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SARS-CoV-2 proteins

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    Elevated HScore is Associated with Poor Clinical Outcomes in COVID-19 MESHD, Even in the Absence of Secondary Hemophagocytic Lymphohistiocytosis MESHD.

    Authors: Rafael Benavente; Camila Peña M.D.; Allyson Cid M.D.; Nicolás Cabello M.D.; Pablo Bustamante M.D.; Marco Álvarez M.D.; Elizabeth Henríquez M.D.; Andrés Soto M.D.; Érika Rubilar M.D.

    doi:10.1101/2021.01.26.21249335 Date: 2021-01-26 Source: medRxiv

    Introduction: Patients with Coronavirus Disease 2019 MESHD ( COVID-19 MESHD) frequently experience a hyperinflammatory syndrome MESHD, that leads to unfavorable outcomes. This condition resembles Secondary Hemophagocytic Lymphohistiocytosis MESHD (sHLH) described in neoplastic, rheumatic MESHD and other infectious diseases MESHD. However, it has not been prospectively studied on these patients. A scoring system (HScore) has been validated for sHLH, and recently proposed to evaluate hyperinflammation in COVID-19 MESHD. Methods: 143 patients aged [≥]18 years admitted because of COVID-19 MESHD were enrolled in a prospective, single-center, cohort study. HScore was calculated within the 72 hours since admission. The incidence of sHLH during hospitalization was evaluated. Additionally, the relationship between HScore [≥]130 points and either the requirement of mechanical ventilation or 60-days mortality was explored. Results: The median age of enrolled patients was 57 (21-100), and 63.6% were male. The median HScore was 96 (33-169). One patient was diagnosed with sHLH (incidence 0,7%), due to a HScore of 169. After adjusting for age, sex, comorbidities and obesity MESHD, HScore [≥]130 was independently associated with the composite clinical outcome (HR 2.13, p=0.022). Conclusion: sHLH is not frequent among COVID-19 MESHD patients. HScore can efficiently predict the risk for poor outcomes.

    COVID-19 MESHD cytokines and the hyperactive immune response: Synergism of TNF-α HGNC and IFN-γ HGNC in triggering inflammation, tissue damage, and death

    Authors: Evan Peter Williams; Lillian Zalduondo; Colleen Beth Jonsson; Alex R Schuurman; Jan Verhoeff; Saskia D van Asten; Hetty J Bontkes; Siebe G Blok; Janwillem Duitman; Harm Jan Bogaard; Leo Heunks; Rene Lutter; Tom van der Poll; Juan J Garcia Vallejo; Qiqi Cao; Fangjin Chen; Yuqing Chen; Xuelian Cheng; Guohong Deng; Wenyu Ding; Yingmei Feng; Rui Gan; Chuang Guo; Shuai He; Chen Jiang; Juanran Liang; Yi-Min Li; Jun Lin; Yun Ling; Haofei Liu; Jianwei Liu; Nianping Liu; Yang Liu; Meng Luo; Qiang Ma; Qibing Song; Wujianan Sun; Gaoxiang Wang; Feng Wang; Ying Wang; Xiaofeng Wen; Qian Wu; Xiaowei Xie; Xinxin Xiong; Xudong Xing; Hao Xu; Chonghai Yin; Dongdong Yu; Kezhuo Yu; Biao Zhang; Tong Zhang; Jincun Zhao; Peidong Zhao; Jianfeng Zhou; Wei Zhou; Sujuan Zhong; Xiaosong Zhong; Shuye Zhang; Lin Zhu; Ping Zhu; Bing Zou; Jiahua Zou; Zengtao Zuo; Fan Bai; Xi Huang; Xiuwu Bian; Penghui Zhou; Qinghua Jiang; Zhiwei Huang; Jin-Xin Bei; Lai Wei; Xindong Liu; Tao Cheng; Xiangpan Li; Fu-Sheng Wang; Hongyang Wang; Bing Su; Kun Qu; Xiaoqun Wang; JieKai Chen; Ronghua Jin; Zemin Zhang

