Evolution of SARS-CoV-2 Variants: Implications on Immune Escape, Vaccination, Therapeutic and Diagnostic Strategies.

The COVID-19 pandemic caused by SARS-CoV-2 is associated with a lower fatality rate than its SARS and MERS counterparts. However, the rapid evolution of SARS-CoV-2 has given rise to multiple variants with varying pathogenicity and transmissibility, such as the Delta and Omicron variants. Individuals with advanced age or underlying comorbidities, including hypertension, diabetes and cardiovascular diseases, are at a higher risk of increased disease severity. Hence, this has resulted in an urgent need for the development of better therapeutic and preventive approaches. This review describes the origin and evolution of human coronaviruses, particularly SARS-CoV-2 and its variants as well as sub-variants. Risk factors that contribute to disease severity and the implications of co-infections are also considered. In addition, various antiviral strategies against COVID-19, including novel and repurposed antiviral drugs targeting viral and host proteins, as well as immunotherapeutic strategies, are discussed. We critically evaluate strategies of current and emerging vaccines against SARS-CoV-2 and their efficacy, including immune evasion by new variants and sub-variants. The impact of SARS-CoV-2 evolution on COVID-19 diagnostic testing is also examined. Collectively, global research and public health authorities, along with all sectors of society, need to better prepare against upcoming variants and future coronavirus outbreaks.

Patterns of preschool children's screen time, parent-child interactions, and cognitive development in early childhood: a pilot study.

BACKGROUND: The primary objective of this study was to explore the feasibility of a virtual study protocol for a future longitudinal study, including recruitment, study measures, and procedures. The secondary objective was to examine preliminary hypotheses of associations, including 1) the correlations between total duration and patterns of screen time and cognitive development, and 2) the differences in quality of parent-child interactions for two screen-based tasks and a storybook reading task. METHODS: Participants included 44 children aged 3 years and their parents from Edmonton, Alberta and surrounding areas. Children's screen time patterns (i.e., type, device, content, context) were parental-reported using a 2-week online daily diary design. Children's cognitive development (i.e., working memory, inhibitory control, self-control, and language) was measured virtually through a recorded Zoom session. Parent-child interactions during three separate tasks (i.e., video, electronic game, and storybook reading) were also measured virtually through a separate recorded Zoom session (n = 42). The quality of the interactions was determined by the Parent-Child Interaction System (PARCHISY). Descriptive statistics, Intra-class correlations (ICC), Spearman's Rho correlations, and a one-way repeated measures ANOVA with a post-hoc Bonferroni test were conducted. RESULTS: All virtual protocol procedures ran smoothly. Most (70%) participants were recruited from four 1-week directly targeted Facebook ads. High completion rates and high inter-rater reliability in a random sample (Diary: 95% for 13/14 days; Cognitive development: 98% 3/4 tests, ICC > 0.93; Parent-child interactions: 100% for 3 tasks, Weighted Kappa ≥ 0.84) were observed for measures. Across cognitive development outcomes, medium effect sizes were observed for five correlations, with positive correlations observed with certain content (i.e., educational screen time) and negative associations observed for total screen time and certain types (show/movie/video viewing) and contexts (i.e., co-use). Medium and large effect sizes were observed for the differences in parent-child interaction quality between the three tasks. CONCLUSIONS: The virtual study protocol appeared feasible. Preliminary findings suggest it may be important to go beyond total duration and consider type, content, and context when examining the association between screen time and cognitive development. A future longitudinal study using this virtual protocol will be conducted with a larger and more generalizable sample.

Multiple-Inputs Convolutional Neural Network for COVID-19 Classification and Critical Region Screening From Chest X-ray Radiographs: Model Development and Performance Evaluation

