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1.
BMC Psychiatry ; 22(1): 219, 2022 03 27.
Article in English | MEDLINE | ID: covidwho-1765443

ABSTRACT

BACKGROUND: There is increasing recognition of the substantial burden of mental health disorders at an individual and population level, including consequent demand on mental health services. Lifestyle-based mental healthcare offers an additional approach to existing services with potential to help alleviate system burden. Despite the latest Royal Australian New Zealand College of Psychiatrists guidelines recommending that lifestyle is a 'first-line', 'non-negotiable' treatment for mood disorders, few such programs exist within clinical practice. Additionally, there are limited data to determine whether lifestyle approaches are equivalent to established treatments. Using an individually randomised group treatment design, we aim to address this gap by evaluating an integrated lifestyle program (CALM) compared to an established therapy (psychotherapy), both delivered via telehealth. It is hypothesised that the CALM program will not be inferior to psychotherapy with respect to depressive symptoms at 8 weeks. METHODS: The study is being conducted in partnership with Barwon Health's Mental Health, Drugs & Alcohol Service (Geelong, Victoria), from which 184 participants from its service and surrounding regions are being recruited. Eligible participants with elevated psychological distress are being randomised to CALM or psychotherapy. Each takes a trans-diagnostic approach, and comprises four weekly (weeks 1-4) and two fortnightly (weeks 6 and 8) 90-min, group-based sessions delivered via Zoom (digital video conferencing platform). CALM focuses on enhancing knowledge, behavioural skills and support for improving dietary and physical activity behaviours, delivered by an Accredited Exercise Physiologist and Accredited Practising Dietitian. Psychotherapy uses cognitive behavioural therapy (CBT) delivered by a Psychologist or Clinical Psychologist, and Provisional Psychologist. Data collection occurs at baseline and 8 weeks. The primary outcome is depressive symptoms (assessed via the Patient Health Questionnaire-9) at 8 weeks. Societal and healthcare costs will be estimated to determine the cost-effectiveness of the CALM program. A process evaluation will determine its reach, adoption, implementation and maintenance. DISCUSSION: If the CALM program is non-inferior to psychotherapy, this study will provide the first evidence to support lifestyle-based mental healthcare as an additional care model to support individuals experiencing psychological distress. TRIAL REGISTRATION: Australia and New Zealand Clinical Trials Register (ANZCTR): ACTRN12621000387820 , Registered 8 April 2021.


Subject(s)
COVID-19 , Telemedicine , Adult , Anxiety , Depression/complications , Depression/therapy , Humans , Life Style , Psychotherapy , Telemedicine/methods , Victoria
2.
Front Psychiatry ; 12: 774858, 2021.
Article in English | MEDLINE | ID: covidwho-1731849

ABSTRACT

The COVID-19 pandemic has afforded the opportunity for some to improve lifestyle behaviours, while for others it has presented key challenges. Adverse changes in global lifestyle behaviours, including physical activity, sleep, and screen time can affect proximal mental health and in turn distal cardiovascular outcomes. We investigated differences in physical activity, sleep, and screen time in parents and children during early stages of the COVID-19 pandemic in Australia compared to pre-COVID-19 national data; and estimated associations between these movement behaviours with parent and child mental health. Cross-sectional baseline data from the COVID-19 Pandemic Adjustment Study (CPAS; N = 2,365) were compared to nationally representative pre-pandemic data from the Longitudinal Study of Australian Children (LSAC; N = 9,438). Participants were parents of children aged ≤ 18 years, residing in Australia. Parents provided self-report measures of mental health, physical activity and sleep quality, and reported on child mental health, physical activity and screen time. Children in CPAS had significantly more sleep problems and more weekend screen time. Their parents had significantly poorer sleep quality, despite increased weekly physical activity. Children's sleep problems were significantly associated with increased mental health problems, after accounting for socioeconomic status, physical activity, and screen time. Poorer parent sleep quality and lower levels of physical activity were significantly associated with poorer mental health. Monitoring this cohort over time will be important to examine whether changes in movement behaviour are enduring or naturally improve with the easing of restrictions; and whether these changes have lasting effects on either parent or child mental health, and in turn, future risk for CVD.

