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The COVID-19 Pandemic: a Call to Action to Identify and Address Racial and Ethnic Disparities.
Laurencin, CT, McClinton, A
Journal of racial and ethnic health disparities. 2020;7(3):398-402
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The severe acute respiratory syndrome coronavirus 2 virus was first identified in late 2019 in Wuhan, China. Various unsubstantiated reports emerged declaring that the genetic constitution of Blacks or even the presence of melanin rendered Blacks immune to the virus. This study is a call of action which reviews preliminary data on race and ethnicity in the peer-reviewed literature for citizens in America affected by COVID-19. Findings demonstrate that communities of colour (Blacks) have a higher rate of infection and death in comparison to their population percentage in the state of Connecticut. However, authors are unable to draw conclusions since race and ethnicity data is missing and the data in this paper is the earliest data available. Therefore, the authors call for action to identify and address racial and ethnic health disparities in the COVID-19 crisis.
Abstract
The Coronavirus disease 2019 (COVID-19) pandemic has significantly impacted and devastated the world. As the infection spreads, the projected mortality and economic devastation are unprecedented. In particular, racial and ethnic minorities may be at a particular disadvantage as many already assume the status of a marginalized group. Black Americans have a long-standing history of disadvantage and are in a vulnerable position to experience the impact of this crisis and the myth of Black immunity to COVID-19 is detrimental to promoting and maintaining preventative measures. We are the first to present the earliest available data in the peer-reviewed literature on the racial and ethnic distribution of COVID-19-confirmed cases and fatalities in the state of Connecticut. We also seek to explode the myth of Black immunity to the virus. Finally, we call for a National Commission on COVID-19 Racial and Ethnic Health Disparities to further explore and respond to the unique challenges that the crisis presents for Black and Brown communities.
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Greater risk of severe COVID-19 in Black, Asian and Minority Ethnic populations is not explained by cardiometabolic, socioeconomic or behavioural factors, or by 25(OH)-vitamin D status: study of 1326 cases from the UK Biobank.
Raisi-Estabragh, Z, McCracken, C, Bethell, MS, Cooper, J, Cooper, C, Caulfield, MJ, Munroe, PB, Harvey, NC, Petersen, SE
Journal of public health (Oxford, England). 2020;42(3):451-460
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The coronavirus disease 2019 (COVID-19) pandemic has to date resulted in over 6 million cases. Growing reports highlight men and Black, Asian and Minority Ethnic (BAME) cohorts as at higher risk of adverse COVID-19 outcomes. The aim of this study was to investigate whether differential patterns of COVID-19 incidence and severity, by sex and ethnicity, might be explained by cardiometabolic, socio-economic, lifestyle and behavioural exposures. This study is a prospective cohort study of over half a million men and women from across the UK. Results showed that male sex, BAME ethnicity, higher body mass index and greater household size were associated with significantly greater odds of a positive result. However, the sex and ethnicity differential pattern of COVID-19 is not adequately explained by variations in cardiometabolic factors, 25(OH)-vitamin D levels, socio-economic or behavioural factors. Authors conclude that investigation of alternative biological and genetic susceptibilities as well as more comprehensive assessment of the complex economic, social and behavioural differences should be prioritised.
