid-derived suppressor cells, plasmacytoid dendritic cells, macrophages, eosinophils, and neutrophils). Additionally, transcription factors, microRNAs, drugs, and chemicals that are closely associated with COVID-19 and HF were identified through the interaction network.

Immunogenicity and reactogenicity of inactivated SARS-CoV-2 vaccines in healthy adults

“…CD69+ is a sign of T cell activation ( 47 ). It can regulate the adaptive immune response through different mechanisms, including the prevention of Th17 differentiation and down regulation of proinflammatory cytokines ( 5 ). CD69+ is required for the trafficking of effector CD4+T cells to the bone marrow, particularly for their relocation and the persistence of their interaction with stromal cells as memory T helper cells ( 47 ).…”

“…These vaccines have been effective and significantly mitigate COVID-19 symptoms and provide protection against serious and fatal infections ( 4 ). Inactivated vaccines have a good preventive effect on various mutations and are widely used in China ( 5 ). Three–doses of the inactivated vaccine have prevented high mortality in elderly people (> 60– year– old) due to Omicron infection ( 6 ).…”

“…CD25 is a late activation marker of lymphocytes and have been reported to be related to the severity of COVID-19 infection ( 18 ). CD69 is a classical early marker of lymphocyte activation, and CD19 CD69 are closely related to heart failure caused by COVID-19 ( 5 ). T cell counts in critical patients, including CD3+T, CD4+T, CD8+T, CD25+CD4+, and CD19+B, were significantly lower in critical patients compared to those in the non-critical patients with COVID‐19 ( 19 ).…”