|151||Persistent SARS-CoV-2 infection in asymptomatic young adults |
Intra-host evolution of SARS-CoV-2 has not been reported among asymptomatic cases, though this phenomenon was observed in a few symptomatic and immunocompromised cases. Here, we identified six asymptomatic cases who were persistently positive for SARS-CoV-2 RNA up to 120 days. Phylogenetic analysis of 40 serial whole-genome sequences from the six cases revealed dynamic mutations of the virus. To explore the possible mechanism contributing to the persistent infection, we investigated immune responses. The six cases had comparable specific antibodies with other 24 non-persistent asymptomatic cases, but they had significantly lower antibody levels than symptomatic cases. Although the virus-specific memory B and T cells were detected in the three groups of cases, the six cases showed an upregulation of CD4 regulatory T cells, which was negatively correlated with low levels of activated CD4(+) and CD8(+) T cells. These findings imply that dysregulation of immune responses might contribute to persistent infection.
|Signal Transduct Target Ther||2022|| ||LitCov and CORD-19|
|152||Covid-19: Even mild infections can cause long-term heart problems, large study finds |
|BMJ||2022|| ||LitCov and CORD-19|
|153||Estimated impact of the 2020 economic downturn on under-5 mortality for 129 countries |
In low- and middle-income countries (LMICs), economic downturns can lead to increased child mortality by affecting dietary, environmental, and care-seeking factors. This study estimates the potential loss of life in children under five years old attributable to economic downturns in 2020. We used a multi-level, mixed effects model to estimate the relationship between gross domestic product (GDP) per capita and under-5 mortality rates (U5MRs) specific to each of 129 LMICs. Public data were retrieved from the World Bank World Development Indicators database and the United Nations World Populations Prospects estimates for the years 1990-2020. Country-specific regression coefficients on the relationship between child mortality and GDP were used to estimate the impact on U5MR of reductions in GDP per capita of 5%, 10%, and 15%. A 5% reduction in GDP per capita in 2020 was estimated to cause an additional 282,996 deaths in children under 5 in 2020. At 10% and 15%, recessions led to higher losses of under-5 lives, increasing to 585,802 and 911,026 additional deaths, respectively. Nearly half of all the potential under-5 lives lost in LMICs were estimated to occur in Sub-Saharan Africa. Because most of these deaths will likely be due to nutrition and environmental factors amenable to intervention, countries should ensure continued investments in food supplementation, growth monitoring, and comprehensive primary health care to mitigate potential burdens.
|PLoS One||2022|| ||CORD-19|
|154||Co-expression analysis to identify key modules and hub genes associated with COVID-19 in platelets |
Corona virus disease 2019 (COVID-19) increases the risk of cardiovascular occlusive/thrombotic events and is linked to poor outcomes. The underlying pathophysiological processes are complex, and remain poorly understood. To this end, platelets play important roles in regulating the cardiovascular system, including via contributions to coagulation and inflammation. There is ample evidence that circulating platelets are activated in COVID-19 patients, which is a primary driver of the observed thrombotic outcome. However, the comprehensive molecular basis of platelet activation in COVID-19 disease remains elusive, which warrants more investigation. Hence, we employed gene co-expression network analysis combined with pathways enrichment analysis to further investigate the aforementioned issues. Our study revealed three important gene clusters/modules that were closely related to COVID-19. These cluster of genes successfully identify COVID-19 cases, relative to healthy in a separate validation data set using machine learning, thereby validating our findings. Furthermore, enrichment analysis showed that these three modules were mostly related to platelet metabolism, protein translation, mitochondrial activity, and oxidative phosphorylation, as well as regulation of megakaryocyte differentiation, and apoptosis, suggesting a hyperactivation status of platelets in COVID-19. We identified the three hub genes from each of three key modules according to their intramodular connectivity value ranking, namely: COPE, CDC37, CAPNS1, AURKAIP1, LAMTOR2, GABARAP MT-ND1, MT-ND5, and MTRNR2L12. Collectively, our results offer a new and interesting insight into platelet involvement in COVID-19 disease at the molecular level, which might aid in defining new targets for treatment of COVID-19–induced thrombosis. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12920-022-01222-y.
