Gender differences in patients with COVID-19: focus on severity and mortality. Feldstein LR, Rose EB, Horwitz SM, Collins JP, Newhams MM, Son MBF, Newburger JW, Kleinman LC, Heidemann SM, Martin AA, Singh AR, Li S, Tarquinio KM, Jaggi P, Oster ME, Zackai SP, Gillen J, Ratner AJ, Walsh RF, Fitzgerald JC, Keenaghan MA, Alharash H, Doymaz S, Clouser KN, Giuliano JS, Gupta A, Parker RM, Maddux AB, Havalad V, Ramsingh S, Bukulmez H, Bradford TT, Smith LS, Tenforde MW, Carroll CL, Riggs BJ, Gertz SJ, Daube A, Lansell A, Coronado Munoz A, Hobbs CV, Marohn KL, Halasa NB, Patel MM, Randolph AG. Ou X, Liu Y, Lei X, Li P, Mi D, Ren L, Guo L, Guo R, Chen T, Hu J, Xiang Z, Mu Z, Chen X, Chen J, Hu K, Jin Q, Wang J, Qian Z. Increasing evidence also suggests the emergence of an associated multisystem inflammatory condition with similar features to Kawasaki disease and toxic shock syndrome in a small subset of pediatric patients (24, 26, 34, 44, 67, 113). 13, 938837. The neurological manifestations of COVID-19 have not been of much focus in the literature, but a few published reports are concerning. SARS-CoV-2 viral entry has been described in detail elsewhere (138). ACE2 is expressed in the kidney, and although previous studies suggested absence of viral particles in postmortem renal specimens from SARS patients (27), electron microscopic examination of 26 postmortem COVID-19 patients demonstrated direct virulence in tubular epithelium and podocytes (126). Aloysius MM, Thatti A, Gupta A, Sharma N, Bansal P, Goyal H. COVID-19 presenting as acute pancreatitis. Gebhard C, Regitz-Zagrosek V, Neuhauser HK, Morgan R, Klein SL. The https:// ensures that you are connecting to the Federal government websites often end in .gov or .mil. Probing the biological basis of the novel virus and evolutionary spread of the COVID-19 disease it causes, a panel of UC San Diego biologists gathered for a special Authors Zhengnan Cen 1 , Bingqing Lu 1 , Yongyan Ji 1 , Jian Chen 1 , Yongqian Liu 1 , Jiakui Jiang 1 , Xue Li 2 , Xiang Li 3 Affiliations A recent, large, multi-center U.S. study of 186 patients who met the broad CDC criteria for MIS-C reported 92% of patients had at least four laboratory results indicating inflammation, including but not limited to elevated CRP and ferritin, lymphocytopenia, neutrophilia, hypoalbuminemia, thrombocytopenia, anemia, as well as elevated D-dimer and fibrinogen (44). Bethesda, MD 20894, Web Policies Wrapp D, Wang N, Corbett KS, Goldsmith JA, Hsieh CL, Abiona O, Graham BS, McLellan JS. Elevations in troponin and brain natriuretic peptide were also observed in the majority of patients (44). government site. FOIA WebThe coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is a highly contagious enveloped positive-strand RNA virus that causes respiratory diseases, fever, and severe pneumonia in humans (13). In WebTo further elucidate the mechanism of COVID-19 severity, we conducted differential expression analysis between moderate disease versus severe disease group in ncMono. Pancreatic injury has also been reported in patients with COVID-19. Here, we review the current literature and summarize key proposed mechanisms of COVID-19 pathophysiological progression (FIGURE 1). The pyrin inflammasome in health and disease. This study, however, is limited by the lack of information regarding whether hospital admission was due to COVID-19 illness or pregnancy-related conditions, complicating interpretation (38). An understanding of the complex and likely multifactorial pathophysiological mechanisms behind kidney failure in COVID-19 is thus needed for early recognition and appropriate treatment selection. No conflicts of interest, financial or otherwise, are declared by the author(s). Viral-mediated cell death causes release of various damage-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs), which are believed to be recognized by pattern-recognition receptors on alveolar macrophages and endothelial cells. Like, check this out -- Rizzo, E. Ivermectin, antiviral properties and COVID-19: a possible new mechanism of action. In particular, IL-6 has emerged as a candidate treatment target due to its robust association with disease progression. The association of GI manifestations with disease severity is not well described, with many conflicting results reported (25, 139, 154). Eroshenko N, Gill T, Keaveney MK, Church GM, Trevejo JM, Rajaniemi H. Implications of