3.
Int J Health Policy Manag ; 2022 Feb 28.
Article in English | MEDLINE | ID: covidwho-1727447

ABSTRACT

Adaptive capacity is a critical component of building resilience in healthcare (RiH). Adaptive capacity comprises the ability of a system to cope with and adapt to disturbances. However, "shocks," such as the current coronavirus disease 2019 (COVID-19) pandemic, can potentially exceed critical adaptation thresholds and lead to systemic collapse. To effectively manage healthcare systems during periods of crises, both adaptive and transformative changes are necessary. This commentary discusses adaptation and transformation as two complementary, integral components of resilience and applies them to healthcare. We treat resilience as an emergent property of complex systems that accounts for multiple, often disparately distinct regimes in which multiple processes (eg, adaptation, recovery) are subsumed and operate. We argue that Convergence Mental Health and other transdisciplinary paradigms such as Brain Capital and One Health can facilitate resilience planning and management in healthcare systems.

4.
Psychiatric Annals ; 52(2):47-48, 2022.
Article in English | ProQuest Central | ID: covidwho-1687102

ABSTRACT

Globally, rates of common mental disorders, like depression, and neurological disorders, like dementia, are significant causes of disability. Since the pandemic onset, there have been 53 million new cases of depression globally. 1 In the United States alone, deaths owing to dementia and Alzheimer's disease have increased by 16% during this time.2 The onset and trajectory of mental and brain disorders are influenced by numerous exposures across the life course, one of which is nutrition. [...]Yung et al. present evidence for the role of diet in the development of depression during the vulnerable periods of childhood and adolescence and provide strategies to help mental health clinicians address diet as part of their practice with youth. [...]Young et al. focus on ways adults with depression can improve their diet quality in mental health settings by harnessing digital health platforms and offer practical advice from their pilot program.

5.
Eur Neuropsychopharmacol ; 54: 21-40, 2022 01.
Article in English | MEDLINE | ID: covidwho-1466347

ABSTRACT

INTRODUCTION: There are few published empirical data on the effects of COVID-19 on mental health, and until now, there is no large international study. MATERIAL AND METHODS: During the COVID-19 pandemic, an online questionnaire gathered data from 55,589 participants from 40 countries (64.85% females aged 35.80 ± 13.61; 34.05% males aged 34.90±13.29 and 1.10% other aged 31.64±13.15). Distress and probable depression were identified with the use of a previously developed cut-off and algorithm respectively. STATISTICAL ANALYSIS: Descriptive statistics were calculated. Chi-square tests, multiple forward stepwise linear regression analyses and Factorial Analysis of Variance (ANOVA) tested relations among variables. RESULTS: Probable depression was detected in 17.80% and distress in 16.71%. A significant percentage reported a deterioration in mental state, family dynamics and everyday lifestyle. Persons with a history of mental disorders had higher rates of current depression (31.82% vs. 13.07%). At least half of participants were accepting (at least to a moderate degree) a non-bizarre conspiracy. The highest Relative Risk (RR) to develop depression was associated with history of Bipolar disorder and self-harm/attempts (RR = 5.88). Suicidality was not increased in persons without a history of any mental disorder. Based on these results a model was developed. CONCLUSIONS: The final model revealed multiple vulnerabilities and an interplay leading from simple anxiety to probable depression and suicidality through distress. This could be of practical utility since many of these factors are modifiable. Future research and interventions should specifically focus on them.


Subject(s)
Anxiety/epidemiology , COVID-19/complications , COVID-19/psychology , Depression/epidemiology , Mental Health , Adult , Anxiety/etiology , COVID-19/epidemiology , Depression/etiology , Female , Global Burden of Disease , Humans , Male , Middle Aged , Pandemics , SARS-CoV-2 , Stress, Psychological/etiology , Suicidal Ideation
7.
J Affect Disord ; 295: 740-751, 2021 12 01.
Article in English | MEDLINE | ID: covidwho-1385792

ABSTRACT

INTRODUCTION: The COVID-19 (coronavirus disease 2019)-related pandemic represents a global source of societal and health burden. Yet, the impact of the pandemic on people with severe mental illness, including bipolar disorder (BD), remains unclear, warranting scoping review on the matter. METHODS: The MEDLINE and EMBASE databases were systematically searched from inception up to April 24, 2021, adopting broad inclusion criteria to assess a variety of clinical and public health themes related to people with a primary diagnosis of BD during the COVID-19 pandemics. The present work complying with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for scoping reviews (PRISMA-ScR) registered in the Open Science Framework (OSF) repository (https://osf.io/7evpx/). RESULTS: Fourteen papers informed the present scoping review. Four major themes were identified: (i) impact of COVID-19-related stressors on BD; (ii) impact of COVID-19 on mental health service utilization among people with BD; (iii) impact of BD on the risk of acquiring SARS-CoV-2 infection; (iv) engagement in preventative behaviors among people with BD. Additional themes warranting further research were nonetheless detected. LIMITATIONS: Further original studies are needed. CONCLUSION: The present study confirmed the high-vulnerability hypothesis concerning people with BD versus the general population, reinforcing the need for further research related to the COVID-19 pandemic. Additional information is warranted to compare the impact of the pandemic period among BD people against pre-pandemic records, the general population, and other severe mental illnesses, namely people with schizophrenia or major depressive disorder, to inform the public health and the delivery of patient-tailored interventions.


