Metformin in SARS-CoV-2 infection: A hidden path – from altered inflammation to reduced mortality. A review from the literature

SARS-CoV-2 infection has been a major threat to human health and a huge challenge to Medicine. In only two years, COVID-19 affected >350 million people, causing >5.6 million deaths. Chronic inflammatory states, such as diabetes or obesity, are known risk factors for COVID-19 poorest outcomes, with higher risk for disease severity and greater mortality. Metformin remains on the first line of the management of hyperglycemia in type 2 diabetes. Through its anti-inflammatory and immunomodulatory mechanisms, metformin appears as an opportunity to control the dysregulated cytokine storm secondary to SARS-CoV-2 infection. Recent studies point towards a potential protective role of metformin in the course of COVID-19, showing that current or previous treatment with metformin associates with better outcomes.     

New onset diabetes,type 1 diabetes and COVID-19

Background and aimsNew data has emerged regarding higher risk of coronavirus disease 2019 (COVID-19), and its severity and complications in patients with type 2 diabetes mellitus (T2DM). However, there is a dearth of evidence regarding type 1 diabetes mellitus (T1DM). This article explores the possibility of COVID 19 induced diabetes and highlights a potential bidirectional link between COVID 19 and T1DM.MethodsA literature search was performed with Medline (PubMed), Scopus, and Google Scholar electronic databases till October 2020, using relevant keywords (COVID-19 induced diabetes; COVID-19 and type 1 diabetes; COVID-19 induced DKA; new-onset diabetes after SARS-CoV-2 infection) to extract relevant studies describing relationship between COVID-19 and T1DM.ResultsPast lessons and new data teach us that severe acute respiratory syndrome coronaviruses (SARS-CoV and SARS-CoV-2) can enter islet cells via angiotensin converting enzyme-2 (ACE-2) receptors and cause reversible β-cell damage and transient hyperglycemia. There have been postulations regarding the potential new-onset T1DM triggered by COVID-19. This article reviews the available evidence regarding the impact and interlink between COVID-19 and Τ1DM. We also explore the mechanisms behind the viral etiology of Τ1DM.ConclusionsSARS-CoV-2 can trigger severe diabetic ketoacidosis at presentation in individuals with new-onset diabetes. However, at present, there is no hard evidence that SARS-CoV-2 induces T1DM on it’s own accord. Long term follow-up of children and adults presenting with new-onset diabetes during this pandemic is required to fully understand the type of diabetes induced by COVID-19.     

Metabolic syndrome and the risk of COVID-19 infection: A nationwide population-based case-control study

Background and aimsMetabolic syndrome (MetS) is a chronic, low-grade inflammatory disease. This study aimed to investigate the impact of MetS on the risk and severity of COVID-19.Methods and resultsWe investigated a nationwide cohort with COVID-19 including all patients who underwent the test for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in Korea. The COVID-19 group included 4070 patients with positive SARS-CoV-2 test results, and the age- and sex-matched control group included 27,618 subjects with negative SARS-CoV-2 test results. The endpoints were SARS-CoV-2 positivity and the severity of COVID-19. The prevalence of MetS was 24.7% and 24.5% in the COVID-19 and control groups, respectively. The presence of MetS was not associated with the risk of developing COVID-19. Among the components of MetS, central obesity was associated with a higher risk of COVID-19 infection (adjusted odds ratio [aOR], 1.17; 95% confidence interval [CI], 1.06–1.28, P = 0.001). The presence of MetS was significantly associated with severe COVID-19 (aOR, 1.25; 95% CI, 0.78–2.00, P = 0.352). Among the individual components of MetS, prediabetes/diabetes mellitus was associated with a higher risk of severe COVID-19 (aOR, 1.61; 95% CI, 1.21–2.13, P = 0.001). The risk of severe COVID-19 linearly increased according to the number of metabolic components (P for trend = 0.005).ConclusionIn this nationwide cohort study, the individuals with MetS had a significant increase in the risk of severe COVID-19 infection. These patients, particularly those with central obesity and insulin resistance, deserve special attention amid the COVID-19 pandemic.     