antibody-dependent enhancement of infection for SARS-CoV-2 countermeasures. Hyperglycemia, hypertriglyceridemia, and acute pancreatitis in COVID-19 infection: clinical implications. Traditional Chinese medicine theory Liver biochemistries in hospitalized patients with COVID-19. The evidence behind these proposals are based on previous experience with similar coronaviruses, as well as clinical characteristics, laboratory testing, and postmortem pathological analysis of COVID-19 patients around the world. Inciardi RM, Lupi L, Zaccone G, Italia L, Raffo M, Tomasoni D, Cani DS, Cerini M, Farina D, Gavazzi E, Maroldi R, Adamo M, Ammirati E, Sinagra G, Lombardi CM, Metra M. Cardiac involvement in a patient with Coronavirus disease 2019 (COVID-19). Following host cell binding, viral and cell membranes fuse, enabling the virus to enter into the cell (89). A recent meta-analysis identified 24 studies, including a total of 624 pediatric cases with PCR-confirmed COVID-19, and reported common laboratory abnormalities in mild and severe disease. In addition to age, emerging clinical and epidemiological data suggest sex-specific differences in the clinical characteristics and case-to-fatality ratio of COVID-19, with worse prognosis observed in males (66, 92). The trinity of COVID-19: immunity, inflammation and intervention. Mao L, Jin H, Wang M, Hu Y, Chen S, He Q, Chang J, Hong C, Zhou Y, Wang D, Miao X, Li Y, Hu B. Neurologic manifestations of hospitalized patients with Coronavirus Disease 2019 in Wuhan, China, Possible link between anosmia and COVID-19: sniffing out the truth. Nevertheless, the exact contribution of direct viral immune cell infection is unknown and highly debated (155). Henry BM, De Oliveira MHS, Benoit S, Plebani M, Lippi G. Hematologic, biochemical and immune biomarker abnormalities associated with severe illness and mortality in coronavirus disease 2019 (COVID-19): A meta-analysis. Severe acute respiratory syndrome and the innate immune responses: modulation of effector cell function without productive infection. Gtzinger F, Santiago-Garca B, Noguera-Julin A, Lanaspa M, Lancella L, Cal Carducci FI, Gabrovska N, Velizarova S, Prunk P, Osterman V, Krivec U, Lo Vecchio A, Shingadia D, Soriano-Arandes A, Melendo S, Lanari M, Pierantoni L, Wagner N, LHuillier AG, Heininger U, Ritz N, Bandi S, Krajcar N, Rogli S, Santos M, Christiaens C, Creuven M, Buonsenso D, Welch SB, Bogyi M, Brinkmann F, Tebruegge M, Pfefferle J, Zacharasiewicz A, Berger A, Berger R, Strenger V, Kohlfrst DS, Zschocke A, Bernar B, Simma B, Haberlandt E, Thir C, Biebl A, Vanden Driessche K, Boiy T, Van Brusselen D, Bael A, Debulpaep S, Schelstraete P, Pavic I, Nygaard U, Glenthoej JP, Heilmann Jensen L, Lind I, Tistsenko M, Uustalu , Buchtala L, Thee S, Kobbe R, Rau C, Schwerk N, Barker M, Tsolia M, Eleftheriou I, Gavin P, Kozdoba O, Zsigmond B, Valentini P, Ivakeviciene I, Ivakevicius R, Vilc V, Schlvinck E, Rojahn A, Smyrnaios A, Klingenberg C, Carvalho I, Ribeiro A, Starshinova A, Solovic I, Falcn L, Neth O, Minguell L, Bustillo M, Gutirrez-Snchez AM, Guarch Ibez B, Ripoll F, Soto B, Ktz K, Zimmermann P, Schmid H, Zucol F, Niederer A, Buettcher M, Cetin BS, Bilogortseva O, Chechenyeva V, Demirjian A, Shackley F, McFetridge L, Speirs L, Doherty C, Jones L, McMaster P, Murray C, Child F, Beuvink Y, Makwana N, Whittaker E, Williams A, Fidler K, Bernatoniene J, Song R, Oliver Z, Riordan A; ptbnet COVID-19 Study Group . A team of Russian researchers has uncovered the mechanisms behind the emergence of new and dangerous coronavirus variants, such as Alpha, Delta, biochemistry, study of the chemical substances and processes that occur in plants, animals, and microorganisms and of the changes they undergo during WebCoronavirus disease 2019 (COVID-19) vaccines can protect people from the infection; however, the action mechanism of vaccine-mediated metabolism remains unclear. The urgent need to appropriately identify these patients has led the World Health Organization (WHO) and other regulatory bodies to develop a preliminary case definition known as Multisystem Inflammatory Disorder in Children and adolescents (MIS-C) (142a). In total, these processes foster an increased secretion of proinflammatory cytokines and chemokines, such as IL-6, type II interferon (IFN), monocyte chemoattractant protein 1 (MCP1), and interferon gamma-induced protein 10 (IP-10), as well as subsequent pulmonary recruitment