Peter Sleight: visionary cardiologist and inspiring leader

Mervyn George Bishop/Fairfax Media/Getty Images Peter Sleight, a professor at Oxford University, helped to transform heart attack treatment and prevent cardiovascular disease with angiotensin converting enzyme inhibitors and statins. Isis methodology influenced the design of studies into other conditions, including the Recovery trial, which showed that dexamethasone reduces covid-19 mortality. [...]unlike many eminent men, he was able, endearingly, to laugh at himself—for example, when medical students lampooned him as Professor BA Flight after he had flown to Tokyo for the day. In the last 10 years of his life, he generated global media interest after demonstrating with his Italian colleague Luciano Bernardi that certain musical rhythms lowered blood pressure.

Renin-Angiotensin System and Sex Differences in COVID-19: A Critical Assessment.

The current epidemic of corona virus disease (COVID-19) has resulted in an immense health burden that became the third leading cause of death and potentially contributed to a decline in life expectancy in the United States. The severe acute respiratory syndrome-related coronavirus-2 binds to the surface-bound peptidase angiotensin-converting enzyme 2 (ACE2, EC 3.4.17.23) leading to tissue infection and viral replication. ACE2 is an important enzymatic component of the renin-angiotensin system (RAS) expressed in the lung and other organs. The peptidase regulates the levels of the peptide hormones Ang II and Ang-(1-7), which have distinct and opposing actions to one another, as well as other cardiovascular peptides. A potential consequence of severe acute respiratory syndrome-related coronavirus-2 infection is reduced ACE2 activity by internalization of the viral-ACE2 complex and subsequent activation of the RAS (higher ratio of Ang II:Ang-[1-7]) that may exacerbate the acute inflammatory events in COVID-19 patients and possibly contribute to the effects of long COVID-19. Moreover, COVID-19 patients present with an array of autoantibodies to various components of the RAS including the peptide Ang II, the enzyme ACE2, and the AT1 AT2 and Mas receptors. Greater disease severity is also evident in male COVID-19 patients, which may reflect underlying sex differences in the regulation of the 2 distinct functional arms of the RAS. The current review provides a critical evaluation of the evidence for an activated RAS in COVID-19 subjects and whether this system contributes to the greater severity of severe acute respiratory syndrome-related coronavirus-2 infection in males as compared with females.

A novel mouse model of COVID-19

OBJECTIVES/GOALS: Rodents are the most widely used experimental animals to study disease mechanisms due to their availability and cost-effectiveness. An international drive to investigate the pathophysiology of COVID-19 is inhibited by the resistance of rats and mice to SARS-CoV-2 infection. Our goal was to establish an appropriate small animal model. METHODS/STUDY POPULATION: To recreate the cytokine storm that is associated with COVID-19, we injected angiotensin converting enzyme 2 knockout (ACE2KO) mice (C57BI/6 strain) with lipopolysaccharide (LPS) intraperitoneally and measured the expression of multiple cytokines as a function of time and LPS dose. We then chose a minimum dose (500ug/kg) and time (3h) when multiple cytokines were elevated to measure lung injury scores using a point-counting technique on tissue sections stained with hematoxylin and eosin. The data are expressed as mean percentage of grid points lying within the peribronchial and superficial area in up to 20 fields. Percentage of peribronchial and superficial intrapulmonary hemorrhage, congestion, neutrophil infiltration and area of alveolar space were all assessed. RESULTS/ANTICIPATED RESULTS: Compared to the wildtype group (WT-G), the LPS-injected ACE2KO mice (LPS-G) exhibited a higher percentage of peribronchial intrapulmonary hemorrhage [(%): LPS-G, 10.56 ± 2.06 vs. WT-G, 5.59 ± 0.53;p DISCUSSION/SIGNIFICANCE: Establishing this novel mouse model of COVID-19 will facilitate studies investigating tissue-specific mechanisms of pathogenesis in this disease. This model can also be used to discover novel therapeutic targets and the design of clinical trials focusing on diagnostics, treatments and outcomes in COVID-19.

In silico phytochemical repurposing of natural molecules as entry inhibitors against RBD of the spike protein of SARS-CoV-2 using molecular docking studies

The receptor binding domain (RBD) of Spike-protein (S-protein) is responsible for virus entry via interaction with host protein ACE2 (angiotensin-converting enzyme 2), present on the cell surface of humans. Therefore, S-protein is an important target to block the entry of the SARS-CoV-2 into the cell for further growth. In the present study, phytochemical repurposing of natural molecules: narirutin, naringin, neohesperidin and hesperidin were performed against the RBD S-protein/ACE2 interface as well as the RBD of the S-protein using molecular docking. These natural molecules were found to have structural similarity to each other and had binding potential against the viral infections. It is first time reported here that the naringin and narirutin are having binding potential against both RBD S-protein/ACE2 interface and active site of RBD of S-protein using binding mode analysis. Hence, this study will open avenues for multitargeting similar natural molecules binding against the SARS-CoV-2 proteins as all reports are made in this single study.

