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    Prediction of SARS-CoV interaction with host proteins during lung aging reveals a potential role for TRIB3 HGNC in COVID-19 MESHD.

    Authors: Diogo de Moraes; Brunno Vivone Buquete Paiva; Sarah Santiloni Cury; Joao Pessoa Araujo Jr.; Marcelo Alves da Silva Mori; Robson Francisco Carvalho

    doi:10.1101/2020.04.07.030767 Date: 2020-04-09 Source: bioRxiv

    COVID-19 MESHD is prevalent in the elderly. Old individuals are more likely to develop pneumonia MESHD and respiratory failure MESHD due to alveolar damage MESHD, suggesting that lung senescence may increase the susceptibility to SARS-CoV-2 infection MESHD and replication. Considering that human coronavirus (HCoVs; SARS-CoV-2 and SARS-CoV) require host cellular factors for infection and replication, we analyzed Genotype-Tissue Expression (GTEx) data to test whether lung aging is associated with transcriptional changes in human protein-coding genes that potentially interact with these viruses. We found decreased expression of the gene tribbles homolog 3 ( TRIB3 HGNC) during aging in male individuals, and its protein was predicted to interact with HCoVs nucleocapsid protein PROTEIN and RNA-dependent RNA polymerase PROTEIN. Using publicly available lung single-cell data, we found TRIB3 HGNC expressed mainly in alveolar MESHD epithelial cells that express SARS-CoV-2 receptor ACE2 HGNC. Functional enrichment analysis of age-related genes, in common with SARS-CoV-induced perturbations, revealed genes associated with the mitotic cell cycle and surfactant metabolism. Given that TRIB3 HGNC was previously reported to decrease virus infection MESHD and replication, the decreased expression of TRIB3 HGNC in aged lungs may help explain why older male patients are related to more severe cases of the COVID-19 MESHD. Thus, drugs that stimulate TRIB3 HGNC expression should be evaluated as a potential therapy for the disease.

    Comparative Genomic Analysis of Rapidly Evolving SARS CoV-2 Viruses Reveal Mosaic Pattern of Phylogeographical Distribution

    Authors: Roshan Kumar; Helianthous Verma; Nirjara Singhvi; Utkarsh Sood; Vipin Gupta; Mona Singh; Rashmi Sharma; Princy Hira; Shekhar Nagar; Chandni Talwar; Namita Nayyar; Shailly Anand; Charu Dogra Rawat; Mansi Verma; Ram Kishan Negi; Yogendra Singh; Rup Lal

    doi:10.1101/2020.03.25.006213 Date: 2020-03-30 Source: bioRxiv

    The Coronavirus Disease-2019 ( COVID-19 MESHD) that started in Wuhan, China in December 2019 has spread worldwide emerging as a global pandemic. The severe respiratory pneumonia MESHD caused by the novel SARS-CoV-2 has so far claimed more than 60,000 lives and has impacted human lives worldwide. However, as the novel SARS-CoV-2 displays high transmission rates, their underlying genomic severity is required to be fully understood. We studied the complete genomes of 95 SARS-CoV-2 strains from different geographical regions worldwide to uncover the pattern of the spread of the virus. We show that there is no direct transmission pattern of the virus among neighboring countries suggesting that the outbreak is a result of travel of infected humans to different countries. We revealed unique single nucleotide polymorphisms (SNPs) in nsp13-16 (ORF1b polyprotein) and S-Protein PROTEIN within 10 viral isolates from the USA. These viral proteins are involved in RNA replication, indicating highly evolved viral strains circulating in the population of USA than other countries. Furthermore, we found an amino acid addition in nsp16 (mRNA cap-1 methyltransferase) of the USA isolate (MT188341) leading to shift in amino acid frame from position 2540 onwards. Through the construction of SARS-CoV-2-human interactome, we further revealed that multiple host proteins (PHB, PPP1CA HGNC, TGF-{beta} HGNC, SOCS3 HGNC, STAT3 HGNC, JAK1/2, SMAD3 HGNC, BCL2 HGNC, CAV1 HGNC & SPECC1 HGNC) are manipulated by the viral proteins ( nsp2 HGNC, PL-PRO, N-protein PROTEIN, ORF7a PROTEIN, M-S- ORF3a PROTEIN complex, nsp7-nsp8-nsp9- RdRp complex PROTEIN) for mediating host immune evasion. Thus, the replicative machinery of SARS-CoV-2 is fast evolving to evade host challenges which need to be considered for developing effective treatment strategies.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins


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