Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1111/febs.16230 http://scihub22266oqcxt.onion/10.1111/febs.16230 34653312!ä!34653312 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       FEBS+J 2023 ; 290 (5): 1384-1392 Nephropedia Template TP {{tp|p=34653312|t=2023. Cellular senescence as a source of SARS-CoV-2 quasispecies |pdf=|usr=}}{{34653312}} gab.com Text Cellular senescence as a source of SARS-CoV-2 quasispecies JO: FEBS J http://www.kidney.de/pget.php?&tw=1&pmid=34653312 #FOAvip In-depth analysis of SARS-CoV-2 biology and pathogenesis is rapidly unraveling the mechanisms through which the virus induces all aspects of COVID-19 pathology. Emergence of hundreds of variants and several important variants of concern has focused research on the mechanistic elucidation of virus mutagenesis. RNA viruses evolve quickly either through the error-prone polymerase or the RNA-editing machinery of the cell. In this review, we are discussing the links between cellular senescence, a natural aging process that has been recently linked to SARS-CoV-2 infection, and virus mutagenesis through the RNA-editing enzymes APOBEC. The action of APOBEC, enhanced by cellular senescence, is hypothesized to assist the emergence of novel variants, called quasispecies, within a cell or organism. These variants when introduced to the community may lead to the generation of a variant of concern, depending on fitness and transmissibility of the new genome. Such a mechanism of virus evolution may highlight the importance of inhibitors of cellular senescence during SARS-CoV-2 clinical treatment. Twit Text FOAVip Cellular senescence as a source of SARS-CoV-2 quasispecies ????FEBS J http://www.kidney.de/pget.php?&tw=1&pmid=34653312 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34653312 #FOAvip English Wikipedia <ref>{{Cite pmid|34653312}}</ref> Cellular senescence as a source of SARS-CoV-2 quasispecies #MMPMID34653312 Karakasiliotis I; Lagopati N; Evangelou K; Gorgoulis VG FEBS J 2023[Mar]; 290 (5): 1384-1392 PMID34653312show ga In-depth analysis of SARS-CoV-2 biology and pathogenesis is rapidly unraveling the mechanisms through which the virus induces all aspects of COVID-19 pathology. Emergence of hundreds of variants and several important variants of concern has focused research on the mechanistic elucidation of virus mutagenesis. RNA viruses evolve quickly either through the error-prone polymerase or the RNA-editing machinery of the cell. In this review, we are discussing the links between cellular senescence, a natural aging process that has been recently linked to SARS-CoV-2 infection, and virus mutagenesis through the RNA-editing enzymes APOBEC. The action of APOBEC, enhanced by cellular senescence, is hypothesized to assist the emergence of novel variants, called quasispecies, within a cell or organism. These variants when introduced to the community may lead to the generation of a variant of concern, depending on fitness and transmissibility of the new genome. Such a mechanism of virus evolution may highlight the importance of inhibitors of cellular senescence during SARS-CoV-2 clinical treatment. |*COVID-19/genetics[MESH] |*Viruses/genetics[MESH] |Cellular Senescence/genetics[MESH] |Humans[MESH] |Quasispecies[MESH] |RNA[MESH]Cellular senescence as a source of SARS-CoV-2 quasispecies (epmc).pdf DeepDyve Pubget Overpricing