|BMC Med Genomics||2022|| ||LitCov and CORD-19|
|155||Impact of COVID-19 on nursing students: what does the evidence tell us? ||Evid Based Nurs||2022|| ||LitCov and CORD-19|
|156||How are vaccines being adapted to meet the changing face of SARS-CoV-2? |
|157||NMOSD typical brain lesions after COVID-19 mRNA vaccination |
|J Neurol||2022|| ||LitCov|
|158||Presence of rare potential pathogenic variants in subjects under 65 years old with very severe or fatal COVID-19 |
|Sci Rep||2022|| ||LitCov|
|159||Aortic dissection and Covid-19; a comprehensive systematic review |
Coronavirus disease 19 (Covid-19) has been declared as a pandemic disease since March 2020; causing wide array of signs and symptoms, many of which result in increased mortality rates worldwide. Although it was initially known as an acute respiratory disease, Covid-19 is accompanied with several extrapulmonary manifestations, of which the cardiovascular ones are of major importance. Among other cardiovascular complications of Covid-19, aortic dissection has been a significant yet underrated problem. The pathophysiology of aortic dissection consists of various inflammatory pathways, that could be influenced by Covid-19 infection. We herein have reviewed articles inclusive of aortic dissection concurrent with Covid-19 infection in a systematic manner, along with the probable similarities in pathophysiology of aortic dissection with Covid-19 infection.
|Curr Probl Cardiol||2022|| ||LitCov and CORD-19|
|160||Ivermectin induced Acute Psychosis in Patients Infected With COVID-19 Pneumonia |
|161||Current RT-qPCR to detect SARS-CoV-2 may give positive results for related coronaviruses |
|Arch Microbiol||2022|| ||LitCov|
|162||Antibodies to combat viral infections: development strategies and progress |
|Nat Rev Drug Discov||2022|| ||LitCov|
|163||Validation of survival prediction models for ECMO in SARS-CoV-2 Related acute respiratory distress syndrome |
|Crit Care||2022|| ||LitCov|
|164||Measuring SARS-CoV-2 T-cell immunity with a scalable qPCR-based assay |
|Nat Biotechnol||2022|| ||LitCov|
|165||Risk of Myocarditis from COVID-19 Infection in People Under Age 20: A Population-Based Analysis |
|166||Investigating a psychological model of mental conditions and coping during the COVID-19 pandemic driven by participatory methods |
|Soc Psychiatry Psychiatr Epide||2022|| ||LitCov|
|167||SARS-CoV-2 productively infects human brain microvascular endothelial cells |
|J Neuroinflammation||2022|| ||LitCov|
|168||COVID-19 conspiracy ideation is associated with the delusion proneness trait and resistance to update of beliefs |
|Sci Rep||2022|| ||LitCov|
|169||Non-pharmaceutical intervention levels to reduce the COVID-19 attack ratio among children |
The attack ratio in a subpopulation is defined as the total number of infections over the total number of individuals in this subpopulation. Using a methodology based on an age-stratified transmission dynamics model, we estimated the attack ratio of COVID-19 among children (individuals 0–11 years) when a large proportion of individuals eligible for vaccination (age 12 and above) are vaccinated to contain the epidemic among this subpopulation, or the effective herd immunity (with additional physical distancing measures). We describe the relationship between the attack ratio among children, the time to remove infected individuals from the transmission chain and the children-to-children daily contact rate while considering the increased transmissibility of virus variants (using the Delta variant as an example). We illustrate the generality and applicability of the methodology established by performing an analysis of the attack ratio of COVID-19 among children in the population of Canada and in its province of Ontario. The clinical attack ratio, defined as the number of symptomatic infections over the total population, can be informed from the attack ratio and both can be reduced substantially via a combination of reduced social mixing and rapid testing and isolation of the children.