Coronavirus disease 2019 and non-alcoholic fatty liver disease

The coronavirus disease 2019(COVID-19) pandemic may present with a broad range of clinical manifestations, from no or mild symptoms to severe disease. Patients with specific pre-existing comorbidities, such as obesity and type 2 diabetes, are at high risk of coming out with a critical form of COVID-19. Nonalcoholic fatty liver disease(NAFLD) is the most common chronic liver disease, and, because of its frequent association with metabolic alterations including obesity and type 2 diabetes, it has recently been re-named as metabolic-associated fatty liver disease(MAFLD). Several studies and systematic reviews pointed out the increased risk of severe COVID-19 in NAFLD/MAFLD patients. Even though dedicated mechanistic studies are missing, this higher probability may be justified by systemic low-grade chronic inflammation associated with immune dysregulation in NAFLD/MAFLD, which could trigger cytokine storm and hypercoagulable state after severe acute respiratory syndrome coronavirus 2 infection. This review focuses on the predisposing role of NAFLD/MAFLD in favoring severe COVID-19, discussing the available information on specific risk factors, clinical features, outcomes, and pathogenetic mechanisms.     

Cardiac Involvement of COVID-19: A Comprehensive Review

Coronavirus Disease 2019 (COVID-19) is an infectious disease caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) virus. SARS-CoV-2 caused COVID-19 has reached a pandemic level. COVID-19 can significantly affect patients’ cardiovascular systems. First, those with COVID-19 and preexisting cardiovascular disease have an increased risk of severe disease and death. Mortality from COVID-19 is strongly associated with cardiovascular disease, diabetes, and hypertension. Second, therapies under investigation for COVID-19 may have cardiovascular side effects of arrhythmia. Third, COVID-19 is associated with multiple direct and indirect cardiovascular complications. Associated with a high inflammatory burden related to cytokine release, COVID-19 can induce vascular inflammation, acute myocardial injury, myocarditis, arrhythmias, venous thromboembolism, metabolic syndrome and Kawasaki disease. Understanding the effects of COVID-19 on the cardiovascular system is essential for providing comprehensive medical care for cardiac and/or COVID-19 patients. We hereby review the literature on COVID-19 regarding cardiovascular virus involvement.     

Companion animals likely do not spread COVID-19 but may get infected themselves

Coronavirus disease 2019 (COVID-19) is a highly contagious infectious disease caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). From the epidemiological data, the picture emerges that the more severe etiopathologies among COVID-19 patients are found in elderly people. The risk of death due to COVID-19 increases exponentially with age. Eight out of 10 COVID-19 related deaths occur in people older than 65 years of age. Older patients with comorbid conditions such as hypertension, heart failure, diabetes mellitus, asthma, chronic obstructive pulmonary disease, and cancer have a much higher case fatality rate. Governments and public health authorities all over the world have realized that protections of vulnerable older adults should be a priority during the COVID-19 pandemic. COVID-19 is a zoonotic disease. The SARS-CoV-2 virus was originally transmitted likely from a bat or a pangolin to humans. Recent evidence suggests that SARS-CoV-2, similar to other coronaviruses, can infect several species of animals, including companion animals such as dogs, cats, and ferrets although their viral loads remain low. While the main source of infection transmission therefore is human to human, there are a few rare cases of pets contracting the infection from a SARS-CoV-2-infected human. Although there is no evidence that pets actively transmit SARS-CoV-2 via animal-to-human transmission, senior pet ownership potentially may pose a small risk to older adults by (1) potentially enabling animal-to-human transmission of SARS-CoV-2 in the most vulnerable population and (2) by increasing the exposition risk for the elderly due to the necessity to care for the pet and, in the case of dogs, to take them outside the house several times per day. In this overview, the available evidence on SARS-CoV-2 infection in pets is considered and the potential for spread of COVID-19 from companion animals to older individuals and the importance of prevention are discussed.

     

Impact of cytokine storm and systemic inflammation on liver impairment patients infected by SARS-CoV-2: Prospective therapeutic challenges

Coronavirus disease 2019 (COVID-19) is a devastating worldwide pandemic infection caused by a severe acute respiratory syndrome namely coronavirus 2 (SARS-CoV-2) that is associated with a high spreading and mortality rate. On the date this review was written, SARS-CoV-2 infected about 96 million people and killed about 2 million people. Several arguments disclosed the high mortality of COVID-19 due to acute respiratory distress syndrome or change in the amount of angiotensin-converting enzyme 2 (ACE2) receptor expression or cytokine storm strength production. In a similar pattern, hepatic impairment patients co-infected with SARS-CoV-2 exhibited overexpression of ACE2 receptors and cytokine storm overwhelming, which worsens the hepatic impairment and increases the mortality rate. In this review, the impact of SARS-CoV-2 on hepatic impairment conditions we overviewed. Besides, we focused on the recent studies that indicated cytokine storm as well as ACE2 as the main factors for high COVID-19 spreading and mortality while hinting at the potential therapeutic strategies.     