    doi:10.1101/2020.10.29.361048 Date: 2020-10-29 Source: bioRxiv

    The COVID-19 MESHD COVID-19 MESHD pandemic has caused significant morbidity and mortality. Currently, there is a critical shortage of proven treatment options and an urgent need to understand the pathogenesis of multi-organ failure MESHD and lung damage MESHD. Cytokine storm is associated with severe inflammation MESHD and organ damage during COVID-19 MESHD. However, a detailed molecular pathway defining this cytokine storm is lacking, and gaining mechanistic understanding of how SARS-CoV-2 elicits a hyperactive inflammatory response is critical to develop effective therapeutics. Of the multiple inflammatory cytokines produced by innate immune cells during SARS-CoV-2 infection MESHD, we found that the combined production of TNF- and IFN-{gamma} specifically induced inflammatory cell death MESHD, PANoptosis, characterized by gasdermin-mediated pyroptosis, caspase-8 HGNC-mediated apoptosis, and MLKL HGNC-mediated necroptosis. Deletion of pyroptosis, apoptosis, or necroptosis mediators individually was not sufficient to protect against cell death. However, cells deficient in both RIPK3 HGNC and caspase-8 HGNC or RIPK3 HGNC and FADD HGNC were resistant to this cell death. Mechanistically, the STAT1 HGNC/ IRF1 HGNC axis activated by TNF- and IFN-{gamma} co-treatment induced iNOS for the production of nitric oxide. Pharmacological and genetic deletion of this pathway inhibited pyroptosis, apoptosis, and necroptosis in macrophages. Moreover, inhibition of PANoptosis protected mice from TNF- and IFN-{gamma}-induced lethal cytokine shock MESHD that mirrors the pathological symptoms of COVID-19 MESHD. In vivo neutralization of both TNF- and IFN-{gamma} in multiple disease models associated with cytokine storm showed that this treatment provided substantial protection against not only SARS-CoV-2 infection MESHD, but also sepsis MESHD, hemophagocytic lymphohistiocytosis MESHD, and cytokine shock models, demonstrating the broad physiological relevance of this mechanism. Collectively, our findings reveal that blocking the COVID-19 MESHD cytokine-mediated inflammatory cell death MESHD signaling pathway identified in this study may benefit patients with COVID-19 MESHD or other cytokine storm-driven syndromes by limiting inflammation MESHD and tissue damage. The findings also provide a molecular and mechanistic description for the term cytokine storm. Additionally, these results open new avenues for the treatment of other infectious and autoinflammatory diseases MESHD and cancers MESHD where TNF- and IFN-{gamma} synergism play key pathological roles.

    Percentage HScore confirms low incidence of secondary haemophagocytic lymphohistiocytosis in hospitalised COVID-19 MESHD patients

    Authors: Michael R Ardern-Jones; Matthew Stammers; Hang T.T. Phan; Florina Borca; Anastasia Koutalopoulou; Ying Teo; James Batchelor; Trevor Smith; Andrew Duncombe

    doi:10.1101/2020.10.19.20214015 Date: 2020-10-21 Source: medRxiv

    Objective: It has been assumed that a significant proportion of COVID-19 MESHD patients show evidence of hyperinflammation of which secondary haemophagocytic lymphohistiocytosis MESHD (sHLH) is the most severe manifestation. To facilitate diagnosis of sHLH the HScore has been developed and validated. We set out to examine the prevalence of sHLH-like hyperinflammation in COVID-19 MESHD. Methods: We retrospectively examined HScore parameters in 626 COVID-19 MESHD cases admitted to our institute of which 567 were suitable for analysis and compared these to a cohort of confirmed infection associated sHLH cases. To account for missing data, we calculated the maximum possible HScore of the recorded parameters (%HScore). Results: Early measurement of HScore parameters (day -1 to 4 from diagnosis) strongly predicted the %HScore over the course of the admission (p <0.0001). The retrospective cohort of sHLH showed significantly higher %HScores as compared to COVID-19 MESHD (median 73.47 vs 18.13 respectively, p <0.0001). The overall prevalence of individuals with an 80% probability of sHLH in our COVID-19 MESHD cohort was 1.59% on admission and only rose to 4.05% during the whole disease course. In the small cohort with scores suggestive of sHLH, there was no excess mortality compared with the whole cohort. %HScores were higher in younger patients (p<0.0001) and did not reliably predict outcome at any cut-off value (AUROC 0.533, p=0.211; OR 0.99). Conclusion: Surprisingly, these findings show that sHLH-type hyperinflammation is not prevalent in COVID-19 MESHD, and %HScores do not predict outcome. Therefore, new algorithms are required to optimise case selection for clinical trials of targeted anti-inflammatory interventions.

