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10.1371/journal.ppat.1009723 http://scihub22266oqcxt.onion/10.1371/journal.ppat.1009723 34214142!8282004!34214142     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+Pathog 2021 ; 17 (7): e1009723 Nephropedia Template TP {{tp|p=34214142|t=2021. ACE2-lentiviral transduction enables mouse SARS-CoV-2 infection and mapping of receptor interactions |pdf=|usr=}}{{34214142}} gab.com Text ACE2-lentiviral transduction enables mouse SARS-CoV-2 infection and mapping of receptor interactions JO: PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=34214142 #FOAvip SARS-CoV-2 uses the human ACE2 (hACE2) receptor for cell attachment and entry, with mouse ACE2 (mACE2) unable to support infection. Herein we describe an ACE2-lentivirus system and illustrate its utility for in vitro and in vivo SARS-CoV-2 infection models. Transduction of non-permissive cell lines with hACE2 imparted replication competence, and transduction with mACE2 containing N30D, N31K, F83Y and H353K substitutions, to match hACE2, rescued SARS-CoV-2 replication. Intrapulmonary hACE2-lentivirus transduction of C57BL/6J mice permitted significant virus replication in lung epithelium. RNA-Seq and histological analyses illustrated that this model involved an acute inflammatory disease followed by resolution and tissue repair, with a transcriptomic profile similar to that seen in COVID-19 patients. hACE2-lentivirus transduction of IFNAR-/- and IL-28RA-/- mouse lungs was used to illustrate that loss of type I or III interferon responses have no significant effect on virus replication. However, their importance in driving inflammatory responses was illustrated by RNA-Seq analyses. We also demonstrate the utility of the hACE2-lentivirus transduction system for vaccine evaluation in C57BL/6J mice. The ACE2-lentivirus system thus has broad application in SARS-CoV-2 research, providing a tool for both mutagenesis studies and mouse model development. Twit Text FOAVip ACE2-lentiviral transduction enables mouse SARS-CoV-2 infection and mapping of receptor interactions ????PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=34214142 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34214142 #FOAvip English Wikipedia <ref>{{Cite pmid|34214142}}</ref> ACE2-lentiviral transduction enables mouse SARS-CoV-2 infection and mapping of receptor interactions #MMPMID34214142 Rawle DJ; Le TT; Dumenil T; Yan K; Tang B; Nguyen W; Watterson D; Modhiran N; Hobson-Peters J; Bishop C; Suhrbier A PLoS Pathog 2021[Jul]; 17 (7): e1009723 PMID34214142show ga SARS-CoV-2 uses the human ACE2 (hACE2) receptor for cell attachment and entry, with mouse ACE2 (mACE2) unable to support infection. Herein we describe an ACE2-lentivirus system and illustrate its utility for in vitro and in vivo SARS-CoV-2 infection models. Transduction of non-permissive cell lines with hACE2 imparted replication competence, and transduction with mACE2 containing N30D, N31K, F83Y and H353K substitutions, to match hACE2, rescued SARS-CoV-2 replication. Intrapulmonary hACE2-lentivirus transduction of C57BL/6J mice permitted significant virus replication in lung epithelium. RNA-Seq and histological analyses illustrated that this model involved an acute inflammatory disease followed by resolution and tissue repair, with a transcriptomic profile similar to that seen in COVID-19 patients. hACE2-lentivirus transduction of IFNAR-/- and IL-28RA-/- mouse lungs was used to illustrate that loss of type I or III interferon responses have no significant effect on virus replication. However, their importance in driving inflammatory responses was illustrated by RNA-Seq analyses. We also demonstrate the utility of the hACE2-lentivirus transduction system for vaccine evaluation in C57BL/6J mice. The ACE2-lentivirus system thus has broad application in SARS-CoV-2 research, providing a tool for both mutagenesis studies and mouse model development. |*Angiotensin-Converting Enzyme 2/biosynthesis/genetics[MESH] |*COVID-19/genetics/metabolism[MESH] |*Gene Expression Profiling[MESH] |*Lentivirus[MESH] |*SARS-CoV-2/genetics/metabolism[MESH] |*Transduction, Genetic[MESH] |Animals[MESH] |Chlorocebus aethiops[MESH] |Disease Models, Animal[MESH] |Humans[MESH] |Mice[MESH] |Mice, Knockout[MESH]ACE2-lentiviral transduction enables mouse SARS-CoV-2 infection and ma(epmc).pdf DeepDyve Pubget Overpricing