Clinical implications of COVID-19 in patients with metabolic-associated fatty liver disease

People across the world are affected by the "coronavirus disease 2019 (COVID-19)", brought on by the "SARS-CoV type-2 coronavirus". Due to its high incidence in individuals with diabetes, metabolic syndrome, and metabolic-associated fatty liver disease (MAFLD), COVID-19 has gained much attention. The metabolic syndrome's hepatic manifestation, MAFLD, carries a significant risk of type-2-diabetes. The link between the above two conditions has also drawn increasing consideration since MAFLD is intricately linked to the obesity epidemic. Independent of the metabolic syndrome, MAFLD may impact the severity of the viral infections, including COVID-19 or may even be a risk factor. An important question is whether the present COVID-19 pandemic has been fueled by the obesity and MAFLD epidemics. Many liver markers are seen elevated in COVID-19. MAFLD patients with associated comorbid conditions like obesity, cardiovascular disease, renal disease, malignancy, hypertension, and old age are prone to develop severe disease. There is an urgent need for more studies to determine the link between the two conditions and whether it might account for racial differences in the mortality and morbidity rates linked to COVID-19. The role of innate and adaptive immunity alterations in MAFLD patients may influence the severity of COVID-19. This review investigates the implications of COVID-19 on liver injury and disease severity and vice-versa. We also addressed the severity of COVID-19 in patients with prior MAFLD and its potential implications and therapeutic administration in the clinical setting.     

Implications of the Immune Polymorphisms of the Host and the Genetic Variability of SARS-CoV-2 in the Development of COVID-19

The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is responsible for the current pandemic affecting almost all countries in the world. SARS-CoV-2 is the agent responsible for coronavirus disease 19 (COVID-19), which has claimed millions of lives around the world. In most patients, SARS-CoV-2 infection does not cause clinical signs. However, some infected people develop symptoms, which include loss of smell or taste, fever, dry cough, headache, severe pneumonia, as well as coagulation disorders. The aim of this work is to report genetic factors of SARS-CoV-2 and host-associated to severe COVID-19, placing special emphasis on the viral entry and molecules of the immune system involved with viral infection. Besides this, we analyze SARS-CoV-2 variants and their structural characteristics related to the binding to polymorphic angiotensin-converting enzyme type 2 (ACE2). Additionally, we also review other polymorphisms as well as some epigenetic factors involved in the immunopathogenesis of COVID-19. These factors and viral variability could explain the increment of infection rate and/or in the development of severe COVID-19.     

Are twindemics occurring?

The emergence and spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease (COVID-19), prompted worldwide COVID-19 surveillance. To investigate the impact of COVID-19 on influenza activity, we used global surveillance data collected since 2019 to compare the number of cases positive for COVID-19 and for influenza across 22 representative countries (Australia, Brazil, Canada, China, Egypt, France, Germany, India, Israel, Italy, Japan, Mexico, The Netherlands, The Philippines, Poland, The Republic of Korea, South Africa, Spain, Thailand, The United Kingdom, The United States, and Vietnam). Our results demonstrate alternating prevalence of SARS-CoV-2 and influenza virus.     

COVID-19 presenting as acute pancreatitis

The ongoing pandemic of Coronavirus disease-2019 (COVID-19) has spread over 200 countries worldwide, affecting >2 million people and >120,000 deaths. COVID-19 is caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). The most common symptoms include cough, shortness of breath, and fever. However, gastrointestinal manifestations of COVID-19 are increasingly being recognized. Herein, we report a case of COVID-19 who presented with acute pancreatitis (AP) without any other risk factors.     