of immune cells, including macrophages and dendritic cells. the contents by NLM or the National Institutes of Health. The pathophysiological mechanisms behind key events in the progression from mild to severe disease remain unclear, warranting further investigation to inform therapeutic decisions. The nuances of age-related immune response appear to play a role, with increasing disease severity observed in older populations (82). Characterization of key events in COVID-19 disease pathophysiological progression. In addition, direct viral infection of immune cells such as monocytes and macrophages have been proposed to contribute to dysregulated immune response, as has been observed in SARS (23, 52, 136). Most of our knowledge on COVID-19 pathophysiological progression has been observed through a laboratory lens, inferring potential causative mechanisms from observed biomarker trends across patients. Bertram S, Glowacka I, Mller MA, Lavender H, Gnirss K, Nehlmeier I, Niemeyer D, He Y, Simmons G, Drosten C, Soilleux EJ, Jahn O, Steffen I, Phlmann S. Cleavage and activation of the severe acute respiratory syndrome coronavirus spike protein by human airway trypsin-like protease. From our preliminary understanding, immunomodulatory therapies are likely to be equally or more effective than solely targeting viral host cell entry. Initial studies have reported varying incidences (315%) of AKI during illness (20, 22, 155). TWC India. This condition appears to be associated with prevalent cutaneous manifestations as well as significant GI symptoms. Comorbidity and its impact on 1590 patients with COVID-19 in China: a nationwide analysis. Richardson S, Hirsch JS, Narasimhan M, Crawford JM, McGinn T, Davidson KW, Barnaby DP, Becker LB, Chelico JD, Cohen SL, Cookingham J, Coppa K, Diefenbach MA, Dominello AJ, Duer-Hefele J, Falzon L, Gitlin J, Hajizadeh N, Harvin TG, Hirschwerk DA, Kim EJ, Kozel ZM, Marrast LM, Mogavero JN, Osorio GA, Qiu M, Zanos TP; the Northwell COVID-19 Research Consortium . COVID-19 Coronavirus origins: genome analysis suggests two viruses may have combined Mar 20, 2020. Once the nucleocapsid is deposited into the cytoplasm of the host cell, the RNA genome is replicated and translated into structural and accessory proteins. However, whether furin-like protease-mediated cleavage is required for SARS-CoV-2 host entry has yet to be determined. Impact of sex and gender on COVID-19 outcomes in Europe, Maternal and neonatal response to COVID-19. The mechanisms of the increase in the incidence of diabetes have been unclear, and there has been discussion on whether the increase results from a direct effect of SARS-CoV-2 infection or other simultaneously altered environmental factors, says Professor Mikael Knip, who headed the study. sharing sensitive information, make sure youre on a federal Some cases of cutaneous manifestations in adult COVID-19 patients have been reported, although varying incidence among patients has been noted (68, 111, 120). Zou X, Chen K, Zou J, Han P, Hao J, Han Z. Single-cell RNA-seq data analysis on the receptor ACE2 expression reveals the potential risk of different human organs vulnerable to 2019-nCoV infection. However, a significant subset of patients present with severe clinical manifestations, requiring life-supporting treatment (51). A multicenter European study of children with PCR-confirmed SARS-CoV-2 infection also reported that 8% of pediatric patients required ICU admission, 4% required mechanical ventilation, 3% required inotropic support, and <1% required extracorporeal membrane oxygenation (49). Dong Y, Mo X, Hu Y, Qi X, Jiang F, Jiang Z, Tong S. Epidemiology of COVID-19 among children in China, Coronavirus infections and Type 2 diabetes-shared pathways with therapeutic implications. Martnez-Rojas MA, Vega-Vega O, Bobadilla NA. In t Complement-mediated pulmonary tissue damage and microvascular injury have been observed in small cohorts with severe COVID-19 (85). official website and that any information you provide is encrypted Indeed, Hoffman and colleagues demonstrated that S-protein priming by transmembrane serine protease 2 (TMPRSS2), which may be substituted by cathepsin B/L, is required to facilitate SARS-CoV-2 entry into host cells (58). Few case reports have observed acute pancreatitis in COVID-19 patients (2, 45, 54), although it is expected to be quite uncommon. This could in part be explained by the viruss It is also important to note that immune-cell infiltration can lead to the excessive secretion of proteases and reactive oxygen species, fostering further damage and hyperinflammation (130). Therefore, Current literature suggests seroconversion in COVID-19 patients occurs ~714 days post symptom onset (12). 