Abstract
BACKGROUND We examined whether the greater severity of coronavirus disease 2019 (COVID-19) amongst men and Black, Asian and Minority Ethnic (BAME) individuals is explained by cardiometabolic, socio-economic or behavioural factors. METHODS We studied 4510 UK Biobank participants tested for COVID-19 (positive, n = 1326). Multivariate logistic regression models including age, sex and ethnicity were used to test whether addition of (1) cardiometabolic factors [diabetes, hypertension, high cholesterol, prior myocardial infarction, smoking and body mass index (BMI)]; (2) 25(OH)-vitamin D; (3) poor diet; (4) Townsend deprivation score; (5) housing (home type, overcrowding) or (6) behavioural factors (sociability, risk taking) attenuated sex/ethnicity associations with COVID-19 status. RESULTS There was over-representation of men and BAME ethnicities in the COVID-19 positive group. BAME individuals had, on average, poorer cardiometabolic profile, lower 25(OH)-vitamin D, greater material deprivation, and were more likely to live in larger households and in flats/apartments. Male sex, BAME ethnicity, higher BMI, higher Townsend deprivation score and household overcrowding were independently associated with significantly greater odds of COVID-19. The pattern of association was consistent for men and women; cardiometabolic, socio-demographic and behavioural factors did not attenuate sex/ethnicity associations. CONCLUSIONS In this study, sex and ethnicity differential pattern of COVID-19 was not adequately explained by variations in cardiometabolic factors, 25(OH)-vitamin D levels or socio-economic factors. Factors which underlie ethnic differences in COVID-19 may not be easily captured, and so investigation of alternative biological and genetic susceptibilities as well as more comprehensive assessment of the complex economic, social and behavioural differences should be prioritised.
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COVID-19: Exposing and addressing health disparities among ethnic minorities and migrants.
Greenaway, C, Hargreaves, S, Barkati, S, Coyle, CM, Gobbi, F, Veizis, A, Douglas, P
Journal of travel medicine. 2020;27(7)
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The coronavirus disease 2019 (COVID-19) has swept across the world affecting all countries. As COVID-19 has spread within countries, vulnerable and marginalized populations, and those with low income and low socioeconomic status have been unduly affected. Every country has vulnerable populations that require special attention from policy makers in their response to the current pandemic. In fact, current literature shows that migrants living in refugee camps, detention centres and reception centres are at particularly high risk for COVID-19 exposure. Therefore, they should be included in national surveillance and be entitled to health care. In addition, it is essential to foster trust between public health practitioners and the leadership of these communities so that they may work together to effectively deliver prevention and intervention strategies. Authors conclude that COVID-19 pandemic has exposed health disparities among ethnic minorities and certain migrant groups. Thus, they highlight the importance of prompting greater health equity for diverse ethnocultural communities.
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COVID-19: Unique public health issues facing Black, Asian and minority ethnic communities.
Abuelgasim, E, Saw, LJ, Shirke, M, Zeinah, M, Harky, A
Current problems in cardiology. 2020;45(8):100621
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The 2019 coronavirus disease (COVID-19), is a public health emergency with serious adverse implications for populations, healthcare systems, and economies globally. The aim of this review was to explore the possible association between ethnicity, incidence and outcomes of COVID-19 using both recent COVID-19 studies and studies of previous pandemics. Findings show that: - ethnic minorities have lower lung function compared to their Caucasian counterparts. - Black, Asian and Minority Ethnics communities are prone to higher rates of cardiovascular disease and are subject to adverse healthcare disparities. - ethnic minorities are disproportionately affected, and experience worse health outcomes compared to other groups. They are also more likely to be socioeconomically disadvantaged compared to white communities. - Africans are at a higher risk of receiving later and more indigent healthcare compared to other ethnic groups. Authors conclude that data on ethnicity should be routinely collected by governments to robustly determine magnitude of association. In addition, governments should also recommend strategies to mitigate risks on minority ethnicities due to socioeconomic disadvantages.
Abstract
The 2019 coronavirus disease is a serious public health emergency, with serious adverse implications for populations, healthcare systems, and economies globally. Recently, concerns have been raised about possible association between ethnicity, incidence and outcomes of COVID-19 arisen from early government data. In this review, we will explore the possible association using both recent COVID-19 studies and studies of previous pandemics. We call for data on ethnicity to be routinely collected by governments, as part of an international collaboration, alongside other patient demographics and further research to robustly determine the magnitude of association. Moreover, governments must learn from previous pandemics and recommended strategies to mitigate risks on minority ethnicities due to socioeconomic disadvantages.
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Persistent Symptoms in Patients After Acute COVID-19.