Subject(s)
Bipolar Disorder , COVID-19 , Depressive Disorder, Major , Bipolar Disorder/epidemiology , Humans , Pandemics , SARS-CoV-2
8.
Cytokine ; 144: 155593, 2021 08.
Article in English | MEDLINE | ID: covidwho-1242912

ABSTRACT

An analysis of published data appertaining to the cytokine storms of COVID-19, H1N1 influenza, cytokine release syndrome (CRS), and macrophage activation syndrome (MAS) reveals many common immunological and biochemical abnormalities. These include evidence of a hyperactive coagulation system with elevated D-dimer and ferritin levels, disseminated intravascular coagulopathy (DIC) and microthrombi coupled with an activated and highly permeable vascular endothelium. Common immune abnormalities include progressive hypercytokinemia with elevated levels of TNF-α, interleukin (IL)-6, and IL-1ß, proinflammatory chemokines, activated macrophages and increased levels of nuclear factor kappa beta (NFκB). Inflammasome activation and release of damage associated molecular patterns (DAMPs) is common to COVID-19, H1N1, and MAS but does not appear to be a feature of CRS. Elevated levels of IL-18 are detected in patients with COVID-19 and MAS but have not been reported in patients with H1N1 influenza and CRS. Elevated interferon-γ is common to H1N1, MAS, and CRS but levels of this molecule appear to be depressed in patients with COVID-19. CD4+ T, CD8+ and NK lymphocytes are involved in the pathophysiology of CRS, MAS, and possibly H1N1 but are reduced in number and dysfunctional in COVID-19. Additional elements underpinning the pathophysiology of cytokine storms include Inflammasome activity and DAMPs. Treatment with anakinra may theoretically offer an avenue to positively manipulate the range of biochemical and immune abnormalities reported in COVID-19 and thought to underpin the pathophysiology of cytokine storms beyond those manipulated via the use of, canakinumab, Jak inhibitors or tocilizumab. Thus, despite the relative success of tocilizumab in reducing mortality in COVID-19 patients already on dexamethasone and promising results with Baricitinib, the combination of anakinra in combination with dexamethasone offers the theoretical prospect of further improvements in patient survival. However, there is currently an absence of trial of evidence in favour or contravening this proposition. Accordingly, a large well powered blinded prospective randomised controlled trial (RCT) to test this hypothesis is recommended.


Subject(s)
Anti-Inflammatory Agents/therapeutic use , Antiviral Agents/therapeutic use , COVID-19 , Cytokine Release Syndrome , Influenza A Virus, H1N1 Subtype/immunology , SARS-CoV-2/immunology , COVID-19/drug therapy , COVID-19/immunology , COVID-19/mortality , COVID-19/pathology , Cytokine Release Syndrome/drug therapy , Cytokine Release Syndrome/immunology , Cytokine Release Syndrome/mortality , Cytokine Release Syndrome/pathology , Disease-Free Survival , Humans , Influenza, Human/drug therapy , Influenza, Human/immunology , Influenza, Human/mortality , Influenza, Human/pathology , Janus Kinases/antagonists & inhibitors , Janus Kinases/metabolism , Lymphocytes/immunology , Lymphocytes/pathology , Survival Rate
9.
Med Sci Monit ; 27: e932220, 2021 May 11.
Article in English | MEDLINE | ID: covidwho-1224335

ABSTRACT

Coronavirus may have a negative impact not only on physical, but also on mental wellbeing. Despite the different approaches of countries to stop the spread of the virus and different infection rates, the dynamically developing pandemic has already affected the entire world. The consequences of the coronavirus for our mental health can be divided into those related to strategies for the prevention of infection, like isolation, quarantine, limitation of social contacts, and remote work, and those related to the direct impact of infection on our nervous system. This review aims to highlight the global effects of the Coronavirus Disease 2019 (COVID-19) pandemic on public mental health following social restrictions, to identify how infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may have direct neurophysiological effects and to compare the impact on public mental health between the USA, Australia, and Poland with Taiwan and Thailand.