|R Soc Open Sci||2022|| ||LitCov and CORD-19|
|170||SARS-CoV-2 Infection and Vaccination Outcomes in Multiple Sclerosis |
|Neurol Clin Pract||2022|| ||LitCov|
|171||Vaccination With Oral Polio Vaccine Reduces COVID-19 Incidence |
|Front Immunol||2022|| ||LitCov|
|172||High viral loads: what drives fatal cases of COVID-19 in vaccinees?-an autopsy study |
The rate of SARS-CoV-2 infections in vaccinees has become a relevant serious issue. This study aimed to determine the causes of death, histological organ alteration, and viral spread in relation to demographic, clinical-pathological, viral variants, and vaccine types for deceased individuals with proven SARS-CoV-2 infection after vaccination who died between January and November 2021. Twenty-nine consecutively collected cases were analyzed and compared to 141 nonvaccinated control cases. Autopsies were performed on 16 partially and 13 fully vaccinated individuals. Most patients were elderly and suffered from several relevant comorbidities. Real-time RT-PCR (RT-qPCR) identified a significantly increased rate of generalized viral dissemination within organ systems in vaccinated cases versus nonvaccinated cases (45% vs. 16%, respectively; P = 0.008) mainly with Ct-values of higher than 25 in non-respiratory samples. However, vaccinated cases also showed high viral loads, reaching Ct-values below 10, especially in the upper airways and lungs. This was accompanied by high rates of pulmonal bacterial or mycotic superinfections and the occurrence of immunocompromising factors, such as malignancies, immunosuppressive drug intake, or decreased immunoglobulin levels. All these findings were particularly accentuated in partially vaccinated patients compared to fully vaccinated individuals. The virus dissemination observed in our case study may indicate that patients with an impaired immune system have a decreased ability to eliminate the virus. However, the potential role of antibody-dependent enhancement must also be ruled out in future studies. Fatal cases of COVID-19 in vaccinees were rare and often associated with severe comorbidities or other immunosuppressive conditions.
|Mod Pathol||2022|| ||LitCov and CORD-19|
|173||Sildenafil for treating patients with COVID-19 and perfusion mismatch: a pilot randomized trial |
BACKGROUND: SARS-CoV-2 seems to affect the regulation of pulmonary perfusion. Hypoperfusion in areas of well-aerated lung parenchyma results in a ventilation–perfusion mismatch that can be characterized using subtraction computed tomography angiography (sCTA). This study aims to evaluate the efficacy of oral sildenafil in treating COVID-19 inpatients showing perfusion abnormalities in sCTA. METHODS: Triple-blinded, randomized, placebo-controlled trial was conducted in Chile in a tertiary-care hospital able to provide on-site sCTA scans and ventilatory support when needed between August 2020 and March 2021. In total, 82 eligible adults were admitted to the ED with RT-PCR-confirmed or highly probable SARS-COV-2 infection and sCTA performed within 24 h of admission showing perfusion abnormalities in areas of well-aerated lung parenchyma; 42 were excluded and 40 participants were enrolled and randomized (1:1 ratio) once hospitalized. The active intervention group received sildenafil (25 mg orally three times a day for seven days), and the control group received identical placebo capsules in the same way. Primary outcomes were differences in oxygenation parameters measured daily during follow-up (PaO(2)/FiO(2) ratio and A-a gradient). Secondary outcomes included admission to the ICU, requirement of non-invasive ventilation, invasive mechanical ventilation (IMV), and mortality rates. Analysis was performed on an intention-to-treat basis. RESULTS: Totally, 40 participants were enrolled (20 in the placebo group and 20 in the sildenafil group); 33 [82.5%] were male; and median age was 57 [IQR 41–68] years. No significant differences in mean PaO(2)/FiO(2) ratios and A-a gradients were found between groups (repeated-measures ANOVA p = 0.67 and p = 0.69). IMV was required in 4 patients who received placebo and none in the sildenafil arm (logrank p = 0.04). Patients in the sildenafil arm showed a significantly shorter median length of hospital stay than the placebo group (9 IQR 7–12 days vs. 12 IQR 9–21 days, p = 0.04). CONCLUSIONS: No statistically significant differences were found in the oxygenation parameters. Sildenafil treatment could have a potential therapeutic role regarding the need for IMV in COVID-19 patients with specific perfusion patterns in sCTA. A large-scale study is needed to confirm these results. Trial Registration: Sildenafil for treating patients with COVID-19 and perfusion mismatch: a pilot randomized trial, NCT04489446, Registered 28 July 2020, https://clinicaltrials.gov/ct2/show/NCT04489446. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13054-021-03885-y.
|Crit Care||2022|| ||LitCov and CORD-19|
|174||Relationship between blood type and outcomes following COVID-19 infection |
Since the onset of the COVID-19 pandemic, a concentrated research effort has been undertaken to elucidate risk factors underlying viral infection, severe illness, and death. Recent studies have investigated the association between blood type and COVID-19 infection. This article aims to comprehensively review current literature and better understand the impact of blood type on viral susceptibility and outcomes.