Background The COVID-19 pandemic is becoming one of the largest, unprecedented health crises, and chest X-ray radiography (CXR) plays a vital role in diagnosing COVID-19. However, extracting and finding useful image features from CXRs demand a heavy workload for radiologists. Objective The aim of this study was to design a novel multiple-inputs (MI) convolutional neural network (CNN) for the classification of COVID-19 and extraction of critical regions from CXRs. We also investigated the effect of the number of inputs on the performance of our new MI-CNN model. Methods A total of 6205 CXR images (including 3021 COVID-19 CXRs and 3184 normal CXRs) were used to test our MI-CNN models. CXRs could be evenly segmented into different numbers (2, 4, and 16) of individual regions. Each region could individually serve as one of the MI-CNN inputs. The CNN features of these MI-CNN inputs would then be fused for COVID-19 classification. More importantly, the contributions of each CXR region could be evaluated through assessing the number of images that were accurately classified by their corresponding regions in the testing data sets. Results In both the whole-image and left- and right-lung region of interest (LR-ROI) data sets, MI-CNNs demonstrated good efficiency for COVID-19 classification. In particular, MI-CNNs with more inputs (2-, 4-, and 16-input MI-CNNs) had better efficiency in recognizing COVID-19 CXRs than the 1-input CNN. Compared to the whole-image data sets, the efficiency of LR-ROI data sets showed approximately 4% lower accuracy, sensitivity, specificity, and precision (over 91%). In considering the contributions of each region, one of the possible reasons for this reduced performance was that nonlung regions (eg, region 16) provided false-positive contributions to COVID-19 classification. The MI-CNN with the LR-ROI data set could provide a more accurate evaluation of the contribution of each region and COVID-19 classification. Additionally, the right-lung regions had higher contributions to the classification of COVID-19 CXRs, whereas the left-lung regions had higher contributions to identifying normal CXRs. Conclusions Overall, MI-CNNs could achieve higher accuracy with an increasing number of inputs (eg, 16-input MI-CNN). This approach could assist radiologists in identifying COVID-19 CXRs and in screening the critical regions related to COVID-19 classifications.

SARS-CoV-2 Non-Structural Proteins and Their Roles in Host Immune Evasion.

Coronavirus disease 2019 (COVID-19) has caused an unprecedented global crisis and continues to threaten public health. The etiological agent of this devastating pandemic outbreak is the severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2). COVID-19 is characterized by delayed immune responses, followed by exaggerated inflammatory responses. It is well-established that the interferon (IFN) and JAK/STAT signaling pathways constitute the first line of defense against viral and bacterial infections. To achieve viral replication, numerous viruses are able to antagonize or hijack these signaling pathways to attain productive infection, including SARS-CoV-2. Multiple studies document the roles of several non-structural proteins (NSPs) of SARS-CoV-2 that facilitate the establishment of viral replication in host cells via immune escape. In this review, we summarize and highlight the functions and characteristics of SARS-CoV-2 NSPs that confer host immune evasion. The molecular mechanisms mediating immune evasion and the related potential therapeutic strategies for controlling the COVID-19 pandemic are also discussed.

Deregulation of the Host Cell Cycle Induced by SARS‐CoV‐2 Nucleocapsid Protein

Introduction: The novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARSCoV2) is the causative agent responsible for the COVID-19 pandemic and has resulted in devastating impacts on global public health. The nucleocapsid (N) protein of other coronaviruses, such as SARS-CoV-1, have been previously implicated in the deregulation of the host cell cycle through interactions with cell cycle checkpoint proteins, Cyclin-Dependent Kinases (CDKs) or cyclins. In this study, we highlight the role of SARS-CoV-2 N-protein in modulating CDK expression, thereby, deregulating the host cell cycle. Methods: A549 cells were transfected with pCMV plasmids, harbouring the SARS-CoV-2 N-protein. Protein extracts of control and Nprotein transfected cells were electrophoresed on SDS-PAGE, transferred onto a nitrocellulose membrane and incubated with CDK2 and CDK4 antibodies. The blots were visualized and protein quantification was performed using ImageJ analysis. Results: Transfection of SARS-CoV-2 N resulted in differential expression of CDK2 and CDK4, which are key regulators that drive cell cycle progression through G0 or G1 phase into S phase. Notably, preliminary findings also demonstrate that N protein results in decreased CDK2 and CDK4 expression. Conclusion: The differential expression of CDKs caused by SARS-CoV-2 N-protein suggests its role in inducing cell cycle arrest at the S phase to facilitate SARS-CoV-2 replication. The results from this research may aid in future characterisation of the mechanisms for SARS-CoV-2-mediated cell cycle arrest, and contribute towards the development of novel antiviral strategies and therapies.