Carfì, A, Bernabei, R, Landi, F
JAMA. 2020;324(6):603-605
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This short article reports the results of a case series of Italian COVID-19 patients who had been hospitalised for the infection and had recovered (shown by 2 negative PCR tests). The aim was to establish any persistent symptoms and quality of life. 143 patients were included in this study, just over a third were women and age range was 19-84 years (mean 56.5 years). After an average of 2 months after recovery, only 13% reported not having any COVOD-19 related symptoms whilst 32% had 1 or 2 and 55% had 3 or more symptoms. None of the patients had symptoms of acute infection, such as fever. The most common symptoms were fatigue (53%), shortness of breath (43%), joint pain (27%) and chest pain (22%). 44% of patients reported a worsening of quality of life after compared to before the infection. Limitations of the study included lack of information of symptoms prior to COVID-19 infection and symptom severity, small sample size and lack of a control group. The authors note that patients with other types of pneumonia can also have persistent symptoms, and this may therefore not be exclusive to COVID-19.
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Persistent fatigue following SARS-CoV-2 infection is common and independent of severity of initial infection.
Townsend, L, Dyer, AH, Jones, K, Dunne, J, Mooney, A, Gaffney, F, O'Connor, L, Leavy, D, O'Brien, K, Dowds, J, et al
PloS one. 2020;15(11):e0240784
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Tiredness is a common symptom of Covid-19; however, it is unknown if this fatigue persists once recovered. This observational study of 128 recovered Covid-19 patients aimed to determine if fatigue persisted after recovery and whether severity of disease could predict fatigue. The results showed that post Covid-19 fatigue was reported in more than half of the participants and was particularly pronounced in females and in those with depression. Severity of disease did not predict fatigue. It was concluded that fatigue appears to outlast infection and fatigue was independent of disease severity. This study could be used by health care practitioners to understand that fatigue is common even after recovery from Covid-19 infection and women and sufferers of depression are the most susceptible.
Abstract
Fatigue is a common symptom in those presenting with symptomatic COVID-19 infection. However, it is unknown if COVID-19 results in persistent fatigue in those recovered from acute infection. We examined the prevalence of fatigue in individuals recovered from the acute phase of COVID-19 illness using the Chalder Fatigue Score (CFQ-11). We further examined potential predictors of fatigue following COVID-19 infection, evaluating indicators of COVID-19 severity, markers of peripheral immune activation and circulating pro-inflammatory cytokines. Of 128 participants (49.5 ± 15 years; 54% female), more than half reported persistent fatigue (67/128; 52.3%) at median of 10 weeks after initial COVID-19 symptoms. There was no association between COVID-19 severity (need for inpatient admission, supplemental oxygen or critical care) and fatigue following COVID-19. Additionally, there was no association between routine laboratory markers of inflammation and cell turnover (leukocyte, neutrophil or lymphocyte counts, neutrophil-to-lymphocyte ratio, lactate dehydrogenase, C-reactive protein) or pro-inflammatory molecules (IL-6 or sCD25) and fatigue post COVID-19. Female gender and those with a pre-existing diagnosis of depression/anxiety were over-represented in those with fatigue. Our findings demonstrate a significant burden of post-viral fatigue in individuals with previous SARS-CoV-2 infection after the acute phase of COVID-19 illness. This study highlights the importance of assessing those recovering from COVID-19 for symptoms of severe fatigue, irrespective of severity of initial illness, and may identify a group worthy of further study and early intervention.
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Laboratory features of severe vs. non-severe COVID-19 patients in Asian populations: a systematic review and meta-analysis.