    Continuous extracorporeal treatments in a dialysis patient with COVID-19 MESHD

    Authors: Yoshihito Nihei; Hajime Nagasawa; Yusuke Fukao; Masao Kihara; Seiji Ueda; Tomohito Gohda; Yusuke Suzuki

    doi:10.21203/rs.3.rs-63251/v2 Date: 2020-08-20 Source: ResearchSquare

    The coronavirus disease 2019 MESHD ( COVID-19 MESHD) pandemic is now a major global health threat. More than half a year have passed since the first discovery of severe acute respiratory syndrome coronavirus-2 MESHD (SARS-CoV2), no effective treatment has been established especially in intensive care unit. Inflammatory cytokine storm caused by SARS-CoV-2 infection MESHD has been reported to play a central role in COVID-19 MESHD; therefore, treatments for suppressing cytokines, including extracorporeal treatments, are considered to be beneficial. However, until today the efficacy of removing cytokines by extracorporeal treatments in patients with COVID-19 MESHD is unclear. Herein, we report our experience with a 66-year-old male patient undergoing maintenance peritoneal dialysis who became critically ill with COVID-19 MESHD and underwent several extracorporeal treatment approaches including plasma exchange, direct hemoperfusion using a polymyxin B-immobilized fiber column and continuous hemodiafiltration. Though the patient developed acute respiratory distress syndrome MESHD ( ARDS MESHD) repeatedly and subacute cerebral infarction MESHD and finally died for respiratory failure MESHD on day 30 after admission, these attempts appeared to dampen the cytokine storm based on the observed decline in serum IL-6 HGNC levels and were effective against ARDS MESHD and secondary haemophagocytic lymphohistiocytosis MESHD. This case suggests the significance of timely initiation of extracorporeal treatment approaches in critically ill MESHD patients with COVID-19 MESHD.

    Deciphering the state of immune silence in fatal COVID-19 MESHD patients

    Authors: Pierre Bost; Francesco De Sanctis; Stefania Cane; Stefano Ugel; Katia Donadello; Monica Castellucci; David Eyal; Alessandra Fiore; Cristina Anselmi; Roza Maria Barouni; Rosalinda Trovato; Simone Caligola; Alessia Lamolinara; Manuela Iezzi; Federica Facciotti; Anna Rita Mazzariol; Davide Gibellini; Pasquale De Nardo; Evelina Tacconelli; Leonardo Gottin; Enrico Polati; Benno Schwikowski; Ido Amit; Vincenzo Bronte

    doi:10.1101/2020.08.10.20170894 Date: 2020-08-13 Source: medRxiv

    Since the beginning of the SARS-CoV-2 pandemic, COVID-19 MESHD has appeared as a unique disease with unconventional tissue and systemic immune features. While COVID-19 MESHD severe forms share clinical and laboratory aspects with various pathologies such as hemophagocytic lymphohistiocytosis MESHD, sepsis MESHD or cytokine release syndrome, their exact nature remains unknown. This is severely impeding the ability to treat patients facing severe stages of the disease. To this aim, we performed an in-depth, single-cell RNA-seq analysis of more than 150.000 immune cells isolated from matched blood samples and broncho- alveolar MESHD lavage fluids of COVID-19 MESHD patients and healthy controls, and integrated it with clinical, immunological and functional ex vivo data. We unveiled an immune signature of disease severity that correlated with the accumulation of naive lymphoid cells in the lung and an expansion and activation of myeloid cells in the periphery. Moreover, we demonstrated that myeloid-driven immune suppression is a hallmark of COVID-19 MESHD evolution and arginase 1 HGNC expression is significantly associated with monocyte immune regulatory features. Noteworthy, we found monocyte and neutrophil immune suppression loss associated with fatal clinical outcome in severe pa-tients. Additionally, our analysis discovered that the strongest association of the patients clinical outcome and immune phenotype is the lung T cell response. We found that patients with a robust CXCR6 HGNC+ effector memory T cell response have better outcomes. This result is line with the rs11385942 COVID-19 MESHD risk allel, which is in proximity to the CXCR6 HGNC gene and suggest effector memory T MESHD cell are a primary feature in COVID-19 MESHD patients. By systemically quantifying the viral landscape in the lung of severe patients, we indeed identified Herpes-Simplex-Virus 1 (HSV-1) as a potential opportunistic virus in COVID-19 MESHD patients. Lastly, we observed an unexpectedly high SARS-CoV-2 viral load in an immuno-compromised patient, allowing us to study the SARS-CoV-2 in-vivo life cycle. The development of myeloid dysfunctions and the impairment of lymphoid MESHD arm establish a condition of immune paralysis MESHD that supports secondary bacteria and virus infection MESHD and can progress to immune silence in patients facing death MESHD.