Studies on the Role of SARS-CoV-2 Nucleocapsid as an Interferon Antagonist

Introduction: The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), responsible for the coronavirus disease 2019 (COVID-19) pandemic, has resulted in significantly disruptive global impacts. Cytokine storm syndrome (CSS) can accompany SARSCoV2 infection, and involves the excessive release of pro-inflammatory cytokines that lead to acute respiratory distress syndrome (ARDS) in infected patients. Given the correlation between ARDS and poor patient prognosis, inflammatory pathways (e.g., interferon-1 (IFN-1)) would be a target area for antiviral development. Our preliminary results have demonstrated a direct correlation between the SARS-CoV-2 nucleocapsid (N) protein and host intracellular IFN-1 pathway components IRF3 and STAT1. Methods: A549 cells were transfected with pCMV-GFP vectors expressing N protein and harvested. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) and Western Blotting were performed. The membranes were then incubated with STAT-1, p-STAT1 and IRF3 antibodies and visualised. Protein content was quantified using ImageJ software. Results: Transfection with SARS-CoV-2 N was correlated with a decrease in intracellular IRF3 and reduced phosphorylation of STAT1, suggesting the involvement of N protein in the delayed IFN-1 response commonly observed in SARS-CoV-2 patients. These findings suggest that IRF3 and STAT1 may be part of the innate immune response affected by SARS-CoV-2 infection. Conclusion: Our results show that IRF3 and STAT1 are responsible for stimulating transcription of interferon signalling genes (ISGs). Future studies on SARS-CoV-2 N and its downstream effectors could provide further insight into the IFN-1 response during infection, and assist in future antiviral development strategies.

Repurposing Molnupiravir for COVID-19: The Mechanisms of Antiviral Activity.

Molnupiravir is a ß-d-N4-hydroxycytidine-5'-isopropyl ester (NHC) compound that exerts antiviral activity against various RNA viruses such as influenza, SARS, and Ebola viruses. Thus, the repurposing of Molnupiravir has gained significant attention for combatting infection with SARS-CoV-2, the etiological agent of COVID-19. Recently, Molnupiravir was granted authorization for the treatment of mild-to-moderate COVID-19 in adults. Findings from in vitro experiments, in vivo studies and clinical trials reveal that Molnupiravir is effective against SARS-CoV-2 by inducing viral RNA mutagenesis, thereby giving rise to mutated complementary RNA strands that generate non-functional viruses. To date, the data collectively suggest that Molnupiravir possesses promising antiviral activity as well as favorable prophylactic efficacy, attributed to its effective mutagenic property of disrupting viral replication. This review discusses the mechanisms of action of Molnupiravir and highlights its clinical utility by disabling SARS-CoV-2 replication, thereby ameliorating COVID-19 severity. Despite relatively few short-term adverse effects thus far, further detailed clinical studies and long-term pharmacovigilance are needed in view of its mutagenic effects.

Repurposing Molnupiravir for COVID-19: The Mechanisms of Antiviral Activity

Molnupiravir is a β-d-N4-hydroxycytidine-5′-isopropyl ester (NHC) compound that exerts antiviral activity against various RNA viruses such as influenza, SARS, and Ebola viruses. Thus, the repurposing of Molnupiravir has gained significant attention for combatting infection with SARS-CoV-2, the etiological agent of COVID-19. Recently, Molnupiravir was granted authorization for the treatment of mild-to-moderate COVID-19 in adults. Findings from in vitro experiments, in vivo studies and clinical trials reveal that Molnupiravir is effective against SARS-CoV-2 by inducing viral RNA mutagenesis, thereby giving rise to mutated complementary RNA strands that generate non-functional viruses. To date, the data collectively suggest that Molnupiravir possesses promising antiviral activity as well as favorable prophylactic efficacy, attributed to its effective mutagenic property of disrupting viral replication. This review discusses the mechanisms of action of Molnupiravir and highlights its clinical utility by disabling SARS-CoV-2 replication, thereby ameliorating COVID-19 severity. Despite relatively few short-term adverse effects thus far, further detailed clinical studies and long-term pharmacovigilance are needed in view of its mutagenic effects.

COVID-19 Related Stressors, Parent-Child Relationship, and Alcohol Use and Mental Health Profiles Among White and Hispanic/Latinx First-Year College Students.