Ghahramani, S, Tabrizi, R, Lankarani, KB, Kashani, SMA, Rezaei, S, Zeidi, N, Akbari, M, Heydari, ST, Akbari, H, Nowrouzi-Sohrabi, P, et al
European journal of medical research. 2020;25(1):30
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The coronavirus disease 2019 (COVID-19) outbreak started in December 2019 in China has spread sharply all over the world. Apart from the clinical symptoms and pulmonary computed tomography findings, a large number of COVID-19 confirmed patients showed laboratory fluctuations. The aim of this study was to quantify the results of previously published studies, comparing the laboratory fluctuations, and some new combined inflammatory laboratory tests in severe/critical versus non-severe confirmed infected cases of COVID-19. This study is a systemic review and meta-analysis which included 22 studies with a total of 3396 patients who were classed into two groups: 720 in severe and 2676 in non-severe groups. Results showed that the results of complete blood count test, liver and kidney function tests, inflammatory/infection markers, serum electrolytes and glucose were significantly different between severe and non-severe cases of COVID-19. In fact, there was significant decreased levels of certain types of white blood cells (lymphocyte, monocyte, eosinophil), haemoglobin, and platelet, whereas elevated neutrophil [white blood cell] counts among the complete blood count indices in severe vs. non-severe patients. Authors conclude that further well-methodologically designed studies from other populations are strongly recommended.
Abstract
BACKGROUND More severe cases of COVID- 19 are more likely to be hospitalized and around one-fifth, needing ICU admission. Understanding the common laboratory features of COVID-19 in more severe cases versus non-severe patients could be quite useful for clinicians and might help to predict the model of disease progression. This systematic review and meta-analysis aimed to compare the laboratory test findings in severe vs. non-severe confirmed infected cases of COVID-19. METHODS Electronic databases were systematically searched in PubMed, EMBASE, Scopus, Web of Science, and Google Scholar from the beginning of 2019 to 3rd of March 2020. Heterogeneity across included studies was determined using Cochrane's Q test and the I2 statistic. We used the fixed or random-effect models to pool the weighted mean differences (WMDs) or standardized mean differences and 95% confidence intervals (CIs). FINDINGS Out of a total of 3009 citations, 17 articles (22 studies, 21 from China and one study from Singapore) with 3396 ranging from 12 to1099 patients were included. Our meta-analyses showed a significant decrease in lymphocyte, monocyte, and eosinophil, hemoglobin, platelet, albumin, serum sodium, lymphocyte to C-reactive protein ratio (LCR), leukocyte to C-reactive protein ratio (LeCR), leukocyte to IL-6 ratio (LeIR), and an increase in the neutrophil, alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin, blood urea nitrogen (BUN), creatinine (Cr), erythrocyte Sedimentation Rate (ESR), C-reactive protein (CRP), Procalcitonin (PCT), lactate dehydrogenase (LDH), fibrinogen, prothrombin time (PT), D-dimer, glucose level, and neutrophil to lymphocyte ratio (NLR) in the severe group compared with the non-severe group. No significant changes in white blood cells (WBC), Creatine Kinase (CK), troponin I, myoglobin, IL-6 and K between the two groups were observed. INTERPRETATION This meta-analysis provides evidence for the differentiation of severe cases of COVID-19 based on laboratory test results at the time of ICU admission. Future well-methodologically designed studies from other populations are strongly recommended.
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The role of cytokine profile and lymphocyte subsets in the severity of coronavirus disease 2019 (COVID-19): A systematic review and meta-analysis.
Akbari, H, Tabrizi, R, Lankarani, KB, Aria, H, Vakili, S, Asadian, F, Noroozi, S, Keshavarz, P, Faramarz, S
Life sciences. 2020;258:118167
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Literature shows that lymphopenia [reduced level of the blood cell lymphocyte] and cytokine release syndrome are among the characteristics caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) - the new infectious Coronavirus Disease 2019 (COVID-19). The main aims of this study were (a) to analyse the different characteristics of cytokine levels, lymphocyte subsets, complete blood count (CBC) indices, and a number of infection-related factors between mild/moderate and severe/critical patients, and (b) to screen out suitable indicators for the prediction of the disease severity in order to provide some insight into the subsequent clinical interventions. This study is a systemic review and meta-analysis of 50 studies (44 articles) with a total of 7865 patients including 2286 in the severe group and 5579 in the non-severe group. Results demonstrated a significant lymphopenia in severe/critical infected cases compared to mild/moderate COVID-19 ones across 46 studies. The severity of COVID-19 has also a significant, positive association with a number of infection related factors (such as C-reactive protein) and ferritin levels. Moreover, with respect to CBC indices, the findings revealed significantly higher levels in white blood cells and neutrophil, while lower lymphocyte and monocyte levels in severe than in non-severe confirmed COVID-19 patients. Authors conclude that it is essential that clinicians have access to reliable quick pathogen tests and feasible differential diagnoses based on the clinical descriptions in their first contact with suspected patients.
