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1.
Nat Med ; 27(4): 601-615, 2021 04.
Article in English | MEDLINE | ID: covidwho-1517636

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the pathogen responsible for the coronavirus disease 2019 (COVID-19) pandemic, which has resulted in global healthcare crises and strained health resources. As the population of patients recovering from COVID-19 grows, it is paramount to establish an understanding of the healthcare issues surrounding them. COVID-19 is now recognized as a multi-organ disease with a broad spectrum of manifestations. Similarly to post-acute viral syndromes described in survivors of other virulent coronavirus epidemics, there are increasing reports of persistent and prolonged effects after acute COVID-19. Patient advocacy groups, many members of which identify themselves as long haulers, have helped contribute to the recognition of post-acute COVID-19, a syndrome characterized by persistent symptoms and/or delayed or long-term complications beyond 4 weeks from the onset of symptoms. Here, we provide a comprehensive review of the current literature on post-acute COVID-19, its pathophysiology and its organ-specific sequelae. Finally, we discuss relevant considerations for the multidisciplinary care of COVID-19 survivors and propose a framework for the identification of those at high risk for post-acute COVID-19 and their coordinated management through dedicated COVID-19 clinics.


Subject(s)
COVID-19/complications , SARS-CoV-2 , Acute Disease , COVID-19/epidemiology , COVID-19/ethnology , COVID-19/therapy , Cardiovascular Diseases/epidemiology , Cardiovascular Diseases/therapy , Humans , Patient Advocacy , Syndrome , Systemic Inflammatory Response Syndrome/epidemiology , Systemic Inflammatory Response Syndrome/therapy , Venous Thromboembolism/epidemiology , Venous Thromboembolism/prevention & control
3.
Eur J Endocrinol ; 183(5): R133-R147, 2020 Nov.
Article in English | MEDLINE | ID: covidwho-695333

ABSTRACT

The SARS-CoV-2 virus responsible for the COVID-19 pandemic has generated an explosion of interest both in the mechanisms of infection leading to dissemination and expression of this disease, and in potential risk factors that may have a mechanistic basis for disease propagation or control. Vitamin D has emerged as a factor that may be involved in these two areas. The focus of this article is to apply our current understanding of vitamin D as a facilitator of immunocompetence both with regard to innate and adaptive immunity and to consider how this may relate to COVID-19 disease. There are also intriguing potential links to vitamin D as a factor in the cytokine storm that portends some of the most serious consequences of SARS-CoV-2 infection, such as the acute respiratory distress syndrome. Moreover, cardiac and coagulopathic features of COVID-19 disease deserve attention as they may also be related to vitamin D. Finally, we review the current clinical data associating vitamin D with SARS-CoV-2 infection, a putative clinical link that at this time must still be considered hypothetical.


Subject(s)
Adaptive Immunity/immunology , Coronavirus Infections/immunology , Cytokine Release Syndrome/immunology , Immunity, Innate/immunology , Immunocompetence/immunology , Lung/immunology , Pneumonia, Viral/immunology , T-Lymphocytes/immunology , Vitamin D/immunology , Antimicrobial Cationic Peptides/immunology , Autophagy/immunology , Betacoronavirus , COVID-19 , Defensins/immunology , Humans , Pandemics , SARS-CoV-2 , T-Lymphocytes, Regulatory/immunology , Th1 Cells/immunology , Th17 Cells/immunology , Th2 Cells/immunology , Vitamin D/analogs & derivatives , Cathelicidins
4.
Nat Med ; 26(7): 1017-1032, 2020 07.
Article in English | MEDLINE | ID: covidwho-639177

ABSTRACT

Although COVID-19 is most well known for causing substantial respiratory pathology, it can also result in several extrapulmonary manifestations. These conditions include thrombotic complications, myocardial dysfunction and arrhythmia, acute coronary syndromes, acute kidney injury, gastrointestinal symptoms, hepatocellular injury, hyperglycemia and ketosis, neurologic illnesses, ocular symptoms, and dermatologic complications. Given that ACE2, the entry receptor for the causative coronavirus SARS-CoV-2, is expressed in multiple extrapulmonary tissues, direct viral tissue damage is a plausible mechanism of injury. In addition, endothelial damage and thromboinflammation, dysregulation of immune responses, and maladaptation of ACE2-related pathways might all contribute to these extrapulmonary manifestations of COVID-19. Here we review the extrapulmonary organ-specific pathophysiology, presentations and management considerations for patients with COVID-19 to aid clinicians and scientists in recognizing and monitoring the spectrum of manifestations, and in developing research priorities and therapeutic strategies for all organ systems involved.


Subject(s)
Betacoronavirus/pathogenicity , Coronavirus Infections/pathology , Organ Specificity , Pneumonia, Viral/pathology , Adaptive Immunity/physiology , Betacoronavirus/physiology , COVID-19 , Coronavirus Infections/diagnosis , Coronavirus Infections/immunology , Coronavirus Infections/therapy , Disease Progression , Endothelium, Vascular/pathology , Endothelium, Vascular/virology , Humans , Inflammation/etiology , Inflammation/pathology , Inflammation/virology , Pandemics , Pneumonia, Viral/diagnosis , Pneumonia, Viral/immunology , Pneumonia, Viral/therapy , Renin-Angiotensin System/physiology , SARS-CoV-2 , Thrombosis/etiology , Thrombosis/pathology , Thrombosis/virology , Virus Internalization
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