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10.3892/mmr.2021.11901 http://scihub22266oqcxt.onion/10.3892/mmr.2021.11901 33576464!7893688!33576464     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33576464&cmd=llinks): Failed to open stream: HTTP request failed! 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Severe acute respiratory syndrome coronavirus 2 for physicians: Molecular characteristics and host immunity (Review) |pdf=|usr=}}{{33576464}} gab.com Text Severe acute respiratory syndrome coronavirus 2 for physicians: Molecular characteristics and host immunity (Review) JO: Mol Med Rep http://www.kidney.de/pget.php?&tw=1&pmid=33576464 #FOAvip Recently, severe acute respiratory syndrome (SARS) coronavirus (CoV) 2 (SARS?CoV?2)?causing CoV disease 2019 (COVID?19) emerged in China and has become a global pandemic. SARS?CoV?2 is a novel CoV originating from beta?CoVs. Major distinctions in the gene sequences between SARS?CoV and SARS?CoV?2 include the spike gene, open reading frame (ORF) 3b and ORF 8. SARS?CoV?2 infection is initiated when the virus interacts with angiotensin?converting enzyme 2 (ACE2) receptors on host cells. Through this mechanism, the virus infects the alveolar, esophageal epithelial, ileum, colon and other cells on which ACE2 is highly expressed, causing damage to target organs. To date, host innate immunity may be the only identified direct factor associated with viral replication. However, increased ACE2 expression may upregulate the viral load indirectly by increasing the baseline level of infectious virus particles. The peak viral load of SARS?CoV?2 is estimated to occur ~10 days following fever onset, causing patients in the acute stage to be the primary infection source. However, patients in the recovery stage or with occult infections can also be contagious. The host immune response in patients with COVID?19 remains to be elucidated. By studying other SARS and Middle East respiratory syndrome coronaviruses, it is hypothesized that patients with COVID?19 may lack sufficient antiviral T?cell responses, which consequently present with innate immune response disorders. This may to a certain degree explain why this type of CoV triggers severe inflammatory responses and immune damage and its associated complications. Twit Text FOAVip Severe acute respiratory syndrome coronavirus 2 for physicians: Molecular characteristics and host immunity (Review) ????Mol Med Rep http://www.kidney.de/pget.php?&tw=1&pmid=33576464 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33576464 #FOAvip English Wikipedia <ref>{{Cite pmid|33576464}}</ref> Severe acute respiratory syndrome coronavirus 2 for physicians: Molecular characteristics and host immunity (Review) #MMPMID33576464 Shang J; Du L; Han N; Lv D; Wang J; Yang H; Bai L; Tang H Mol Med Rep 2021[Apr]; 23 (4): � PMID33576464show ga Recently, severe acute respiratory syndrome (SARS) coronavirus (CoV) 2 (SARS?CoV?2)?causing CoV disease 2019 (COVID?19) emerged in China and has become a global pandemic. SARS?CoV?2 is a novel CoV originating from beta?CoVs. Major distinctions in the gene sequences between SARS?CoV and SARS?CoV?2 include the spike gene, open reading frame (ORF) 3b and ORF 8. SARS?CoV?2 infection is initiated when the virus interacts with angiotensin?converting enzyme 2 (ACE2) receptors on host cells. Through this mechanism, the virus infects the alveolar, esophageal epithelial, ileum, colon and other cells on which ACE2 is highly expressed, causing damage to target organs. To date, host innate immunity may be the only identified direct factor associated with viral replication. However, increased ACE2 expression may upregulate the viral load indirectly by increasing the baseline level of infectious virus particles. The peak viral load of SARS?CoV?2 is estimated to occur ~10 days following fever onset, causing patients in the acute stage to be the primary infection source. However, patients in the recovery stage or with occult infections can also be contagious. The host immune response in patients with COVID?19 remains to be elucidated. By studying other SARS and Middle East respiratory syndrome coronaviruses, it is hypothesized that patients with COVID?19 may lack sufficient antiviral T?cell responses, which consequently present with innate immune response disorders. This may to a certain degree explain why this type of CoV triggers severe inflammatory responses and immune damage and its associated complications. |Adaptive Immunity[MESH] |Angiotensin-Converting Enzyme 2/metabolism[MESH] |COVID-19/immunology/*pathology/virology[MESH] |Humans[MESH] |Immunity, Innate[MESH] |SARS-CoV-2/genetics/immunology/isolation & purification/*physiology[MESH] |Spike Glycoprotein, Coronavirus/genetics/metabolism[MESH]Severe acute respiratory syndrome coronavirus 2 for physicians: Molecu(epmc).pdf DeepDyve Pubget Overpricing