ABSTRACT
Corona virus infection rapidly spreading and producing morbidity and mortality in all over the world over the past one and half year. The virus triggered immune system dysfunction leading to life threatening cytokine storm indicating severe forms of lung injury .Need to understand the clinical profile and risk factors leading to mortality is much needed . Aim(s): To determine the clinical profile of patients having COVID 19 using the inflammatory markers at a semi urban center Methods and materials: A retrospective study conducted on cases that were admitted in CAIMS during the period of 3 months, with CT chest grading CORADS > 3, COVID RT-PCR or rapid antigen test positive, pulse oximetre saturation less than 90% Conclusion(s): 515 cases were taken into study,clinical presentation was observed .Most cases were likely to have CT chest CORADS grading > 3, inflammatory markers like LDH, Sr Ferritin, CRP have been elevated. Cases have shown high IL-6, which was estimated selectively in cases with oxygen support suggesting cytokine storm.16.4 % cases showed mortality. This is attributed among cases with severe form of Covid 19.Copyright © 2020 Ubiquity Press. All rights reserved.
ABSTRACT
Visceral adiposity is a risk factor for severe COVID-19, and a link between adipose tissue infection and disease progression has been proposed. Here we demonstrate that SARS-CoV-2 infects human adipose tissue and undergoes productive infection in fat cells. However, susceptibility to infection and the cellular response depends on the anatomical origin of the cells and the viral lineage. Visceral fat cells express more ACE2 and are more susceptible to SARS-CoV-2 infection than their subcutaneous counterparts. SARS-CoV-2 infection leads to inhibition of lipolysis in subcutaneous fat cells, while in visceral fat cells, it results in higher expression of pro-inflammatory cytokines. Viral load and cellular response are attenuated when visceral fat cells are infected with the SARS-CoV-2 gamma variant. A similar degree of cell death occurs 4-days after SARS-CoV-2 infection, regardless of the cell origin or viral lineage. Hence, SARS-CoV-2 infects human fat cells, replicating and altering cell function and viability in a depot- and viral lineage-dependent fashion.