    The Association of HScore Parameters with Severe COVID-19 MESHD: a Systematic Review and Meta-Analysis

    Authors: Elham Roshandel; Mohammad Hossein Kazemi; Bentolhoda Kuhestani Dehaghi; Hossein Bonakchi; Sayeh Parkhideh; Mahshid Mehdizadeh; Abbas Hajifathali

    doi:10.21203/rs.3.rs-54490/v1 Date: 2020-08-06 Source: ResearchSquare

    Several reports associated the severe Coronavirus disease-2019 (s COVID-19 MESHD) with secondary-haemophagocytic lymphohistiocytosis MESHD ( sHLH MESHD) and proposed the HScore table for s COVID-19 MESHD patients. We conducted a meta-analysis to found the possible association of HScore parameters with severity in COVID-19 MESHD patients. Systematic search was performed in Medline (PubMed), EMBASE, and Cochrane databases using all HScore and COVID-19 MESHD keywords. The records were screened based on inclusion/exclusion criteria. Random/fixed-effect models were employed. The pooled mean differences were estimated for continuous parameters. The pooled odds-ratio was estimated for fever MESHD. Eighteen studies met the criteria and included in the meta-analysis (2459 patients). Significant higher levels of leukocyte, neutrophil, aspartate-transaminase ( AST HGNC), ferritin, and fibrinogen HGNC, as well as lower level of lymphocyte, platelet, and hemoglobin were found in s COVID-19 MESHD patients compared to non-severe ones. Fever MESHD was nearly associated with 2 times increased odds of s COVID-19 MESHD (p-value = 0.051). Lymphopenia MESHD, thrombocytopenia MESHD, hypohemoglobinemia, hyperferritinemia, high levels of AST HGNC, and fever MESHD are common features of both s COVID-19 MESHD and HLH. However, leukocytosis MESHD, neutrophilia, and hyperfibrinogenemia found in s COVID-19 MESHD contrast with HScore. Conclusively, HScore parameters could be risk factors for the severity of COVID-19 MESHD. However, some parameters’ roles are contradictory, suggesting further investigation and a new way of HScore interpretation for s COVID-19 MESHD patients.

    A network-informed analysis of SARS-CoV-2 and hemophagocytic lymphohistiocytosis genes' interactions points to Neutrophil Extracellular Traps as mediators of thrombosis in COVID-19 MESHD

    Authors: Jun Ding; David Earl Hostallero; Mohamed Reda El Khili; Gregory J Fonseca; Simon Milette; Nuzha Noorah; Myriam Guay-Belzile; Jonathan Spicer; Noriko Daneshtalab; Martin Sirois; Karine Tremblay; Amin Emad; Simon Rousseau

    doi:10.1101/2020.07.01.20144121 Date: 2020-07-02 Source: medRxiv

    Abnormal coagulation MESHD and an increased risk of thrombosis MESHD are features of severe COVID-19 MESHD, with parallels proposed with hemophagocytic lymphohistiocytosis MESHD ( HLH MESHD), a life-threating condition associated with hyperinflammation. The presence of HLH MESHD was described in severely ill patients during the H1N1 influenza epidemic, presenting with pulmonary vascular thrombosis MESHD. We tested the hypothesis that genes causing primary HLH MESHD regulate pathways linking pulmonary thromboembolism MESHD to the presence of SARS-CoV-2 using novel network-informed computational algorithms. This approach led to the identification of Neutrophils Extracellular Traps (NETs) as plausible mediators of vascular thrombosis MESHD in severe COVID-19 MESHD in children and adults. Taken together, the network-informed analysis led us to propose the following model: the release of NETs in response to inflammatory signals acting in concert with SARS-CoV-2 damage MESHD the endothelium and direct platelet-activation promoting abnormal coagulation MESHD leading to serious complications of COVID-19 MESHD. The underlying hypothesis is that genetic and/or environmental conditions that favor the release of NETs may predispose individuals to thrombotic MESHD complications of COVID-19 MESHD due to an increase risk of abnormal coagulation MESHD. This would be a common pathogenic mechanism in conditions including autoimmune/infectious diseases, hematologic and metabolic disorders MESHD.