1) Potential mechanisms of COVID-pain (SARS-CoV-2/COVID-19-induced pain) (A) ACE2/RAS pathway and the direct virus-induced damage. Khalil A, Kalafat E, Benlioglu C, OBrien P, Morris E, Draycott T, Thangaratinam S, Le Doare K, Heath P, Ladhani S, von Dadelszen P, Magee LA. Gu J, Gong E, Zhang B, Zheng J, Gao Z, Zhong Y, Zou W, Zhan J, Wang S, Xie Z, Zhuang H, Wu B, Zhong H, Shao H, Fang W, Gao D, Pei F, Li X, He Z, Xu D, Shi X, Anderson VM, Leong ASY. Accessibility Trippella G, Ciarci M, Ferrari M, Buzzatti C, Maccora I, Azzari C, Dani C, Galli L, Chiappini E. COVID-19 in pregnant women and neonates: a systematic review of the literature with quality assessment of the studies. 1Molecular Medicine, Research Institute, The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada, 2Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada, 3Department of Physiology, University of Toronto, Toronto, Ontario, Canada. Biological mechanisms for these neurological symptoms need to be investigated and may include both direct and indirect effects of the virus on the brain and spinal cord. Some authors have proposed this is due to direct exocrine damage, whereas others suggest it is likely resultant from the gastrointestinal symptoms observed in many COVID-19 patients (32). This review presents various potential pathophysiological mechanisms behind SARS-CoV-2 infection. 1) Potential mechanisms of COVID-pain (SARS-CoV-2/COVID-19-induced pain) (A) ACE2/RAS pathway and the direct virus-induced damage. Toscano G, Palmerini F, Ravaglia S, Ruiz L, Invernizzi P, Cuzzoni MG, Franciotta D, Baldanti F, Daturi R, Postorino P, Cavallini A, Micieli G. Guillain-Barr Syndrome associated with SARS-CoV-2. Notably, the cytokine concentrations observed in hospitalized COVID-19 patients are rarely elevated to the same extent as in secondary hemophagocytic lymphohistiocytosis and cytokine release syndrome following CAR-T cell treatment (64). Zhou F, Yu T, Du R, Fan G, Liu Y, Liu Z, Xiang J, Wang Y, Song B, Gu X, Guan L, Wei Y, Li H, Wu X, Xu J, Tu S, Zhang Y, Chen H, Cao B. FIGURE 3. Firstly, deformable convolution is used to extract features in the horizontal and vertical directions, respectively. Although currently available commercial serological assays do not provide information on whether SARS-CoV-2 antibodies confer immune protection, recent reports using specialized laboratory-based neutralization assays have observed a marked correlation between the levels of SARS-CoV-2 spike/receptor binding domain (RBD) antibodies and the neutralization capacity of patient sera, suggesting its potential beneficial role in clearance (3, 98, 103, 107, 160). Bohn MK, Lippi G, Horvath A, Sethi S, Koch D, Ferrari M, Wang C-B, Mancini N, Steele S, Adeli K. Molecular, serological, and biochemical diagnosis and monitoring of COVID-19: IFCC taskforce evaluation of the latest evidence. Gastrointestinal manifestations of SARS-CoV-2 infection and virus load in fecal samples from the Hong Kong cohort and systematic review and meta-analysis. Although the clinical and laboratory characteristics of COVID-19 patients have been well characterized, the pathophysiological mechanisms underlying disease severity and progression remain unclear. Guo T, Fan Y, Chen M, Wu X, Zhang L, He T, Wang H, Wan J, Wang X, Lu Z. Cardiovascular Implications of Fatal Outcomes of Patients with Coronavirus Disease 2019 (COVID-19). In addition to cytokine release and immune cell recruitment, another potential mechanism that could contribute to successful viral clearance is antibody neutralization. Meng Y, Wu P, Lu W, Liu K, Ma K, Huang L, Cai J, Zhang H, Qin Y, Sun H, Ding W, Gui L, Wu P. Sex-specific clinical characteristics and prognosis of coronavirus disease-19 infection in Wuhan, China: a retrospective study of 168 severe patients, Pathological inflammation in patients with COVID-19: a key role for monocytes and macrophages, Host cell entry of Middle East respiratory syndrome coronavirus after two-step, furin-mediated activation of the spike protein. Traditional Chinese medicine theory-driven natural drug research and development (TCMT-NDRD) is a feasible method to address this issue as the traditional Chinese medicine formulae have been shown Blocking or inhibiting these processing enzymes may serve as a potential antiviral target (130). Although much progress has been made in our understanding of the mechanisms underlying SARS-CoV-2 invasion, additional research is needed to delineate exactly how cleavage of the S proteins by TMPRSS2 confers viral particle entry as well as how S-protein cleavage by membrane proteases contributes to viral penetration. Coronavirus fulminant myocarditis saved with glucocorticoid and human immunoglobulin. Characterization of spike glycoprotein of SARS-CoV-2 on virus entry and its immune cross-reactivity with SARS-CoV. In a more recent study, hyperlipasemia was reported in 12.1% of COVID-19 patients (n = 71) but was not associated with worse outcome (91). Specifically, in a study of 417 COVID-19 patients, 76.3% had abnormal liver tests, and 21.5% had liver injury during hospitalization (14). Conclusion Evidence on why persistent symptoms occur is still limited, and available studies are heterogeneous. Biological mechanisms for these neurological symptoms need to be investigated and may include both direct and indirect effects of the virus on the brain and spinal cord. Wang F, Wang H, Fan J, Zhang Y, Wang H, Zhao Q. Pancreatic injury patterns in patients with Coronavirus Disease 19 pneumonia. Diabetic ulcers (DUs) are one of the most serious complications of diabetes mellitus. Diabetic ulcers (DUs) are one of the most serious complications of diabetes mellitus. SARS-CoV-2 infection in pregnancy: a systematic review and meta-analysis of clinical features and pregnancy outcomes. That variant, classified as XBB.1.16 by the World Health Organization, was designated as a variant under monitoring by the organization last month. The most common GI manifestations reported in both adult and especially pediatric COVID-19 patients include diarrhea, nausea, vomiting, and abdominal pain (16, 133, 157). They describe settings where transmission of the COVID-19 virus spreads more easily: Crowded places; Close-contact settings, especially where people have Importantly, it is possible that the neurological manifestations of COVID-19 could be a result of hypoxia, respiratory, and/or metabolic acidosis at end-stage disease (6). The condition is typically treated with either an infusion of antibodies, known as immunoglobulin therapy, or plasma exchange, in which a patients blood plasma is removed and replaced. Larsen CP, Bourne TD, Wilson JD, Saqqa O, Sharshir MA. In addition to GI manifestations, several studies have reported elevated liver enzymes and higher rates of liver injury in patients with severe COVID-19. In a case study series of >2,000 children with suspected or confirmed COVID-19 in China, 5% of symptomatic children had dyspnea or hypoxemia, and only 0.6% progressed to ARDS or MOF (36). A more plausible mechanism behind liver dysfunction in COVID-19 is the observed systemic inflammatory response, as described previously, leading to cytotoxic T-cell-mediated necrosis and MOF. Xu X, Chen P, Wang J, Feng J, Zhou H, Li X, Zhong W, Hao P. Evolution of the novel coronavirus from the ongoing Wuhan outbreak and modeling of its spike protein for risk of human transmission. Clinical, laboratory and imaging features of COVID-19: A systematic review and meta-analysis. For example, Toll-like receptors (TLRs) recognize PAMPs in mostly the extracellular space, triggering induction of proinflammatory cytokine transcription factors such as NF-, as well as activating interferon regulatory factors that mediate the type I interferon-dependent antiviral response (122, 125). Received 2020 Jun 23; Revised 2020 Jul 7; Accepted 2020 Jul 7. coagulation, COVID-19, cytokine storm, multisystem organ failure, pathophysiolog. Severe acute respiratory syndrome Coronavirus 2-specific antibody responses in Coronavirus Disease 2019 patients. HHS Vulnerability Disclosure, Help Hasnain M, Pasha MF, Ghani I, Budiarto R. Protection challenges of pregnant women against vertical transmission during COVID-19 epidemic: a narrative review. M.K.B. reported that 17% of COVID-19 patients in their cohort (n = 52) had serologic evidence of exocrine pancreatic injury, defined as elevated amylase or lipase (140). Hadi A, Werge M, Kristiansen KT, Pedersen UG, Karstensen JG, Novovic S, Gluud LL. The emerging impasse of angiotensin blockade, Coronaviruses post-SARS: update on replication and pathogenesis. Jin JM, Bai P, He W, Wu F, Liu XF, Han DM, Liu S, Yang JK. It is thus hypothesized that the GI manifestations observed in COVID-19 are a result of SARS-CoV-2 infection of intestinal enterocytes and subsequent dysfunction in the ileum and colon (16). Chai X, Hu L, Zhang Y, Han W, Lu Z, Ke A, Zhou J, Shi G, Fang N, Fan J, Cai J, Fan J, Lan F. Specific ACE2 expression in cholangiocytes may cause liver damage after 2019-nCoV infection. Direct renal infection and damage presents one potential contributing mechanism. 