Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the neuroendocrine stress axis

Steenblock, Charlotte; Todorov, Vladimir; Kanczkowski, Waldemar; Eisenhofer, Graeme; Schedl, Andreas; Wong, Ma-Li; Licinio, Júlio; Bauer, Michael; Young, Allan H.; Gainetdinov, Raul R.; Bornstein, Stefan R.

doi:10.1038/s41380-020-0758-9

Cited by 81 publications

(85 citation statements)

References 82 publications

(82 reference statements)

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“…Further, in COVID-19 patients receiving antiviral medications and/or steroids long-term consequences on HPA axis dysfunction need to be considered [12] to avoid an adrenal crisis. Finally, dysregulation of the HPA axis may result in an aggravation of other chronic disorders including cardiometabolic and mental disease [13].…”

Section: Resultsmentioning

confidence: 99%

Inflammatory Cell Infiltration of Adrenals in COVID-19

et al. 2020

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AbstractSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was originated in November–December 2019 in Wuhan, China, and has rapidly spread around the world causing severe health and socioeconomical damage to the entire civilization. The key feature of coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, is upper respiratory tract infection, which may be complicated by bilateral pneumonia. Angiotensin converting enzyme 2 (ACE2) has been identified as a key host factor, required for virus entry into cells. Interestingly, ACE2 is expressed not only in the respiratory system, but also in the other organs and systems including adrenal glands. Here we provide the first description of the pathomorphological changes in adrenal glands in patients with severe COVID-19 characterized by perivascular infiltration of CD3+ and CD8+ T-lymphocytes. Due to the central role of the adrenals in the stress response of the organism, this finding is of potential clinical relevance, because infection with the SARS-CoV-2 virus might critically impair adrenal function under pathophysiological conditions.

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Section: Resultsmentioning

confidence: 99%

Inflammatory Cell Infiltration of Adrenals in COVID-19

et al. 2020

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“…Patients who suffer from COVID-19 complications, including hospitalization and being isolated from their family members, experience a great deal of psychological stress [41]. Being isolated is similar to the stress of physical immobilization, which is associated with a sharp increase in cortisol and steroid levels [41].…”

Section: Pathophysiology Of Neurological Abnormalities In Covid-19mentioning

confidence: 99%

Neurobiology of COVID-19

Fotuhi

Mian

Meysami

et al. 2020

JAD

349

391

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Anosmia, stroke, paralysis, cranial nerve deficits, encephalopathy, delirium, meningitis, and seizures are some of the neurological complications in patients with coronavirus disease-19 (COVID-19) which is caused by acute respiratory syndrome coronavirus 2 (SARS-Cov2). There remains a challenge to determine the extent to which neurological abnormalities in COVID-19 are caused by SARS-Cov2 itself, the exaggerated cytokine response it triggers, and/or the resulting hypercoagulapathy and formation of blood clots in blood vessels throughout the body and the brain. In this article, we review the reports that address neurological manifestations in patients with COVID-19 who may present with acute neurological symptoms (e.g., stroke), even without typical respiratory symptoms such as fever, cough, or shortness of breath. Next, we discuss the different neurobiological processes and mechanisms that may underlie the link between SARS-Cov2 and COVID-19 in the brain, cranial nerves, peripheral nerves, and muscles. Finally, we propose a basic "NeuroCovid" classification scheme that integrates these concepts and highlights some of the short-term challenges for the practice of neurology today and the longterm sequalae of COVID-19 such as depression, OCD, insomnia, cognitive decline, accelerated aging, Parkinson's disease, or Alzheimer's disease in the future. In doing so, we intend to provide a basis from which to build on future hypotheses and investigations regarding SARS-Cov2 and the nervous system.

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“…Mallick et al [17] reported broncho alveolar stem cells as important target for SARS-CoV infection. Hence, the hypothetical explanation of the rapid deterioration and delay in recovery of COVID-19 pneumonia cases may be due to destruction of lung stem cells along with pneumocytes by the novel corona virus, SARA-CoV-2 [18,19].…”

Section: Mechanism Of Virus Entry Into Cells and Clinical Symptomsmentioning

confidence: 99%

An Assessment on Impact of COVID-19 Infection in a Gender Specific Manner

Agrawal

Das

Nathani

et al. 2020

Stem Cell Rev and Rep

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Coronavirus disease 2019 (COVID-19) is caused by novel coronavirus Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It was first time reported in December 2019 in Wuhan, China and thereafter quickly spread across the globe. Till September 19, 2020, COVID-19 has spread to 216 countries and territories. Severe infection of SARS-CoV-2 cause extreme increase in inflammatory chemokines and cytokines that may lead to multi-organ damage and respiratory failure. Currently, no specific treatment and authorized vaccines are available for its treatment. Renin angiotensin system holds a promising role in human physiological system specifically in regulation of blood pressure and electrolyte and fluid balance. SARS-CoV-2 interacts with Renin angiotensin system by utilizing angiotensin-converting enzyme 2 (ACE2) as a receptor for its cellular entry. This interaction hampers the protective action of ACE2 in the cells and causes injuries to organs due to persistent angiotensin II (Ang-II) level. Patients with certain comorbidities like hypertension, diabetes, and cardiovascular disease are under the high risk of COVID-19 infection and mortality. Moreover, evidence obtained from several reports also suggests higher susceptibility of male patients for COVID-19 mortality and other acute viral infections compared to females. Analysis of severe acute respiratory syndrome coronavirus (SARS) and Middle East respiratory syndrome coronavirus (MERS) epidemiological data also indicate a gender-based preference in disease consequences. The current review addresses the possible mechanisms responsible for higher COVID-19 mortality among male patients. The major underlying aspects that was looked into includes smoking, genetic factors, and the impact of reproductive hormones on immune systems and inflammatory responses. Detailed investigations of this gender disparity could provide insight into the development of patient tailored therapeutic approach which would be helpful in improving the poor outcomes of COVID-19.

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the neuroendocrine stress axis

Cited by 81 publications

References 82 publications

Inflammatory Cell Infiltration of Adrenals in COVID-19

Inflammatory Cell Infiltration of Adrenals in COVID-19

Neurobiology of COVID-19

An Assessment on Impact of COVID-19 Infection in a Gender Specific Manner

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