Abstract
AIMS: This study aimed to make a comparison between the clinical laboratory-related factors, complete blood count (CBC) indices, cytokines, and lymphocyte subsets in order to distinguish severe coronavirus disease 2019 (COVID-19) cases from the non-severe ones. MATERIALS AND METHODS Relevant studies were searched in PubMed, Embase, Scopus, and Web of Science databases until March 31, 2020. Cochrane's Q test and the I2 statistic were used to determine heterogeneity. We used the random-effect models to pool the weighted mean differences (WMDs) and 95% confidence intervals (CIs). KEY FINDINGS Out of a total of 8557 initial records, 44 articles (50 studies) with 7865 patients (ranging from 13 to 1582), were included. Our meta-analyses with random-effect models showed a significant decrease in lymphocytes, monocyte, CD4+ T cells, CD8+ T cells, CD3 cells, CD19 cells, and natural killer (NK) cells and an increase in the white blood cell (WBC), neutrophils, neutrophil to lymphocyte ratio (NLR), C-reactive protein (CRP)/hs-CRP, erythrocyte sedimentation rate (ESR), ferritin, procalcitonin (PCT), and serum amyloid A (SAA), interleukin-2 (IL-2), IL-2R, IL-4, IL-6, IL-8, IL-10, tumor necrosis factor-alpha (TNF-α), and interferon-gamma (INF-γ) in the severe group compared to the non-severe group. However, no significant differences were found in IL-1β, IL-17, and CD4/CD8 T cell ratio between the two groups. SIGNIFICANCE Decrease in total lymphocytes and lymphocyte subsets as well as the elevation of CRP, ESR, SAA, PCT, ferritin, and cytokines, but not IL-1β and IL-17, were closely associated with COVID-19 severity, implying reliable indicators of severe COVID-19.
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Potential Anti-SARS-CoV-2 Therapeutics That Target the Post-Entry Stages of the Viral Life Cycle: A Comprehensive Review.
Al-Horani, RA, Kar, S
Viruses. 2020;12(10)
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The covid-19 pandemic has required the identification of therapies to prevent infection and limit severity. A previous paper by the same authors reviewed therapies that block the virus in the early stages of its lifecycle. This very large review of over 300 papers aimed to summarise therapeutics which are aimed at blocking the lifecycle of the virus after it has entered the body’s cells. The authors began by reviewing the lifecycle of the covid-19 virus explaining how it enters the body’s cells, replicates inside and then is released to infect new cells. Several antivirals, antimalarials and natural products were then reviewed. Of note, Remdesivir is being trialled in covid-19 patients, with mixed results, however, is being recommended in the US for the treatment of hospitalised covid-19 patients with severe disease. Ribavirin, which is being trialled in combination with other antivirals is also showing promising results in shortening hospitalisation times in covid-19 patients. It was concluded that any stage of the covid-19 lifecycle could be a target for therapeutics and combining therapies is likely to be more successful than monotherapy. This paper could be used by health care professionals to understand the most recent therapeutic research for covid-19.