    Cytokine release syndrome is not usually caused by secondary hemophagocytic lymphohistiocytosis in a cohort of 19 critically ill COVID-19 MESHD patients

    Authors: Georg Lorenz; Philipp Moog; Quirin Bachmann; Paul La Rosee; Heike Schneider; Michaela Schlegl; Christoph Spinner; Uwe Heemann; Roland M Schmid; Hana Algül; Tobias Lahmer; Wolfgang Huber; Christoph Schmaderer

    doi:10.21203/rs.3.rs-31847/v1 Date: 2020-05-27 Source: ResearchSquare

    Background: Severe COVID-19 MESHD associated respiratory failure MESHD, poses the one challenge of our days. Assessment and treatment of COVID-19 MESHD associated hyperinflammation may be key to improve outcomes. It was speculated that in subgroups of patients secondary hemophagocytic lymphohistiocytosis MESHD (sHLH) or cytokine release syndrome (CRS) with features of macrophage activation syndrome MESHD might drive severe disease trajectories. If confirmed, profound immunosuppressive therapy would be a rationale treatment approach.Methods: Over a median observation period of 11 (IQR: 8; 16) days, 19 consecutive confirmed severe COVID-19 MESHD-patients admitted to our intensive-care-unit were tested for presence of sHLH by two independent experts. HScores and 2004-HLH diagnostic criteria were assessed. Patients were grouped according to short-term clinical courses: discharge from ICU versus ongoing ARDS or death MESHD at time of analysis.Results: The median HScore at admission was 157 (IQR: 98;180), without the key clinical triad of HLH, i.e. progressive cytopenia MESHD, persistent fever MESHD and organomegaly MESHD. Independent expert chart review revealed the absence of sHLH in all cases. No patient reached more than 3/6 of modified HLH 2004 criteria. Nevertheless, patients presented hyperinflammation with peripheral neutrophilic signatures (neutrophil/lymphocyte-ratio>3.5). The latter best paralleled their short-term clinical courses, with declining relative neutrophil numbers prior to extubation (4.4, [IQR: 2.5;6.3]; n=8) versus those with unfavourable courses (7.6, [IQR: 5.2;31], n=9).Conclusion: Our study rules out virus induced sHLH as the leading cause of most severe- COVID-19 MESHD trajectories. Instead, an associated innate neutrophilic hyperinflammatory response or virus-associated-CRS appears dominant in patients with an unfavourable clinical course. Therapeutic implications are discussed.

    Pathophysiology of SARS-CoV-2: targeting of endothelial cells renders a complex disease with thrombotic microangiopathy and aberrant immune response. The Mount Sinai COVID-19 MESHD autopsy experience

    Authors: Clare Bryce; Zachary Grimes; Elisabet Pujadas; Sadhna Ahuja; Mary Beth Beasley; Randy Albrecht; Tahyna Hernandez; Aryeh Stock; Zhen Zhao; Mohamed Al Rasheed; Joyce Chen; Li Li; Diane Wang; Adriana Corben; Kenneth Haines; William Westra; Melissa Umphlett; Ronald E Gordon; Jason Reidy; Bruce Petersen; Fadi Salem; MariaIsabel Fiel; Siraj M El Jamal; Nadejda M Tsankova; Jane Houldsworth; Zarmeen Mussa; Wen-Chun Liu; Brandon Veremis; Emilia Sordillo; Melissa Gitman; Michael Nowak; Rachel Brody; Noam Harpaz; Miriam Merad; Sacha Gnjatic; Ryan Donnelly; Patricia Seigler; Calvin Keys; Jennifer Cameron; Isaiah Moultrie; Kae-Lynn Washington; Jacquelyn Treatman; Robert Sebra; Jeffrey Jhang; Adolfo Firpo; John Lednicky; Alberto Paniz-Mondolfi; Carlos Cordon-Cardo; Mary Fowkes