Liver dysfunction during COVID-19 pandemic: Contributing role of associated factors in disease progression and severity

In December 2019, a new strain of coronavirus was discovered in China, and the World Health Organization declared it a pandemic in March 2020. The majority of people with coronavirus disease 19 (COVID-19) exhibit no or only mild symptoms such as fever, cough, anosmia, and headache. Meanwhile, approximately 15% develop a severe lung infection over the course of 10 d, resulting in respiratory failure, which can lead to multi-organ failure, coagulopathy, and death. Since the beginning of the pandemic, it appears that there has been consideration that pre-existing chronic liver disease may predispose to deprived consequences in conjunction with COVID-19. Furthermore, extensive liver damage has been linked to immune dysfunction and coagulopathy, which leads to a more severe COVID-19 outcome. Besides that, people with COVID-19 frequently have abnormal liver function, with more significant elevations in alanine aminotransferase and aspartate aminotransferase in patients with severe COVID-19 compared to those with mild/moderate disease. This review focuses on the pathogenesis of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection in the liver, as well as the use of liver chemistry as a prognostic tool during COVID-19. We also evaluate the findings for viral infection of hepatocytes, and look into the potential mechanisms behind SARS-CoV-2-related liver damage.     

COVID-19 cynomolgus macaque model reflecting human COVID-19 pathological conditions

The pandemic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a global threat to human health and life. A useful pathological animal model accurately reflecting human pathology is needed to overcome the COVID-19 crisis. In the present study, COVID-19 cynomolgus monkey models including monkeys with underlying diseases causing severe pathogenicity such as metabolic disease and elderly monkeys were examined. Cynomolgus macaques with various clinical conditions were intranasally and/or intratracheally inoculated with SARS-CoV-2. Infection with SARS-CoV-2 was found in mucosal swab samples, and a higher level and longer period of viral RNA was detected in elderly monkeys than in young monkeys. Pneumonia was confirmed in all of the monkeys by computed tomography images. When monkeys were readministrated SARS-CoV-2 at 56 d or later after initial infection all of the animals showed inflammatory responses without virus detection in swab samples. Surprisingly, in elderly monkeys reinfection showed transient severe pneumonia with increased levels of various serum cytokines and chemokines compared with those in primary infection. The results of this study indicated that the COVID-19 cynomolgus monkey model reflects the pathophysiology of humans and would be useful for elucidating the pathophysiology and developing therapeutic agents and vaccines.

At the end of 2019, cases of infection with a novel coronavirus, later named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), that causes various respiratory symptoms expanded globally from China. On 11 March 2020, the World Health Organization declared a pandemic status based on the spread of infection worldwide and increase in the number of deaths. The outbreak of SARS-CoV-2 has resulted in a miserable reality for global health and life, and infection cases are continuing to increase worldwide. A detailed understanding of pathological conditions and development of effective therapeutic agents are needed to overcome the pandemic of diseases caused by SARS-CoV-2 infection, which has been named COVID-19. A new strategy including the development of pharmaceutical products and the use of appropriate animal models reflecting the human pathogenesis of COVID-19 is required.The common clinical features of COVID-19 are respiratory symptoms associated with pneumonia including fever, cough, myalgia, fatigue, dyspnea, and lymphopenia (1). COVID-19 symptoms range from no symptoms to severe symptoms. COVID-19 has shown severe pathogenicity in people with underlying diseases and in elderly people (2, 3). The period from onset of COVID-19 symptoms to death varies depending on the age of the patient and underlying disease status of the patient (4). Therefore, in addition to elucidating the pathological features in healthy individuals, it is necessary to elucidate the pathological conditions in patients with underlying diseases and in elderly patients.Cynomolgus monkeys (CMs), which are common laboratory animals among nonhuman primates (NHPs), show various human-like characteristics, including higher brain functions, long life span, single pregnancy, and regular menstrual periods, which are not found in other experimental animals. In the present study, COVID-19 model CMs, including healthy young CMs, elderly CMs (23 to 30 y of age, equivalent to 69 to 90 y of age in humans), and CMs with underlying diseases including diabetes and hyperlipidemia were experimentally infected with SARS-CoV-2 as animal models reflecting human pathology.     