Abstract
The coronavirus disease-2019 (COVID-19) pandemic continues to challenge health care systems around the world. Scientists and pharmaceutical companies have promptly responded by advancing potential therapeutics into clinical trials at an exponential rate. Initial encouraging results have been realized using remdesivir and dexamethasone. Yet, the research continues so as to identify better clinically relevant therapeutics that act either as prophylactics to prevent the infection or as treatments to limit the severity of COVID-19 and substantially decrease the mortality rate. Previously, we reviewed the potential therapeutics in clinical trials that block the early stage of the viral life cycle. In this review, we summarize potential anti-COVID-19 therapeutics that block/inhibit the post-entry stages of the viral life cycle. The review presents not only the chemical structures and mechanisms of the potential therapeutics under clinical investigation, i.e., listed in clinicaltrials.gov, but it also describes the relevant results of clinical trials. Their anti-inflammatory/immune-modulatory effects are also described. The reviewed therapeutics include small molecules, polypeptides, and monoclonal antibodies. At the molecular level, the therapeutics target viral proteins or processes that facilitate the post-entry stages of the viral infection. Frequent targets are the viral RNA-dependent RNA polymerase (RdRp) and the viral proteases such as papain-like protease (PLpro) and main protease (Mpro). Overall, we aim at presenting up-to-date details of anti-COVID-19 therapeutics so as to catalyze their potential effective use in fighting the pandemic.
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Harnessing the immune system to overcome cytokine storm and reduce viral load in COVID-19: a review of the phases of illness and therapeutic agents.
Khadke, S, Ahmed, N, Ahmed, N, Ratts, R, Raju, S, Gallogly, M, de Lima, M, Sohail, MR
Virology journal. 2020;17(1):154
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Severe manifestations of COVID-19 infection and mortality are associated with a cytokine storm. This is an excessive inflammatory response to the infection leading to an overproduction of pro-inflammatory signalling molecules, which consequently contributes to tissue and organ damage. This literature review summarised current knowledge, as of June 2020, about virus-associated cytokine storm, virus-host interactions and immunological mechanism, to gain a better understanding of the phenomena observed in COVID-19 infections and devise better treatment strategies. The review briefly outlines the epidemiology of COVID-19, predictors of severity of disease, mode of transmission, testing, viral structure, mechanism of invasion of the host cell, replication and immune invasion and the progression of the four stages of the cytokine storm. The second part of the review discusses antiviral therapeutics of interest with a table summarising drugs, mechanism and available data. This article may be of interest to those who like to delve further into the mechanisms and immune components involved in a cytokine storm and gain an oversight of the pathways targeted by allopathic agents that have been put forward as treatment options.
Abstract
BACKGROUND Coronavirus disease 2019 (COVID-19) is caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2, previously named 2019-nCov), a novel coronavirus that emerged in China in December 2019 and was declared a global pandemic by World Health Organization by March 11th, 2020. Severe manifestations of COVID-19 are caused by a combination of direct tissue injury by viral replication and associated cytokine storm resulting in progressive organ damage. DISCUSSION We reviewed published literature between January 1st, 2000 and June 30th, 2020, excluding articles focusing on pediatric or obstetric population, with a focus on virus-host interactions and immunological mechanisms responsible for virus associated cytokine release syndrome (CRS). COVID-19 illness encompasses three main phases. In phase 1, SARS-CoV-2 binds with angiotensin converting enzyme (ACE)2 receptor on alveolar macrophages and epithelial cells, triggering toll like receptor (TLR) mediated nuclear factor kappa-light-chain-enhancer of activated B cells (NF-ƙB) signaling. It effectively blunts an early (IFN) response allowing unchecked viral replication. Phase 2 is characterized by hypoxia and innate immunity mediated pneumocyte damage as well as capillary leak. Some patients further progress to phase 3 characterized by cytokine storm with worsening respiratory symptoms, persistent fever, and hemodynamic instability. Important cytokines involved in this phase are interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α. This is typically followed by a recovery phase with production of antibodies against the virus. We summarize published data regarding virus-host interactions, key immunological mechanisms responsible for virus-associated CRS, and potential opportunities for therapeutic interventions. CONCLUSION Evidence regarding SARS-CoV-2 epidemiology and pathogenesis is rapidly evolving. A better understanding of the pathophysiology and immune system dysregulation associated with CRS and acute respiratory distress syndrome in severe COVID-19 is imperative to identify novel drug targets and other therapeutic interventions.