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2.
Am J Physiol Lung Cell Mol Physiol ; 319(1): L115-L120, 2020 07 01.
Article in English | MEDLINE | ID: covidwho-558506

ABSTRACT

COVID-19 can be divided into three clinical stages, and one can speculate that these stages correlate with where the infection resides. For the asymptomatic phase, the infection mostly resides in the nose, where it elicits a minimal innate immune response. For the mildly symptomatic phase, the infection is mostly in the pseudostratified epithelium of the larger airways and is accompanied by a more vigorous innate immune response. In the conducting airways, the epithelium can recover from the infection, because the keratin 5 basal cells are spared and they are the progenitor cells for the bronchial epithelium. There may be more severe disease in the bronchioles, where the club cells are likely infected. The devastating third phase is in the gas exchange units of the lung, where ACE2-expressing alveolar type II cells and perhaps type I cells are infected. The loss of type II cells results in respiratory insufficiency due to the loss of pulmonary surfactant, alveolar flooding, and possible loss of normal repair, since type II cells are the progenitors of type I cells. The loss of type I and type II cells will also block normal active resorption of alveolar fluid. Subsequent endothelial damage leads to transudation of plasma proteins, formation of hyaline membranes, and an inflammatory exudate, characteristic of ARDS. Repair might be normal, but if the type II cells are severely damaged alternative pathways for epithelial repair may be activated, which would result in some residual lung disease.


Subject(s)
Alveolar Epithelial Cells/virology , Betacoronavirus/pathogenicity , Coronavirus Infections/virology , Epithelial Cells/virology , Pneumonia, Viral/virology , Alveolar Epithelial Cells/metabolism , Coronavirus Infections/diagnosis , Coronavirus Infections/therapy , Epithelial Cells/metabolism , Epithelium/metabolism , Epithelium/virology , Humans , Lung/metabolism , Pandemics , Pneumonia, Viral/diagnosis , Pneumonia, Viral/therapy , Respiratory Mucosa/metabolism , Respiratory Mucosa/virology
3.
Obesity (Silver Spring) ; 28(9): 1586-1589, 2020 09.
Article in English | MEDLINE | ID: covidwho-306140

ABSTRACT

OBJECTIVE: Mortality from coronavirus disease 2019 (COVID-19) is increased in patients with chronic obstructive pulmonary disease (COPD). Furthermore, higher BMI is related to severe disease. Severe acute respiratory syndrome coronavirus 2 utilizes angiotensin converting enzyme 2 (ACE2) to gain cellular entry. METHODS: Whether ACE2 bronchial epithelial expression is increased in COPD patients who have overweight compared with those who do not was investigated by RNA sequencing. RESULTS: Increased ACE2 expression was observed in patients with COPD with overweight (mean BMI, 29 kg/m2 ) compared with those without overweight (mean BMI, 21 kg/m2 ) (P = 0.004). CONCLUSIONS: Increased ACE2 expression may cause increased severe acute respiratory syndrome coronavirus 2 infection of the respiratory tract. Overweight COPD patients may be at greater risk for developing severe COVID-19.


Subject(s)
Bronchi , Epithelium/metabolism , Overweight/complications , Peptidyl-Dipeptidase A/genetics , Pulmonary Disease, Chronic Obstructive/genetics , Aged , Betacoronavirus , Coronavirus Infections , Female , Gene Expression Regulation , Humans , Male , Middle Aged , Pandemics , Pneumonia, Viral , Pulmonary Disease, Chronic Obstructive/complications
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