No abstract

The coronavirus disease 2019 (COVID-19) pandemic, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has attracted increasing worldwide attention (1). Obesity commonly aggravates the severity of respiratory diseases, but it is currently not known whether obese patients are also more likely to have greater COVID-19 severity of illness. We investigated the association between obesity and COVID-19 severity of illness among patients with laboratoryconfirmed SARS-CoV-2 infection. We enrolled adult patients with COVID-19 from three hospitals in China between 17 January 2020 and 11 February 2020. Seventy-five patients were diagnosed as obese (i.e., case subjects). We randomly matched each case subject with one control subject (nonobese) by sex (1:1) and age (65 years). The cohort thus comprised 150 patients with COVID-19. The study protocol was approved by local ethics committees of the three hospitals.

Risk of severe illness from COVID-19 in patients with metabolic dysfunctionassociated fatty liver disease and increased fibrosis scores A recent study reported that patients with severe COVID-19 were more likely to have non-alcoholic fatty liver disease (NAFLD) compared with those with non-severe COVID-19 illness. 1 However, the prognosis of NAFLD (recently renamed metabolic dysfunction-associated fatty liver disease (MAFLD) 2) is determined by the severity of liver fibrosis. 3 4 We therefore postulated that patients with MAFLD with increased noninvasive liver fibrosis scores are at higher risk of severe illness from COVID-19. We studied 310 patients with laboratoryconfirmed COVID-19 who were consecutively hospitalised at four sites in Zhejiang Province, China, between January and February 2020. Some of these patients (n=150) have been included in a prior study examining the association between obesity and COVID-19 severity. 5 Patients with viral hepatitis, excessive alcohol consumption, chronic pulmonary diseases or active cancers were excluded. Clinical and laboratory data were collected at hospital admission. All patients were screened for hepatic steatosis by computed tomography and subsequently diagnosed as MAFLD. 6 The originally validated cut-points for fibrosis-4 (FIB-4) index and NAFLD fibrosis score (NFS) were used to categorise liver fibrosis probability as low, intermediate or high. 7 COVID-19 severity was classified as severe and non-severe. 8 The study protocol was approved by the local ethics committees of the four hospitals. In our cohort of 310 confirmed cases of COVID-19, 94 (30.3%) patients had MAFLD. As shown in table 1, patients with MAFLD with intermediate or high FIB-4 scores were more likely to be older, obese, have diabetes and have higher NFS, higher liver enzymes, higher C reactive protein, as well as lower levels of lymphocyte count, platelet count, triglycerides and high-density lipoprotein cholesterol compared with their counterparts with low FIB-4 score or those without MAFLD. Notably, the severity

No abstract

CD8 + T cells (TCD8) confer protective immunity against many infectious diseases, suggesting that microbial TCD8 determinants are promising vaccine targets. Nevertheless, current T cell antigen identification approaches do not discern which epitopes drive protective immunity during active infection -information that is critical for the rational design of TCD8-targeted vaccines. We employed a proteomics-based approach for large-scale discovery of naturally processed determinants derived from a complex pathogen, vaccinia virus (VACV), that are presented by the most frequent representatives of four major HLA class I supertypes. Immunologic characterization revealed that many previously unidentified VACV determinants were recognized by smallpox-vaccinated human peripheral blood cells in a variegated manner. Many such determinants were recognized by HLA class I-transgenic mouse immune TCD8 too and elicited protective TCD8 immunity against lethal intranasal VACV infection. Notably, efficient processing and stable presentation of immune determinants as well as the availability of naive TCD8 precursors were sufficient to drive a multifunctional, protective TCD8 response. Our approach uses fundamental insights into T cell epitope processing and presentation to define targets of protective TCD8 immunity within human pathogens that have complex proteomes, suggesting that this approach has general applicability in vaccine sciences.

We declare no competing interests.Please refer to the accompanying ICMJE disclosure forms for further details.Authors' contributions DJ, EQ, JX, and DZ treated the patients. DJ, GC, YW and GL processed statistical data and drafted the manuscript. DJ and GL had the idea for and designed the study.

The outbreak of coronavirus disease 2019 (COVID‐19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), has been recently declared a pandemic by the World Health Organization. In addition to its acute respiratory manifestations, SARS‐CoV‐2 may also adversely affect other organ systems. To date, however, there is a very limited understanding of the extent and management of COVID‐19‐related conditions outside of the pulmonary system. This narrative review provides an overview of the current literature about the extrapulmonary manifestations of COVID‐19 that may affect the urinary, cardiovascular, gastrointestinal, hematological, hematopoietic, neurological, or reproductive systems. This review also describes the current understanding of the extrapulmonary complications caused by COVID‐19 to improve the management and prognosis of patients with COVID‐19.

Background and AimCoronavirus disease 2019 (COVID‐19) has attracted increasing worldwide attention. While diabetes is known to aggravate COVID‐19 severity, it is not known whether nondiabetic patients with metabolic dysfunction are also more prone to more severe disease. The association of metabolic associated fatty liver disease (MAFLD) with COVID‐19 severity in nondiabetic patients was investigated here.MethodsThe study cohort comprised 65 patients with (i.e. cases) and 65 patients without MAFLD (i.e. controls). Each case was randomly matched with one control by sex (1:1) and age (±5 years). The association between the presence of MAFLD (as exposure) and COVID‐19 severity (as the outcome) was assessed by binary logistic regression analysis.ResultsIn nondiabetic patients with COVID‐19, the presence of MAFLD was associated with a four‐fold increased risk of severe COVID‐19; the risk increased with increasing numbers of metabolic risk factors. The association with COVID‐19 severity persisted after adjusting for age, sex, and coexisting morbid conditions.ConclusionHealth‐care professionals caring for nondiabetic patients with COVID‐19 should be cognizant of the increased likelihood of severe COVID‐19 in patients with MAFLD.