4: dendritic cells phagocytose virus in the lungs, migrate to secondary lymphoid organs, and activate antigen-specific T cells, which travel to the lungs and destroy virally infected alveolar cells. Gadiparthi C, Bassi M, Yegneswaran B, Ho S, Pitchumoni CS. However, a recent report in Blood characterized bleeding as a significant cause of morbidity in COVID-19 patients, emphasizing the need for randomized trials on the benefit of escalated prophylaxis (1). The application of a functional dressing is a crucial step in DU treatment and is associated with the patient's recovery and prognosis. In brief, SARS-CoV-2 consists of four main structural glycoproteins: spike (S), membrane (M), envelope (E), and nucleocapsid (N). Overall, the predominant mechanism seems that encompassing SARS-CoV-2-induced endothelial damage fosters monocyte recruitment and activation, along with tissue factor exposure, which then activates blood coagulation. A new variant of COVID-19 starting to spread around the United States could be responsible for a new symptom that is unlike any weve seen with the virus so far. This work was supported by a Foundation Grant from the Canadian Institutes of Health Research (CIHR) (grant no. In most COVID-19 patients, the combined immune response of initial cytokine release and activation of antiviral interferon response followed by immune-cell recruitment should result in successful SARS-CoV-2 clearance from the lungs (FIGURE 2). Although hepatocytes have not been shown to exhibit high ACE2 expression, previous studies have demonstrated a high level of ACE2 expression in cholangiocytes, suggesting direct bile duct infection/damage as a potential cause of abnormal liver enzymes (17). Collapsing glomerulopathy in a patient with Coronavirus Disease 2019 (COVID-19). The involvement of the gastrointestinal (GI) tract and hepatic system in COVID-19 disease progression is being increasingly reported. Recruitment of neutrophils by activated endothelial cells can also synthesize and release multiple cytokines into the circulation, further accelerating this process (93). Presenting characteristics, comorbidities, and outcomes among 5700 patients hospitalized with COVID-19 in the New York City area. The cell uses the mRNA from the vaccine as the blueprint to build the SARS-CoV-2 spike protein. Liu F, Long X, Zhang B, Zhang W, Chen X, Zhang Z. ACE2 expression in pancreas may cause pancreatic damage after SARS-CoV-2 infection, Clinical features of COVID-19 in elderly patients: A comparison with young and middle-aged patients. However, despite evidence of mild COVID-19 in pregnant patients, a recent report by the CDC suggests pregnant women may be at higher risk for more severe outcomes, estimating a higher proportion of pregnant women with COVID-19 undergo hospitalization compared with nonpregnant women (38). Lei F, Liu YM, Zhou F, Qin JJ, Zhang P, Zhu L, Zhang XJ, Cai J, Lin L, Ouyang S, Wang X, Yang C, Cheng X, Liu W, Li H, Xie J, Wu B, Luo H, Xiao F, Chen J, Tao L, Cheng G, She ZG, Zhou J, Wang H, Lin J, Luo P, Fu S, Zhou J, Ye P, Xiao B, Mao W, Liu L, Yan Y, Liu L, Chen G, Li H, Huang X, Zhang BH, Yuan Y. Longitudinal association between markers of liver injury and mortality in COVID-19 in China, Functional assessment of cell entry and receptor usage for SARS-CoV-2 and other lineage B betacoronaviruses, Evidence for a common evolutionary origin of coronavirus spike protein receptor-binding subunits, Expression of the SARS-CoV-2 cell receptor gene ACE2 in a wide variety of human tissues, Cardiac troponin I in patients with coronavirus disease 2019 (COVID-19): Evidence from a meta-analysis, Laboratory abnormalities in patients with COVID-2019 infection, Defining the epidemiology of Covid-19 - Studies needed.
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