Transitioning to college during the novel coronavirus disease 2019 (COVID-19) pandemic may increase risk for alcohol use and mental health problems. We examined how COVID-19 related stressors and parent-child relationships are independently and interactively associated with alcohol use and mental health profiles in a sample of first-year college students (N = 425, 34.8% Hispanic/Latinx; 74.9% female) who completed an online survey in October 2020. Latent profile analysis identified four profiles: well-adjusted (53.2%), mental health problems only (21.6%), alcohol use only (17.4%), and comorbid (7.8%). COVID-19 related stressful events increased risk of being in the alcohol use only and comorbid profiles, whereas COVID-19 related worries increased risk of being in the mental health problems only profile. Parent-child relationship quality lowered risk of being in the mental health problems only and the comorbid profiles. In addition, parent-child relationship quality moderated the role of COVID-19 related worries such that COVID-19 related worries were associated with lower odds of being in the comorbid profile when parent-child relationship quality was high but not when parent-child relationship quality was low. Strengthening parent-child relationship quality appears important for promoting college students' well-being.

Genetic characteristics and nucleic acid detection results of SARS-CoV-2 in 2297 clinical samples

Objective To analyze the genomics characteristics and nucleic acid detection results of the severe Acute respiratory syndrome coronavirus 2（SARS-CoV-2） in 2 297 clinical samples collected in January and February, 2020 in Laboratory of Microbiology of Changsha Municipal Center for Disease Control and Prevention. Methods Viral RNA of throat swabs or respiratory tract specimens of coronavirus disease 2019（COVID-19） suspected cases from January 19, 2020 to February 29, 2020 was extracted and SARS-CoV-2 nucleic acid was detected by real-time reverse transcription polymerase chain reaction.The full length genome of SARS-CoV-2 in positive samples was enriched by using viral genome capture kit and sequenced on Illumina MiSeq platform.The raw reads were mapped and aligned with SPAdes software v 3.13.0.Reference SARS-CoV-2 sequences were obtained from GISAID（https://www.gisaid.org） andviral genetic evolution and antigen variation were analyzed. Results A total of 215 SARS-Co V2-nucleic acid positive samples were identified from 2 297 clinical samples.Among the SARS-Co V2-positive samples, 110 were males and 105 were from females.The male to female ratio was 1.05∶1.The highest positive rate was among 40-<60 years old people（11.35%） and the lowest positive rate was in children under 6 years old（5.49%）.The peak of newly confirmed cases was in the 5 th week（January 26 to February 1, 2020） and then decreased.There was no newly positive case after February 25, 2020.Five SARS-Co V2-whole genome sequences were obtained and there were 4 to 6 nucleotide mutations compared to the Wuhan reference strain, and the homology was more than 99.90%.Most mutations occurred only once except C8782 T and T28144 C, indicating random mutations.Phylogenetic analysis revealed that the 5 sequences belonged to the L/B or S/A lineages and were highly homologous with strains prevalent in other provinces of China at the same time. Conclusions With the quick nucleic acid tests and quarantine measures, the SARS-Co V2-positive cases in Changsha began to decline after a 2-week increasing period, and there was no new confirmed cases 6 weeks later.The genomes of SARS-Co V-2 prevalent in Changsha are highly homology with the Wuhan strains in the early 2020 and no obvious mutation is found in the local pandemic period. Reset

Identification of COVID-19 Type Respiratory Disorders Using Channel State Analysis of Wireless Communications Links.

One deadly aspect of COVID-19 is that those infected can often be contagious before exhibiting overt symptoms. While methods such as temperature checks and sinus swabs have aided with early detection, the former does not always provide a reliable indicator of COVID-19, and the latter is invasive and requires significant human and material resources to administer. This paper presents a non-invasive COVID-19 early screening system implementable with commercial off-the-shelf wireless communications devices. The system leverages the Doppler radar principle to monitor respiratory-related chest motion and identifies breathing rates that indicate COVID-19 infection. A prototype was developed from software-defined radios (SDRs) designed for 5G NR wireless communications and system performance was evaluated using a robotic mover simulating human breathing, and using actual breathing, resulting in a consistent respiratory rate accuracy better than one breath per minute, exceeding that used in common medical practice.Clinical Relevance-This establishes the potential efficacy of wireless communications based radar for recognizing respiratory disorders such as COVID-19.

Repositioning Ivermectin for Covid-19 treatment: Molecular mechanisms of action against SARS-CoV-2 replication.