COVID-19 vaccination in pregnant and lactating diabetic women

AimTo discuss available information on the opportunity for pregnant women affected by diabetes/obesity to receive COVID-19 vaccine.Data synthesisPregnant women with SARS-CoV-2 (COVID-19) infection are at high risk for severe acute respiratory syndrome and adverse outcomes. Pregnant women with severe COVID-19 present increased rates of preterm delivery (<37 gestational weeks), cesarean delivery and neonatal admissions to the intensive care unit. Comorbidity such as diabetes (pregestational or gestational) or obesity further increased maternal and fetal complications. It is known that diabetic or obese patients with COVID-19 present an unfavorable course and a worse prognosis, with a direct association between worse outcome and suboptimal glycol-metabolic control or body mass index (BMI) levels. Critical COVID-19 infection prevention is important for both mother and fetus. Vaccination during pregnancy is a common practice. Vaccines against COVID-19 are distributed across the world with some population considered to have a priority. Since pregnant women are excluded from clinical trials very little information are available on safety and efficacy of COVD-19 vaccines during pregnancy. However, it is well known the concept of passive immunization of the newborn obtained with transplacental passage of protective antibodies into the fetal/neonatal circulation after maternal infection or vaccination. Moreover, it has been reported that COVID-19 vaccine-induced IgG pass to the neonates through breastmilk. Therefore, maternal vaccination can protect mother, fetus and baby.ConclusionsAfter an individual risk/benefit evaluation pregnant and lactating women should be counselled to receive COVID-19 vaccines.     

Human ACE2 Polymorphisms from Different Human Populations Modulate SARS-CoV-2 Infection

The COVID-19 pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has resulted in over 6 million deaths worldwide. The high variability in COVID-19 symptoms remains one of the most interesting mysteries of the pandemic. Genetic and environmental factors are likely to be key determinants of COVID-19 symptomatology. Here, we explored ACE2 as a genetic determinant for SARS-CoV-2 infection and COVID-19 symptomatology. Each human genome encodes two alleles of ACE2, which encodes the cell entry receptor for SARS-CoV-2. Here, we determined whether naturally occurring human ACE2 (hACE2) polymorphisms in the human population affect SARS-CoV-2 infection and the severity of COVID-19 symptoms. ACE2 variants S19P, I21V, E23K, K26R, K31R, N33I, H34R, E35K, and T92I showed increased virus infection compared to wild-type ACE2; thus, these variants could increase the risk for COVID-19. In contrast, variants D38V, Y83H, I468V, and N638S showed reduced infection, indicating a potential protective effect. hACE2 variants K26R and T92I increased infection by three-fold without changing the levels of ACE2 on the surface of the cells, suggesting that these variants may increase the risk of severe COVID-19. On the contrary, hACE2 variants D38V and Y83H decreased SARS-CoV-2 infection by four- and ten-fold, respectively, without changing surface expression, suggesting that these variants may protect against severe COVID-19. Remarkably, all protective hACE2 Polymorphisms were found almost exclusively in Asian populations, which may provide a partial explanation for the low COVID-19 mortality rates in Asian countries. Thus, hACE2 polymorphisms may modulate susceptibility to SARS-CoV-2 in the host and partially account for the differences in severity of COVID-19 among different ethnic groups.     

Insights into disparities observed with COVID-19

The onset of human disease by infection with SARS-CoV-2 causing COVID-19 has revealed risk factors for disease severity. There are four identified factors that put one at high risk for infection and/or mortality creating a disparity: age, co-morbidities, race/ethnicity and gender. Data indicate that the older a person is, and/or the presence of obesity and diabetes, cardiovascular disease and chronic kidney disease place one at higher risk for COVID-19. In the United States, specific race/ethnicities, particularly African Americans and Native Americans, are strong COVID-19 risk components. Male gender has also emerged as a severity risk factor. For age and racial/ethnicities, the accumulation of health co-morbidities is common precipitating mechanisms. In particular, underlying socio-economic structures in the United States likely drive development of co-morbidities, putting affected populations at higher risk for severe COVID-19. Sudden cardiac death triggered by a common sodium channel variant in African Americans with COVID-19 has not been evaluated as a cause for racial disparity. There is no evidence that racial/ethnic differences for COVID-19 are caused by ABO blood groups, use of angiotensin-converting enzyme (ACE) inhibitors or from amino acid substitutions in the SARS-CoV-2 spike protein. There is growing evidence that androgen-enabled expression of ACE2 receptors and the serine protease TMPRSS2, two permissive elements engaging the SARS-CoV-2 spike protein for infection, may contribute to severe COVID-19 in men. Overall, COVID-19 has generated disparities for who is infected and the severity of that infection. Understanding the mechanisms for the disparity will help nullify the differences in risk for COVID-19.     