Subject(s)
COVID-19/psychology , Mental Health/statistics & numerical data , Public Health/statistics & numerical data , Australia/epidemiology , Humans , Pandemics , Poland/epidemiology , Taiwan/epidemiology , Thailand/epidemiology , United States/epidemiology
13.
J Affect Disord ; 282: 442-447, 2021 03 01.
Article in English | MEDLINE | ID: covidwho-1002677

ABSTRACT

BACKGROUND: It is unclear how those with bipolar disorder (BD) have been affected by the coronavirus (COVID-19) pandemic. This study aimed to obtain a more detailed understanding of the current mental health needs of these individuals, which is important for both the development of intervention strategies to better manage patient distress and to better prepare for similar circumstances in future. METHODS: The sample comprised 43 individuals with a verified diagnosis of BD and 24 healthy controls. Data about pandemic-related mental health support use, socio-demographics, mood, lifestyle, social rhythm and subjective cognitive dysfunction data were collected and compared between groups. Inter-relationships between scores were also examined. RESULTS: No between-group differences were found in terms of age, sex, living situation, job loss or reduced work hours due to COVID-19. Most patients with BD reported a history of ongoing formal psychological support (68.3%), with most continuing this support throughout the pandemic (82.1%). A large, statistically significant pandemic-related increase in subjective cognitive dysfunction was evident in the BD group. Subjective cognitive dysfunction was significantly associated with negative symptomology, suicidal thoughts, and quality of life ratings. LIMITATIONS: Data was collected in self-report format in an online survey and objective symptom measures were not used at this time CONCLUSION: The absenceof substantial differences between patients and controls in terms of mood symptoms, COVID-19 fear or lifestyle factors and social rhythms suggests a degree of resilience in BD patients; despite large pandemic related increases in subjective cognitive dysfunction.


Subject(s)
Bipolar Disorder , COVID-19 , Bipolar Disorder/epidemiology , Humans , Life Style , Mental Health , Quality of Life , SARS-CoV-2
14.
Life Sci ; 264: 118617, 2021 Jan 01.
Article in English | MEDLINE | ID: covidwho-880558

ABSTRACT

BACKGROUND: COVID-19-associated acute respiratory distress syndrome (ARDS) is associated with significant morbidity and high levels of mortality. This paper describes the processes involved in the pathophysiology of COVID-19 from the initial infection and subsequent destruction of type II alveolar epithelial cells by SARS-CoV-2 and culminating in the development of ARDS. MAIN BODY: The activation of alveolar cells and alveolar macrophages leads to the release of large quantities of proinflammatory cytokines and chemokines and their translocation into the pulmonary vasculature. The presence of these inflammatory mediators in the vascular compartment leads to the activation of vascular endothelial cells platelets and neutrophils and the subsequent formation of platelet neutrophil complexes. These complexes in concert with activated endothelial cells interact to create a state of immunothrombosis. The consequence of immunothrombosis include hypercoagulation, accelerating inflammation, fibrin deposition, migration of neutrophil extracellular traps (NETs) producing neutrophils into the alveolar apace, activation of the NLRP3 inflammazome, increased alveolar macrophage destruction and massive tissue damage by pyroptosis and necroptosis Therapeutic combinations aimed at ameliorating immunothrombosis and preventing the development of severe COVID-19 are discussed in detail.


Subject(s)
COVID-19/immunology , COVID-19/physiopathology , Respiratory Distress Syndrome/complications , Respiratory Distress Syndrome/prevention & control , SARS-CoV-2/pathogenicity , Thrombosis/complications , Thrombosis/physiopathology , Alveolar Epithelial Cells/physiology , Blood Platelets/physiology , COVID-19/complications , COVID-19/drug therapy , Cytokines/physiology , Endothelial Cells/physiology , Humans , Macrophages, Alveolar/physiology , Neutrophils/physiology , Respiratory Distress Syndrome/immunology , Respiratory Distress Syndrome/pathology , Thrombosis/immunology
15.
Life Sci ; 262: 118541, 2020 Dec 01.
Article in English | MEDLINE | ID: covidwho-816772