    doi:10.1101/2020.05.18.20099960 Date: 2020-05-22 Source: medRxiv

    BACKGROUND Severe Acute Respiratory Syndrome Coronavirus-2 MESHD (SARS-CoV-2) and its associated clinical syndrome COVID-19 MESHD are causing overwhelming morbidity and mortality around the globe, disproportionately affecting New York City. A comprehensive, integrative autopsy series that advances the mechanistic discussion surrounding this disease process is still lacking. METHODS Autopsies were performed at the Mount Sinai Hospital on 67 COVID-19 MESHD positive patients and data from the clinical records were obtained from the Mount Sinai Data Warehouse. The experimental design included a comprehensive microscopic examination carried out by a team of expert pathologists, along with transmission electron microscopy, immunohistochemistry, RNA in situ hybridization, as well as immunology and serology assays. RESULTS Laboratory results of our COVID-19 MESHD cohort show elevated inflammatory markers, abnormal coagulation values, and elevated cytokines IL-6 HGNC, IL-8 HGNC and TNF HGNC. Autopsies revealed large pulmonary emboli MESHD in four cases. We report microthrombi in multiple organ systems including the brain, as well as conspicuous hemophagocytosis MESHD and a secondary hemophagocytic lymphohistiocytosis-like syndrome MESHD in many of our patients. We provide electron microscopic, immunofluorescent and immunohistochemical evidence of the presence of the virus and the ACE2 HGNC receptor in our samples. CONCLUSIONS We report a comprehensive autopsy series of 67 COVID-19 MESHD positive patients revealing that this disease, so far conceptualized as a primarily respiratory viral illness MESHD, also causes endothelial dysfunction, a hypercoagulable state, and an imbalance of both the innate and adaptive immune responses. Novel findings reported here include an endothelial phenotype of ACE2 HGNC in selected organs, which correlates with clotting abnormalities and thrombotic microangiopathy MESHD, addressing the prominent coagulopathy and neuropsychiatric symptoms MESHD. Another original observation is that of macrophage activation syndrome MESHD, with hemophagocytosis MESHD and a hemophagocytic lymphohistiocytosis-like disorder MESHD, underlying the microangiopathy MESHD and excessive cytokine release. We discuss the involvement of critical regulatory pathways.

    SARS-CoV-2 Infection MESHD Associated Hemophagocytic Lymphohistiocytosis: An autopsy series with clinical and laboratory correlation.

    Authors: Andrey Prilutskiy; Michael Kritselis; Artem Shevtsov; Ilyas Yambayev; Charitha Vadlamudi; Qing Zhao; Yachana Kataria; Shayna Sarosiek; Adam Lerner; John Mark Sloan; Karen Quillen; Eric Burks

    doi:10.1101/2020.05.07.20094888 Date: 2020-05-12 Source: medRxiv

    Background: A subset of COVID-19 MESHD patients exhibit clinical features of cytokine storm. However, clinicopathologic features diagnostic of hemophagocytic lymphohistiocytosis MESHD ( HLH MESHD) have not been reported. Pathologic studies to date have largely focused on the pulmonary finding of diffuse alveolar damage MESHD (DAD). To this aim, we study the reticuloendothelial organs of four consecutive patients dying of COVID-19 MESHD and correlate with clinical and laboratory parameters to detect HLH MESHD. Methods: Autopsies restricted to chest and abdomen were performed on four patients who succumbed to COVID-19 MESHD. Spleen, liver, and multiple pulmonary hilar/mediastinal lymph nodes were sampled in all cases. Bone marrow was obtained by rib squeeze in a subset of cases. Routine H&E staining as well as immunohistochemical staining for CD163 HGNC was performed to detect hemophagocytosis. Clinical and laboratory results from pre-mortem blood samples were used to calculate H-scores. Findings: All four cases demonstrated DAD within the lungs. Three of the four cases had histologic evidence of hemophagocytosis within pulmonary hilar/mediastinal lymph nodes. One case showed hemophagocytosis in the spleen but none showed hemophagocytosis in liver MESHD or bone marrow. Lymphophagocytosis was the predominant form of hemophagocytosis observed. One patient showed diagnostic features of HLH MESHD with an H-score of 217 while a second patient was likely HLH MESHD with a partial H-score of 145 due to missing triglyceride level. Both patients exhibited high fever and early onset rise in serum ferritin; however, neither bicytopenia, pancytopenia MESHD, nor hypofibrinogenemia were observed in either. The remaining two patients had H-scores of 131 and 96. Interpretation: This is the first report of SARS-CoV-2 associated HLH MESHD. Identification of HLH MESHD in a subset of patients with severe COVID-19 MESHD will inform clinical trials of therapeutic strategies.

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