Network-based Approach to Identify Pathways and Macromolecule Interactions that Mediate Influences of COVID-19 on the Progression of Respiratory System Diseases

COVID-19 is an infectious illness concerning coronavirus that is transmitted through droplets propagated by an infected person exhales, coughs, or sneezes. People affected by coronavirus have a risk to occur respiratory diseases (RDs). The longevity of COVID-19 may appear a vital risk of manifesting RDs. To address these issues, we explored transcriptomic data to identify the genetic effects of COVID-19 on the development of RDs such as Bronchitis (BC), Asthma (AT), Lung cancer (LC), and Pulmonary Edema (PE). We explored GEO datasets from NCBI for COVID-19, BC, AT, LC, PE case, and control subjects. We identified COVID-19 is associated with RDs by sharing 16, 19, 27, and 59 commonly DEGs accordingly. By using these genes we performed some bioinformatics analysis and constructed diseasome networks, identified functional and ontological pathways. We formed PPIs networks and PDIs network. On the basis of PPIs and PDIs, we have identified hub proteins and constructed hub proteins network. We have successfully developed a quantitative model to identify the genetic effects of COVID-19 on the progression of RDs. We also validated our investigations through gold-benchmark datasets. Our results are an effective resource to mark out the most important influences on the development of RDs for COVID-19. © 2022 IEEE.

Genetic Effects of Covid 19 on the Development of Neurodegenerative Diseases

The coronavirus disease (COVID-19) caused by SARS-COV-2, a highly infectious pathogen, genetically similar to SARS-COV is an unprecedented worldwide health crisis. Rapidly accumulating clinical research revealed that COVID-19 is manifested by various neurological symptoms and also affects the brain in many ways including direct infection to systemic inflammation. Which indicates it may substantially increase the incidence of developing neurodegenerative diseases (NDGDs). To discourse this issue we studied the computable frameworks to address the gene expression association of COVID-19 and NDGDs to identify the link among them. We analyzed GEO microarray datasets from COVID-19 and NDGDs including Epilepsy, Stroke, Multiple Sclerosis, Alzheimer's disease, and Parkinson's disease. We constructed disease-gene relationship networks and identified dysregulated pathways, ontological pathways, protein-protein interaction (PPI) network, and protein-drug interaction (PDI) network. We observed that COVID-19 associated genes share 19, 26, 20, 19, 22 differentially expressed genes with Epilepsy, Stroke, Multiple Sclerosis, Alzheimer's disease, and Parkinson's disease respectively. Gene expression dysregulation, PPI and PDI relationship networks, different pathways suggest that COVID-19 may have a significant link to the development of these NDGDs. This analysis may help to develop therapeutic strategies and raise awareness about the influence of COVID-19 on the progression of NDGDs. © 2021 IEEE.

Enrichment of SARS-CoV-2 Entry Factors and Interacting Intracellular Genes in Tissue and Circulating Immune Cells.

SARS-CoV-2 uses ACE2 and TMPRSS2 to gain entry into the cell. However, recent studies have shown that SARS-CoV-2 may use additional host factors that are required for the viral lifecycle. Here we used publicly available datasets, CoV-associated genes, and machine learning algorithms to explore the SARS-CoV-2 interaction landscape in different tissues. We found that in general a small fraction of cells express ACE2 in the different tissues, including nasal, bronchi, and lungs. We show that a small fraction of immune cells (including T cells, macrophages, dendritic cells) found in tissues also express ACE2. We show that healthy circulating immune cells do not express ACE2 and TMPRSS2. However, a small fraction of circulating immune cells (including dendritic cells, monocytes, T cells) in the PBMC of COVID-19 patients express ACE2 and TMPRSS2. Additionally, we found that a large spectrum of cells (in tissues and circulation) in both healthy and COVID-19-positive patients were significantly enriched for SARS-CoV-2 factors, such as those associated with RHOA and RAB GTPases, mRNA translation proteins, COPI- and COPII-mediated transport, and integrins. Thus, we propose that further research is needed to explore if SARS-CoV-2 can directly infect tissue and circulating immune cells to better understand the virus' mechanism of action.

Neurological manifestations of COVID-19: available evidences and a new paradigm.

The recent pandemic outbreak of coronavirus is pathogenic and a highly transmittable viral infection caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV2). In this time of ongoing pandemic, many emerging reports suggested that the SARS-CoV-2 has inimical effects on neurological functions, and even causes serious neurological damage. The neurological symptoms associated with COVID-19 include headache, dizziness, depression, anosmia, encephalitis, stroke, epileptic seizures, and Guillain-Barre syndrome along with many others. The involvement of the CNS may be related with poor prognosis and disease worsening. Here, we review the evidence of nervous system involvement and currently known neurological manifestations in COVID-19 infections caused by SARS-CoV-2. We prioritize the 332 human targets of SARS-CoV-2 according to their association with brain-related disease and identified 73 candidate genes. We prioritize these 73 genes according to their spatio-temporal expression in the different regions of brain and also through evolutionary intolerance analysis. The prioritized genes could be considered potential indicators of COVID-19-associated neurological symptoms and thus act as a possible therapeutic target for the prevention and treatment of CNS manifestations associated with COVID-19 patients.