ABSTRACT

The possibility is examined that immunomodulatory pharmacotherapy may be clinically useful in managing the pandemic coronavirus disease 2019 (COVID-19), known to result from infection by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a positive-sense single-stranded RNA virus. The dominant route of cell entry of the coronavirus is via phagocytosis, with ensconcement in endosomes thereafter proceeding via the endosomal pathway, involving transfer from early (EEs) to late endosomes (LEs) and ultimately into lysosomes via endolysosomal fusion. EE to LE transportation is a rate-limiting step for coronaviruses. Hence inhibition or dysregulation of endosomal trafficking could potentially inhibit SARS-CoV-2 replication. Furthermore, the acidic luminal pH of the endolysosomal system is critical for the activity of numerous pH-sensitive hydrolytic enzymes. Golgi sub-compartments and Golgi-derived secretory vesicles also depend on being mildly acidic for optimal function and structure. Activation of endosomal toll-like receptors by viral RNA can upregulate inflammatory mediators and contribute to a systemic inflammatory cytokine storm, associated with a worsened clinical outcome in COVID-19. Such endosomal toll-like receptors could be inhibited by the use of pharmacological agents which increase endosomal pH, thereby reducing the activity of acid-dependent endosomal proteases required for their activity and/or assembly, leading to suppression of antigen-presenting cell activity, decreased autoantibody secretion, decreased nuclear factor-kappa B activity and decreased pro-inflammatory cytokine production. It is also noteworthy that SARS-CoV-2 inhibits autophagy, predisposing infected cells to apoptosis. It is therefore also suggested that further pharmacological inhibition of autophagy might encourage the apoptotic clearance of SARS-CoV-2-infected cells.


Subject(s)
Antiviral Agents/pharmacology , Autophagy/drug effects , COVID-19/drug therapy , COVID-19/virology , Endosomes/drug effects , Lysosomes/drug effects , SARS-CoV-2/drug effects , Azithromycin/adverse effects , Azithromycin/pharmacology , Azithromycin/therapeutic use , Humans , Hydroxychloroquine/adverse effects , Hydroxychloroquine/pharmacology , Hydroxychloroquine/therapeutic use , Pandemics
16.
Life Sci ; 258: 118166, 2020 Oct 01.
Article in English | MEDLINE | ID: covidwho-703163

ABSTRACT

In this paper, a model is proposed of the pathophysiological processes of COVID-19 starting from the infection of human type II alveolar epithelial cells (pneumocytes) by SARS-CoV-2 and culminating in the development of ARDS. The innate immune response to infection of type II alveolar epithelial cells leads both to their death by apoptosis and pyroptosis and to alveolar macrophage activation. Activated macrophages secrete proinflammatory cytokines and chemokines and tend to polarise into the inflammatory M1 phenotype. These changes are associated with activation of vascular endothelial cells and thence the recruitment of highly toxic neutrophils and inflammatory activated platelets into the alveolar space. Activated vascular endothelial cells become a source of proinflammatory cytokines and reactive oxygen species (ROS) and contribute to the development of coagulopathy, systemic sepsis, a cytokine storm and ARDS. Pulmonary activated platelets are also an important source of proinflammatory cytokines and ROS, as well as exacerbating pulmonary neutrophil-mediated inflammatory responses and contributing to systemic sepsis by binding to neutrophils to form platelet-neutrophil complexes (PNCs). PNC formation increases neutrophil recruitment, activation priming and extraversion of these immune cells into inflamed pulmonary tissue, thereby contributing to ARDS. Sequestered PNCs cause the development of a procoagulant and proinflammatory environment. The contribution to ARDS of increased extracellular histone levels, circulating mitochondrial DNA, the chromatin protein HMGB1, decreased neutrophil apoptosis, impaired macrophage efferocytosis, the cytokine storm, the toll-like receptor radical cycle, pyroptosis, necroinflammation, lymphopenia and a high Th17 to regulatory T lymphocyte ratio are detailed.