|Semin Vasc Surg||2021|| ||LitCov and CORD-19|
|175||Covid-19 vaccines and treatments: we must have raw data, now |
|BMJ||2022|| ||LitCov and CORD-19|
|176||Correlates to psychological distress in frail older community-dwellers undergoing lockdown during the COVID-19 pandemic |
|BMC Geriatr||2022|| ||LitCov|
|177||Unethical studies of ivermectin for covid-19 |
|BMJ||2022|| ||LitCov and CORD-19|
|178||The EMA covid-19 data leak and what it tells us about mRNA instability |
|BMJ||2021|| ||LitCov and CORD-19|
|179||Disentangling the relative importance of T-cell responses in COVID-19: leading actors or supporting cast? |
The rapid development of multiple vaccines providing strong protection from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been a major achievement. There is now compelling evidence for the role of neutralizing antibodies in protective immunity. T cells may play a role in resolution of primary SARS-CoV-2 infection, and there is a widely expressed view that T cell-mediated immunity also plays an important role in vaccine-mediated protection. Here we discuss the role of vaccine-induced T cells in two distinct stages of infection: firstly, in protection from acquisition of symptomatic SARS-CoV-2 infection following exposure; secondly, if infection does occur, the potential for T cells to reduce the risk of developing severe COVID-19. We describe several lines of evidence that argue against a direct impact of vaccine-induced memory T cells in preventing symptomatic SARS-CoV-2 infection. However, the contribution of T cell immunity in reducing the severity of infection, particularly in infection with SARS-CoV-2 variants, remains to be determined. A detailed understanding of the role of T cells in COVID-19 is critical for next-generation vaccine design and development. Here we discuss the challenges in determining a causal relationship between vaccine-induced T cell immunity and protection from COVID-19 and propose an approach to gather the necessary evidence to clarify any role for vaccine-induced T cell memory in protection from severe COVID-19.
|Nat Rev Immunol||2022|| ||LitCov and CORD-19|
|180||It is not too late to achieve global covid-19 vaccine equity |
Gavin Yamey and colleagues say that a new, urgent push for global vaccine equity could help avert suffering and deaths, protect economies, and prevent new virus variants
|BMJ||2022|| ||LitCov and CORD-19|
|181||Survey of COVID-19 infection control policies at leading US academic hospitals in the context of the initial pandemic surge of the severe acute respiratory coronavirus virus 2 omicron variant |
|Infect Control Hosp Epidemiol||2022|| ||LitCov|
|182||"No Regrets" Purchasing in a pandemic: making the most of advance purchase agreements |
|Global Health||2022|| ||LitCov|
|183||Anti-nucleocapsid antibodies enhance the production of IL-6 induced by SARS-CoV-2 N protein |
A cytokine storm induces acute respiratory distress syndrome, the main cause of death in coronavirus disease 2019 (COVID-19) patients. However, the detailed mechanisms of cytokine induction due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remain unclear. To examine the cytokine production in COVID-19, we mimicked the disease in SARS-CoV-2-infected alveoli by adding the lysate of SARS-CoV-2-infected cells to cultured macrophages or induced pluripotent stem cell-derived myeloid cells. The cells secreted interleukin (IL)-6 after the addition of SARS-CoV-2-infected cell lysate. Screening of 25 SARS-CoV-2 protein-expressing plasmids revealed that the N protein-coding plasmid alone induced IL-6 production. The addition of anti-N antibody further enhanced IL-6 production, but the F(ab’)(2) fragment did not. Sera from COVID-19 patients also enhanced IL-6 production, and sera from patients with severer disease induced higher levels of IL-6. These results suggest that anti-N antibody promotes IL-6 production in SARS-CoV-2-infected alveoli, leading to the cytokine storm of COVID-19.
|Sci Rep||2022|| ||LitCov and CORD-19|
|184||SARS-CoV-2 and Its Variants: The Pandemic of Unvaccinated ||Front Microbiol||2021|| ||LitCov and CORD-19|
|185||Under pressure and overlooked: the impact of COVID-19 on teachers in NSW public schools |
The COVID-19 pandemic has put unprecedented pressure on teachers around the world, raising significant concerns about their workload and wellbeing. Our comparison of 2019 (pre-pandemic) and 2020 (first year of the pandemic) survey data (n = 362) from teachers in New South Wales, Australia, demonstrates that their morale and efficacy declined significantly during COVID-19, even with the relatively short period of school closure (8 weeks) during 2020. Interviews with teachers and school leaders (n = 18) reinforced these findings and highlighted the depth to which teachers felt dispensable and unappreciated, despite working incredibly hard for their students. The pressure to adapt to online teaching and learning, in trying circumstances, also challenged their confidence in their teaching. We argue that practical and emotional support for teachers both during periods of remote learning and upon students’ return to the classroom is essential to support teacher’s wellbeing and a robust teaching workforce into the future.