Ivermectin (IVM) is an FDA approved macrocyclic lactone compound traditionally used to treat parasitic infestations and has shown to have antiviral potential from previous in-vitro studies. Currently, IVM is commercially available as a veterinary drug but have also been applied in humans to treat onchocerciasis (river blindness - a parasitic worm infection) and strongyloidiasis (a roundworm/nematode infection). In light of the recent pandemic, the repurposing of IVM to combat SARS-CoV-2 has acquired significant attention. Recently, IVM has been proven effective in numerous in-silico and molecular biology experiments against the infection in mammalian cells and human cohort studies. One promising study had reported a marked reduction of 93% of released virion and 99.98% unreleased virion levels upon administration of IVM to Vero-hSLAM cells. IVM's mode of action centres around the inhibition of the cytoplasmic-nuclear shuttling of viral proteins by disrupting the Importin heterodimer complex (IMPα/ß1) and downregulating STAT3, thereby effectively reducing the cytokine storm. Furthermore, the ability of IVM to block the active sites of viral 3CLpro and S protein, disrupts important machinery such as viral replication and attachment. This review compiles all the molecular evidence to date, in review of the antiviral characteristics exhibited by IVM. Thereafter, we discuss IVM's mechanism and highlight the clinical advantages that could potentially contribute towards disabling the viral replication of SARS-CoV-2. In summary, the collective review of recent efforts suggests that IVM has a prophylactic effect and would be a strong candidate for clinical trials to treat SARS-CoV-2.

The Suppressor of Cytokine Signalling family of proteins and their potential impact on COVID-19 disease progression.

The family of Suppressor of Cytokine Signalling (SOCS) proteins plays pivotal roles in cytokine and immune regulation. Despite their key roles, little attention has been given to the SOCS family as compared to other feedback regulators. To date, SOCS proteins have been found to be exploited by viruses such as herpes simplex virus (HSV), hepatitis B virus (HBV), hepatitis C virus (HCV), Zika virus, respiratory syncytial virus (RSV), Ebola virus, influenza A virus (IAV) and SARS-CoV, just to name a few. The hijacking and subsequent upregulation of the SOCS proteins upon viral infection, suppress the associated JAK-STAT signalling activities, thereby reducing the host antiviral response and promoting viral replication. Two SOCS protein family members, SOCS1 and SOCS3 are well-studied and their roles in the JAK-STAT signalling pathway are defined as attenuating interferon (IFN) signalling upon viral infection. The upregulation of SOCS protein by SARS-CoV during the early stages of infection implies strong similarity with SARS-CoV-2, given their closely related genomic organisation. Thus, this review aims to outline the plausibility of SOCS protein inhibitors as a potential therapeutic regimen for COVID-19 patients. We also discuss the antagonists against SOCS protein to offer an overview on the previous 'successes' of SOCS protein inhibition in various viral infections that may portray possible clues for COVID-19 disease management.

SARS coronavirus outbreaks past and present-a comparative analysis of SARS-CoV-2 and its predecessors.

The Coronavirus Disease 2019 (COVID-19), a pneumonic disease caused by the SARS Coronavirus 2 (SARS-CoV-2), is the 7th Coronavirus to have successfully infected and caused an outbreak in humans. Genome comparisons have shown that previous isolates, the SARS-related coronavirus (SARSr-CoV), including the SARS-CoV are closely related, yet different in disease manifestation. Several explanations were suggested for the undetermined origin of SARS-CoV-2, in particular, bats, avian and Malayan pangolins as reservoir hosts, owing to the high genetic similarity. The general morphology and structure of all these viral isolates overlap with analogous disease symptoms such as fever, dry cough, fatigue, dyspnoea and headache, very similar to the current SARS-CoV-2. Chest CT scans for SARS-CoV-2, SARS-CoV and MERS-CoV reveal pulmonary lesions, bilateral ground-glass opacities, and segmental consolidation in the lungs, a common pathological trait. With greatly overlapping similarities among the previous coronavirus, the SARS-CoV, it becomes interesting to observe marked differences in disease severity of the SARS-CoV-2 thereby imparting it the ability to rapidly transmit, exhibit greater stability, bypass innate host defences, and increasingly adapt to their new host thereby resulting in the current pandemic. The most recent B.1.1.7, B.1.351 and P.1 variants of SARS-CoV-2, highlight the fact that changes in amino acids in the Spike protein can contribute to enhanced infection and transmission efficiency. This review covers a comparative analysis of previous coronavirus outbreaks and highlights the differences and similarities among different coronaviruses, including the most recent isolates that have evolved to become easily transmissible with higher replication efficiency in humans.