Severe SARS-CoV-2 Infection in a Cat with Hypertrophic Cardiomyopathy

Coronavirus disease 19 (COVID-19), has claimed millions of human lives worldwide since the emergence of the zoonotic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in China in December 2019. Notably, most severe and fatal SARS-CoV-2 infections in humans have been associated with underlying clinical conditions, including diabetes, hypertension and heart diseases. Here, we describe a case of severe SARS-CoV-2 infection in a domestic cat (Felis catus) that presented with hypertrophic cardiomyopathy (HCM), a chronic heart condition that has been described as a comorbidity of COVID-19 in humans and that is prevalent in domestic cats. The lung and heart of the affected cat presented clear evidence of SARS-CoV-2 replication, with histological lesions similar to those observed in humans with COVID-19 with high infectious viral loads being recovered from these organs. The study highlights the potential impact of comorbidities on the outcome of SARS-CoV-2 infection in animals and provides important information that may contribute to the development of a feline model with the potential to recapitulate the clinical outcomes of severe COVID-19 in humans.     

Alterations of the gut microbiota in coronavirus disease 2019 and its therapeutic potential

The coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) poses a serious threat to global health. SARS-CoV-2 infects host cells primarily by binding to angiotensin-converting enzyme 2, which is coexpressed in alveolar type 2 cells and gut epithelial cells. It is known that COVID-19 often presents with gastrointestinal symptoms and gut dysbiosis, mainly characterized by an increase in opportunistic pathogens and a decrease in beneficial commensal bacteria. In recent years, multiple studies have comprehensively explored gut microbiota alterations in COVID-19 and highlighted the clinical correlation between dysbiosis and COVID-19. SARS-CoV-2 causes gastrointestinal infections and dysbiosis mainly through fecal-oral transmission and the circulatory and immune pathways. Studies have shown that the gut microbiota and its metabolites can regulate the immune response and modulate antiviral effects. In addition, the gut microbiota is closely related to gastrointestinal symptoms, such as diarrhea, a common gastrointestinal symptom among COVID-19. Therefore, the contribution of the gut microbiota in COVID-19 should not be overlooked. Strategies targeting the gut microbiota via probiotics, prebiotics and fecal microbiota transplantation should be considered to treat this patient population in the future. However, the specific alterations and mechanisms as well as the contributions of gut microbiota in COVID-19 should be urgently further explored.     

SARS-CoV-2 Infection Hospitalization Rate and Infection Fatality Rate Among the Non-Congregate Population in Connecticut

BackgroundInfection fatality rate and infection hospitalization rate, defined as the proportion of deaths and hospitalizations, respectively, of the total infected individuals, can estimate the actual toll of coronavirus disease 2019 (COVID-19) on a community, as the denominator is ideally based on a representative sample of a population, which captures the full spectrum of illness, including asymptomatic and untested individuals.ObjectiveTo determine the COVID-19 infection hospitalization rate and infection fatality rate among the non-congregate population in Connecticut between March 1 and June 1, 2020.MethodsThe infection hospitalization rate and infection fatality rate were calculated for adults residing in non-congregate settings in Connecticut prior to June 2020. Individuals with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) antibodies were estimated using the seroprevalence estimates from the recently conducted Post-Infection Prevalence study. Information on total hospitalizations and deaths was obtained from the Connecticut Hospital Association and the Connecticut Department of Public Health, respectively.ResultsPrior to June 1, 2020, nearly 113,515 (90% confidence interval [CI] 56,758-170,273) individuals were estimated to have SARS-CoV-2 antibodies, and there were 7792 hospitalizations and 1079 deaths among the non-congregate population. The overall COVID-19 infection hospitalization rate and infection fatality rate were estimated to be 6.86% (90% CI, 4.58%-13.72%) and 0.95% (90% CI, 0.63%-1.90%), respectively, and there was variation in these rate estimates across subgroups; older people, men, non-Hispanic Black people, and those belonging to 2 of the counties had a higher burden of adverse outcomes, although the differences between most subgroups were not statistically significant.ConclusionsUsing representative seroprevalence estimates, the overall COVID-19 infection hospitalization rate and infection fatality rate were estimated to be 6.86% and 0.95%, respectively, among community residents in Connecticut.     

Influence of COVID-19 pandemic and related quarantine procedures on metabolic risk

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has changed the lives of many people across the globe. In addition to the effect of the virus on the biological functions in those infected individuals, many countries have launched government policy with additional impact of these quarantine procedures on the metabolic health of many people worldwide. This mini-review aimed to highlight current evidence regarding the influence of metabolic health due to these quarantine procedures including decrease in physical activity, changes in unhealthy eating habits, increase in stress, and provide recommendations of healthy lifestyle during COVID-19 pandemic.