|Aust Educ Res||2022|| ||LitCov and CORD-19|
|186||Recognition and inhibition of SARS-CoV-2 by humoral innate immunity pattern recognition molecules |
|Nat Immunol||2022|| ||LitCov and CORD-19|
|187||Risk Factors for SARS-CoV-2 Infection and Illness in Cats and Dogs(1) |
|Emerg Infect Dis||2022|| ||LitCov and CORD-19|
|188||Major candidate variables to guide personalised treatment with steroids in critically ill patients with COVID-19: CIBERESUCICOVID study |
|Intensive Care Med||2022|| ||LitCov|
|189||Deaths in children and young people in England after SARS-CoV-2 infection during the first pandemic year |
|Nat Med||2022|| ||LitCov and CORD-19|
|190||Covid and flu: what do the numbers tell us about morbidity and deaths? |
|BMJ||2021|| ||LitCov and CORD-19|
|191||SARS-CoV-2 non-structural protein 6 triggers NLRP3-dependent pyroptosis by targeting ATP6AP1 |
|Cell Death Differ||2022|| ||LitCov and CORD-19|
|192||ESCMID rapid guidelines for assessment and management of long COVID |
SCOPE: The aim of these guidelines is to provide evidence-based recommendations for assessment and management of individuals with persistent symptoms after acute COVID-19 infection, and provide a definition for this entity, termed “long COVID”. METHODS: We performed a search of the literature on studies addressing epidemiology, symptoms, assessment, and treatment of long COVID. The recommendations were grouped by these headings and by organ systems for assessment and treatment. An expert opinion definition of long COVID is provided. Symptoms were reviewed by a search of the available literature. For assessment recommendations, we aimed to perform a diagnostic meta-analysis, but no studies provided relevant results. For treatment recommendations we performed a systematic review of the literature in accordance with the PRISMA statement. We aimed to evaluate patient-related outcomes, including quality of life, return to baseline physical activity, and return to work. Quality assessment of studies included in the systematic review is provided according to study design. RECOMMENDATIONS: Evidence was insufficient to provide any recommendation other than conditional guidance. The panel recommends considering routine blood tests, chest imaging and pulmonary functions tests for patients with persistent respiratory symptoms at 3 months. Other tests should be performed mainly to exclude other conditions according to symptoms. For management, no evidence-based recommendations could be provided. Physical and respiratory rehabilitation should be considered. On the basis of limited evidence, the panel suggests designing high quality prospective clinical studies/trials, including a control group, to further evaluate assessment and management of individuals with persistent symptoms of COVID-19.
|Clin Microbiol Infect||2022|| ||LitCov and CORD-19|
|193||A comprehensive review about immune responses and exhaustion during coronavirus disease |
|Cell Commun Signal||2022|| ||LitCov|
|194||Comprehensive clinical assessment identifies specific neurocognitive deficits in working-age patients with long-COVID |
|PLoS One||2022|| ||LitCov|
|195||Side Effects and Perceptions of COVID-19 Vaccination in Saudi Arabia: A Cross-Sectional Study |
|Front Med (Lausanne)||2022|| ||LitCov|
|196||Long COVID occurrence in COVID-19 survivors |
This cross-sectional study aimed to investigate the post-acute consequences of COVID-19. We conducted a self-administered questionnaire survey on sequelae, psychological distress (K6), impairments in work performance (WFun), and COVID-19–related experiences of stigma and discrimination in two designated COVID-19 hospitals in Hiroshima Prefecture, Japan, between August 2020 and March 2021. The prevalence of sequelae was calculated by age and COVID-19 severity. Factors independently associated with sequelae or psychological distress were identified using logistic regression analysis. Among 127 patients who had recovered from COVID-19, 52.0% had persistent symptoms at a median of 29 days [IQR 23–128] after COVID-19 onset. Among patients with mild COVID-19, 49.5% had sequelae. The most frequent symptoms were olfactory disorders (15.0%), taste disorders (14.2%), and cough (14.2%). Multivariate analysis showed that age was an independent risk factor for sequelae (adjusted odds ratios [AOR] for ≥ 60 years vs. < 40 years 3.63, p = 0.0165). Possible psychological distress was noted in 30.7% (17.9% of males and 45.0% of females). Female sex and the presence of sequelae were independent risk factors for psychological distress. Of all participants, 29.1% had possible impairments in work performance. Experiences of stigma and discrimination were reported by 43.3% of participants. This study revealed the significant impacts of Long COVID on health in local communities. A large-scale, long-term cohort study is desired.