Drug Repositioning: New Approaches and Future Prospects for Life-Debilitating Diseases and the COVID-19 Pandemic Outbreak.

Traditionally, drug discovery utilises a de novo design approach, which requires high cost and many years of drug development before it reaches the market. Novel drug development does not always account for orphan diseases, which have low demand and hence low-profit margins for drug developers. Recently, drug repositioning has gained recognition as an alternative approach that explores new avenues for pre-existing commercially approved or rejected drugs to treat diseases aside from the intended ones. Drug repositioning results in lower overall developmental expenses and risk assessments, as the efficacy and safety of the original drug have already been well accessed and approved by regulatory authorities. The greatest advantage of drug repositioning is that it breathes new life into the novel, rare, orphan, and resistant diseases, such as Cushing's syndrome, HIV infection, and pandemic outbreaks such as COVID-19. Repositioning existing drugs such as Hydroxychloroquine, Remdesivir, Ivermectin and Baricitinib shows good potential for COVID-19 treatment. This can crucially aid in resolving outbreaks in urgent times of need. This review discusses the past success in drug repositioning, the current technological advancement in the field, drug repositioning for personalised medicine and the ongoing research on newly emerging drugs under consideration for the COVID-19 treatment.

Drug Repositioning: New Approaches and Future Prospects for Life-Debilitating Diseases and the COVID-19 Pandemic Outbreak

Traditionally, drug discovery utilises a de novo design approach, which requires high cost and many years of drug development before it reaches the market. Novel drug development does not always account for orphan diseases, which have low demand and hence low-profit margins for drug developers. Recently, drug repositioning has gained recognition as an alternative approach that explores new avenues for pre-existing commercially approved or rejected drugs to treat diseases aside from the intended ones. Drug repositioning results in lower overall developmental expenses and risk assessments, as the efficacy and safety of the original drug have already been well accessed and approved by regulatory authorities. The greatest advantage of drug repositioning is that it breathes new life into the novel, rare, orphan, and resistant diseases, such as Cushing"s syndrome, HIV infection, and pandemic outbreaks such as COVID-19. Repositioning existing drugs such as Hydroxychloroquine, Remdesivir, Ivermectin and Baricitinib shows good potential for COVID-19 treatment. This can crucially aid in resolving outbreaks in urgent times of need. This review discusses the past success in drug repositioning, the current technological advancement in the field, drug repositioning for personalised medicine and the ongoing research on newly emerging drugs under consideration for the COVID-19 treatment.

Manifestations of blood coagulation and its relation to clinical outcomes in severe COVID-19 patients: Retrospective analysis.

INTRODUCTION: Characteristics of blood coagulation and its relation to clinical outcomes in COVID-19 patients are still rarely reported. We aimed to investigate the blood coagulation function and its influences on clinical outcomes of patients with syndrome coronavirus 2 (SARS-CoV-2) infection. METHODS: A total of 71 severe patients with confirmed SARS-CoV-2 infection who were treated in Wuhan First Hospital from February 12 to March 20, 2020, were enrolled. The blood coagulation data in these patients and in 61 healthy controls were collected. The patients with COVID-19 were divided into two groups: the aggravated group and the nonaggravated group, respectively, basing on whether the patients' conditions turned to critically ill or not after admission. RESULTS: Compared with healthy controls, patients with COVID-19 had significant performances with coagulation dysfunction, including dramatically elevated values of FIB, PT, APTT, INR, FDP, and D-Dimers but markedly reduced AT value (P < .05). Importantly, more noteworthy coagulation disorders similar to the differences between patients and controls were found in the aggravated patients with conditions deterioration after admission than those in the nonaggravated patients without conditions deterioration (P < .05). Moreover, the aggravated patients possessed a longer hospital stay and a higher mortality compared with the nonaggravated patients (P < .001). The coagulation parameters of COVID-19 patients were widely and closely related to the indexes of liver function and inflammation (P < .05), indicating the coagulation dysfunction of these patients may be caused by liver injury and inflammatory storm. CONCLUSION: Severe patients with SARS-CoV-2 infection often possess coagulation dysfunction on admission. A certain correlation exists in coagulation disorder and adverse clinical outcome among severe COVID-19 patients.