Single-Cell RNA Expression Profiling of ACE2, the Receptor of SARS-CoV-2

Zhao, Yu; Zhao, Zhongyang; Wang, Yujia; Zhou, Yueqing; Ma, Yu; Zuo, Wei

doi:10.1164/rccm.202001-0179le

Cited by 635 publications

(396 citation statements)

References 24 publications

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“…It is suggested that since ACE2 is mostly expressed in type II alveolar cells, the injury to these cells explains the severe alveolar damage and minimal upper airway symptoms 16 observed in these patients, seen as bilateral ground-glass opacity and subsegmental areas of consolidation by chest computed tomography. 6 The systemic inflammatory response syndrome 25 is a cardinal feature of lung disease caused by SARS-CoV-2, as evidenced by elevated levels of CRP, procalcitonin, and serum amyloid A.…”

Section: Physiopathology Of the Inflammatory Response In Sars-cov-2-imentioning

confidence: 99%

“…13,15 Thus, the tropism of virus infection is determined by tissue expression and distribution of the receptor. 16 As with all CoVs, SARS-CoV-2 has a positive singlestranded RNA genome which contains two genomic open reading frames (ORFs: ORF1a and ORF1b) and nine ORFs that are part of the sub-genomic RNA. The translation of ORF1a and ORF1b encodes a polyprotein containing the replicase which has proteases that cleave the polyprotein to release nonstructural proteins (nsp) to form the replicase-transcriptase complex.…”

Section: Sars-cov-2 Infection Mechanismsmentioning

confidence: 99%

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Direct or Collateral Liver Damage in SARS-CoV-2–Infected Patients

et al. 2020

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Liver injury can result from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection with more than one-third of COVID-19 patients exhibiting elevated liver enzymes. Microvesicular steatosis, inflammation, vascular congestion, and thrombosis in the liver have been described in autopsy samples from COVID-19 patients. Several factors, including direct cytopathic effect of the virus, immune-mediated collateral damage, or an exacerbation of preexisting liver disease may contribute to liver pathology in COVID-19. Due to its immunological functions, the liver is an organ likely to participate in the viral response against SARS-CoV-2 and this may predispose it to injury. A better understanding of the mechanism contributing to liver injury is needed to develop and implement early measures to prevent serious liver damage in patients suffering from COVID-19. This review summarizes current reports of SARS-CoV-2 with an emphasis on how direct infection and subsequent severe inflammatory response may contribute to liver injury in patients with and without preexisting liver disease.

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Section: Physiopathology Of the Inflammatory Response In Sars-cov-2-imentioning

confidence: 99%

Section: Sars-cov-2 Infection Mechanismsmentioning

confidence: 99%

Direct or Collateral Liver Damage in SARS-CoV-2–Infected Patients

et al. 2020

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“…Recent virological assessments suggest that the pathophysiological mechanisms of SARS-CoV-2 are similar to that of SARS-CoV, where there is evidence to prove that both viruses predominantly infect airway and alveolar epithelial cells, vascular endothelial cells, and macrophages of humans (Zhao et al, 2020;Zhou et al, 2020). Some of the most common symptoms of COVID-19 are fever, cough, fatigue, and myalgia (Guan et al, 2020;Goyal et al, 2020;Young et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

Long-term Air Pollution Exposure Impact on COVID-19 Morbidity in China

Zhan

Zhao

2021

Aerosol Air Qual. Res.

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Although previous studies have proved the association between air pollution and respiratory viral infection, given the relatively short history of human infection with the severe acute respiratory syndrome coronavirus (SARS-CoV-2), the linkage between long-term air pollution exposure and the morbidity of 2019 novel coronavirus (COVID-19) pneumonia remains poorly understood. To fill this gap, this study investigates the influences of particulate matters (PM 2.5 and PM 10), nitrogen dioxide (NO 2), ozone (O 3), sulfur dioxide (SO 2) and carbon monoxide (CO) on COVID-19 incidence rate based on the prefecture-level morbidity count and air quality data in China. Annual means for ambient PM 2.5 , PM 10 , SO 2 , NO 2 , CO and O 3 concentrations in each prefecture are used to estimate the population's exposure. We leverage identical statistical methods, i.e., Spearman's rank correlation and negative binomial regression model, to demonstrate that people who are chronically exposed to ambient air pollution are more likely to be infected by COVID-19. Our statistical analysis indicates that a 1 µg m-3 increase of PM 2.5 , PM 10 , NO 2 and O 3 can result in 1.95% (95% CI: 0.83-3.08%), 0.55% (95% CI:-0.05-1.17%), 4.63% (95% CI: 3.07-6.22%) rise and 2.05% (95% CI: 0.51-3.59%) decrease of COVID-19 morbidity. However, we observe nonsignificant association with long-term SO 2 and CO exposure to COVID-19 morbidity in this study. Our results' robustness is examined based on sensitivity analyses that adjust for a wide range of confounders, including socioeconomic, demographic, weather, healthcare, and mobility-related variables. We acknowledge that more laboratory results are required to prove the etiology of these associations.

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“…As the ACE2 gene is located on the X chromosome, its potential escape from the X chromosome inactivation process could favor its differential expression in males and females. Whether ACE2 expression varies according to gender remains unclear (37,38). An indepth analysis of ACE2 expression within different tissues was reported and found to be up-regulated by type I interferons (39).…”

Section: Discussionmentioning

confidence: 99%