|Sci Rep||2022|| ||LitCov and CORD-19|
|197||Covid-19 vaccines: In the rush for regulatory approval, do we need more data? |
|BMJ||2021|| ||LitCov and CORD-19|
|198||Spatially distributed infection increases viral load in a computational model of SARS-CoV-2 lung infection |
A key question in SARS-CoV-2 infection is why viral loads and patient outcomes vary dramatically across individuals. Because spatial-temporal dynamics of viral spread and immune response are challenging to study in vivo, we developed Spatial Immune Model of Coronavirus (SIMCoV), a scalable computational model that simulates hundreds of millions of lung cells, including respiratory epithelial cells and T cells. SIMCoV replicates viral growth dynamics observed in patients and shows how spatially dispersed infections can lead to increased viral loads. The model also shows how the timing and strength of the T cell response can affect viral persistence, oscillations, and control. By incorporating spatial interactions, SIMCoV provides a parsimonious explanation for the dramatically different viral load trajectories among patients by varying only the number of initial sites of infection and the magnitude and timing of the T cell immune response. When the branching airway structure of the lung is explicitly represented, we find that virus spreads faster than in a 2D layer of epithelial cells, but much more slowly than in an undifferentiated 3D grid or in a well-mixed differential equation model. These results illustrate how realistic, spatially explicit computational models can improve understanding of within-host dynamics of SARS-CoV-2 infection.
|PLoS Comput Biol||2021|| ||LitCov and CORD-19|
|199||Long-Term COVID-19 Sequelae in Adolescents: the Overlap with Orthostatic Intolerance and ME/CFS |
PURPOSE OF REVIEW: To discuss emerging understandings of adolescent long COVID or post-COVID-19 conditions, including proposed clinical definitions, common symptoms, epidemiology, overlaps with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and orthostatic intolerance, and preliminary guidance on management. RECENT FINDINGS: The recent World Health Organization clinical case definition of post-COVID-19 condition requires a history of probable or confirmed SARS-CoV-2 infection, with symptoms starting within 3 months of the onset of COVID-19. Symptoms must last for at least 2 months and cannot be explained by an alternative diagnosis. Common symptoms of the post-COVID-19 condition include, but are not limited to, fatigue, shortness of breath, and cognitive dysfunction. These symptoms generally have an impact on everyday functioning. The incidence of prolonged symptoms following SARS-CoV-2 infection has proven challenging to define, but it is now clear that those with relatively mild initial infections, without severe initial respiratory disease or end-organ injury, can still develop chronic impairments, with symptoms that overlap with conditions like ME/CFS (profound fatigue, unrefreshing sleep, post-exertional malaise, cognitive dysfunction, and orthostatic intolerance). SUMMARY: We do not yet have a clear understanding of the mechanisms by which individuals develop post-COVID-19 conditions. There may be several distinct types of long COVID that require different treatments. At this point, there is no single pharmacologic agent to effectively treat all symptoms. Because some presentations of post-COVID-19 conditions mimic disorders such as ME/CFS, treatment guidelines for this and related conditions can be helpful for managing post-COVID-19 symptoms. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s40124-022-00261-4.
|Curr Pediatr Rep||2022|| ||LitCov and CORD-19|
|200||The law of regression to the tail: How to survive Covid-19, the climate crisis and other disasters |
Regression to the mean is nice and reliable. Regression to the tail is reliably scary. We live in the age of regression to the tail. It is only a matter of time until a pandemic worse than covid-19 will hit us, and climate more extreme than any we have seen. What are the basic principles that generate such extreme risk, and for navigating it, for government, business, and the public?
|Environ Sci Policy||2020|| ||LitCov and CORD-19|