Subject(s)
Betacoronavirus/physiology , Coronavirus Infections/physiopathology , Pneumonia, Viral/physiopathology , Respiratory Distress Syndrome/physiopathology , Alveolar Epithelial Cells/immunology , Alveolar Epithelial Cells/pathology , Animals , Betacoronavirus/immunology , COVID-19 , Coronavirus Infections/complications , Coronavirus Infections/immunology , Coronavirus Infections/therapy , Humans , Immunity, Innate , Inflammation/etiology , Inflammation/immunology , Inflammation/physiopathology , Inflammation/therapy , Macrophage Activation , Macrophages, Alveolar/immunology , Macrophages, Alveolar/pathology , Neutrophil Activation , Pandemics , Platelet Activation , Pneumonia, Viral/complications , Pneumonia, Viral/immunology , Pneumonia, Viral/therapy , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/immunology , Respiratory Distress Syndrome/therapy , SARS-CoV-2 , Thrombophilia/etiology , Thrombophilia/immunology , Thrombophilia/physiopathology , Thrombophilia/therapy
17.
Brain Behav Immun Health ; 5: 100096, 2020 May.
Article in English | MEDLINE | ID: covidwho-598856

ABSTRACT

The Coronavirus Disease-2019 (COVID-19) pandemic has led to a global health care crisis. Emerging research suggest an unanticipated impact of COVID-19 on mental and/or psychological health of both the general community and affected individuals. The fear of the COVID-19 epidemic and the consequent lockdown and economic crisis has led to globally increased psychological distress. The biological bases of immediate and new onset of psychiatric symptoms in individuals with COVID-19 are not yet known. COVID-19 infection may lead to activated immune-inflammatory pathways and a cytokine storm. Activated immune-inflammatory pathways, especially chronic low-grade inflammation, are associated with major psychiatric disorders in at least a subset of individuals. We propose that both the (sub)chronic inflammatory response and cytokine storm might crucially be involved in the immediate manifestation of neuropsychiatric symptoms in individuals with COVID-19 infection as well as heightened expression of psychiatric symptoms in COVID-19 infected individuals with prior psychiatric conditions. These events might expand concepts in psychoneuroimmunology, with the importance of chronic-low grade inflammation augmented by the cytokine storm hypothesis. Additionally, this might augment and refine diagnosis and prognostic management as well as treatment.

18.
FASEB J ; 34(7): 8787-8795, 2020 07.
Article in English | MEDLINE | ID: covidwho-593467

ABSTRACT

The dynamics, such as transmission, spatial epidemiology, and clinical course of Coronavirus Disease-2019 (COVID-19) have emerged as the most intriguing features and remain incompletely understood. The genetic landscape of an individual in particular, and a population in general seems to play a pivotal role in shaping the above COVID-19 dynamics. Considering the implications of host genes in the entry and replication of SARS-CoV-2 and in mounting the host immune response, it appears that multiple genes might be crucially involved in the above processes. Herein, we propose three potentially important genetic gateways to COVID-19 infection; these could explain at least in part the discrepancies of its spread, severity, and mortality. The variations within Angiotensin-converting enzyme 2 (ACE2) gene might constitute the first genetic gateway, influencing the spatial transmission dynamics of COVID-19. The Human Leukocyte Antigen locus, a master regulator of immunity against infection seems to be crucial in influencing susceptibility and severity of COVID-19 and can be the second genetic gateway. The genes regulating Toll-like receptor and complement pathways and subsequently cytokine storm induced exaggerated inflammatory pathways seem to underlie the severity of COVID-19, and such genes might represent the third genetic gateway. Host-pathogen interaction is a complex event and some additional genes might also contribute to the dynamics of COVID-19. Overall, these three genetic gateways proposed here might be the critical host determinants governing the risk, severity, and outcome of COVID-19. Genetic variations within these gateways could be key in influencing geographical discrepancies of COVID-19.


Subject(s)
Betacoronavirus/physiology , Complement Activation/genetics , Coronavirus Infections/genetics , HLA Antigens/genetics , Host-Pathogen Interactions/genetics , Pandemics , Peptidyl-Dipeptidase A/genetics , Pneumonia, Viral/genetics , Receptors, Virus/genetics , Toll-Like Receptors/genetics , Angiotensin-Converting Enzyme 2 , COVID-19 , Coronavirus Infections/complications , Coronavirus Infections/immunology , Coronavirus Infections/transmission , Cytokine Release Syndrome/etiology , Cytokine Release Syndrome/genetics , Disease Resistance/immunology , Genetic Predisposition to Disease , Genetic Variation , HLA Antigens/immunology , Host-Pathogen Interactions/immunology , Humans , Inflammation , Metagenomics , Mutation, Missense , Peptidyl-Dipeptidase A/physiology , Pneumonia, Viral/complications , Pneumonia, Viral/immunology , Pneumonia, Viral/transmission , Prognosis , Quantitative Trait Loci , Receptors, Virus/physiology , Risk , SARS-CoV-2 , Toll-Like Receptors/immunology , Treatment Outcome
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