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10.1096/fj.202001025

http://scihub22266oqcxt.onion/10.1096/fj.202001025
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32427393!7276714!32427393
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suck abstract from ncbi

pmid32427393      FASEB+J 2020 ; 34 (6): 7247-7252
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  • Telomeres and COVID-19 #MMPMID32427393
  • Aviv A
  • FASEB J 2020[Jun]; 34 (6): 7247-7252 PMID32427393show ga
  • The medical, public health, and scientific communities are grappling with monumental imperatives to contain COVID-19, develop effective vaccines, identify efficacious treatments for the infection and its complications, and find biomarkers that detect patients at risk of severe disease. The focus of this communication is on a potential biomarker, short telomere length (TL), that might serve to identify patients more likely to die from the SARS-CoV-2 infection, regardless of age. The common thread linking these patients is lymphopenia, which largely reflects a decline in the numbers of CD4/CD8 T cells but not B cells. These findings are consistent with data that lymphocyte TL dynamics impose a limit on T-cell proliferation. They suggest that T-cell lymphopoiesis might stall in individuals with short TL who are infected with SARS-CoV-2.
  • |*Betacoronavirus[MESH]
  • |*Models, Biological[MESH]
  • |*Telomere Shortening[MESH]
  • |Biomarkers[MESH]
  • |Bone Marrow/pathology[MESH]
  • |COVID-19[MESH]
  • |Cell Division[MESH]
  • |Coronavirus Infections/genetics/immunology/mortality/*pathology[MESH]
  • |Disease Progression[MESH]
  • |Hematopoietic Stem Cells/pathology[MESH]
  • |Humans[MESH]
  • |Lymphocyte Activation[MESH]
  • |Lymphocyte Count[MESH]
  • |Lymphopenia/*etiology/pathology[MESH]
  • |Lymphopoiesis[MESH]
  • |Pandemics[MESH]
  • |Pneumonia, Viral/genetics/immunology/mortality/*pathology[MESH]
  • |Prognosis[MESH]
  • |Risk[MESH]
  • |SARS-CoV-2[MESH]
  • |T-Lymphocyte Subsets/*ultrastructure[MESH]


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