Paying Attention to Circadian Rhythms in the Treatment of COVID-19

The bidirectional association between the circadian system and innate-adaptive immune functions has been highlighted in many investigations. Viruses are a submicroscopic infectious agent that activate the immune system after entering the human host cell. A novel virus, so-called Coronavirus Disease 2019 (COVID-19), which has recently emerged, is an infectious disease caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Previous investigations show that the factors that are strongly controlled by circadian rhythms, such as clock genes and melatonin, modulate the immune response and may, therefore, influence the healing processes of COVID-19. Moreover, the mechanism of COVID-19 shows that some host cell factors, such as an angiotensin-converting enzyme, exhibit daily rhythms. In this review, we explore key findings that show a link between circadian rhythms and viral infection. The results of these findings could be helpful for clinical and preclinical studies to discover a useful and highly effective treatment for eradicating the COVID-19 disease.

A Review on COVID-19: Primary Receptor, Endothelial Dysfunction, Related Comorbidities, and Therapeutics

Since December 2019, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has caused a global pandemic named coronavirus disease-19 (COVID-19) and resulted in a worldwide economic crisis. Utilizing the spike-like protein on its surface, the SARS-CoV-2 binds to the receptor angiotensin-converting enzyme 2 (ACE2), which highly expresses on the surface of many cell types. Given the crucial role of ACE2 in the renin–angiotensin system, its engagement by SARS-CoV-2 could potentially result in endothelial cell perturbation. This is supported by the observation that one of the most common consequences of COVID-19 infection is endothelial dysfunction and subsequent vascular damage. Furthermore, endothelial dysfunction is the shared denominator among previous comorbidities, including hypertension, kidney disease, cardiovascular diseases, etc., which are associated with an increased risk of severe disease and mortality in COVID-19 patients. Several vaccines and therapeutics have been developed and suggested for COVID-19 therapy. The present review summarizes the relationship between ACE2 and endothelial dysfunction and COVID-19, also reviews the most common comorbidities associated with COVID-19, and finally reviews several categories of potential therapies against COVID-19.

The role of angiotensin I converting enzyme insertion/deletion polymorphism in the severity and outcomes of COVID-19 patients.

The pandemic of coronavirus disease in 2019 has led to a global crisis. COVID-19 shows distinct clinical manifestations of the severity of symptoms. Numerous patients with no associated risk factors demonstrate acute respiratory distress syndrome (ARDS). The role of genetic factors in determining the severity and outcome of the disease remains unresolved. The purpose of this study was to see if a correlation exists between Angiotensin I Converting Enzyme (ACE) insertion/deletion (I/D) polymorphism and the severity of COVID-19 patients' symptoms. 120 COVID-19 patients admitted to Masih Daneshvari Hospital in Tehran with their consent to participate entered the study. Based on the World Health Organization classification, patients were divided into moderate and severe groups, which were primarily affected by O2 saturation levels. The effects of the patients' ACE insertion/deletion polymorphism, background disease, Angiotensin receptor blocker (ARB) drug consumption, and demographic parameters on the severity risk were calculated statistically. The ACE D allele was associated with an increased risk of disease severity (OR = 6.766, p = 0.012), but had no effect on mortality.

Angiotensin converting enzyme as a possible biomarker to predict effect of obstetric anesthesia on pregnant women with COVID-19 infection

We retrospectively investigated 68 parturients with or without COVID-19 undergone emergency cesarean section with combined spinal-epidural anesthesia(CSEA) from a single tertiary university hospital in Wuhan, China. The cases were divided into 2 groups: patients with COVID-19 pneumonia(Group 1) and cases without COVID-19 pneumonia(Group 2). The patients in Group 1 were later divided into 2 groups: patients with low-angiotensin converting enzyme(ACE)(Group 3) and patients with normal-ACE(Group 4). The ACE levels, blood pressure and anesthesia management between the patients of Group 1 and Group 2, Group 3 and Group 4 were recorded as the primary outcome. The secondary outcome included perioperative symptoms, laboratory parameters and vital signs. Compared with Group 2, the patients in Group 1 had different ACE level and lower blood pressure after CSEA. Compared with Group 4, the patients in Group 3 showed lower SBP after CSEA(127 vs. 130 mm Hg, p=0.028), accompanied with more partus matures and younger age(28 vs. 32 years, p=0.007). ACE may be a possible biomarker to predict the anesthesia effects on patients with COVID-19 infections undergoing emergency cesarean delivery.

A single centre retrospective analysis of new patients presented to the hepatology clinic with non-alcoholic fatty liver disease post-covid era

OP06 Table 1Demographics of patients Valid (n=) Missing (n=) Mean Std. Deviation Minimum Maximum Age (years) 134 0 55.522 15.111 17 87 Metabolic risk factors BMI in kg/m2 129 5 34.875 7.168 21.5 59.3 HbA1c (mmol/mol) 118 16 47.398 14.793 27 94 Total cholesterol (mmol/L) 119 15 4.646 1.195 1.9 7.4 Triglyceride level (mmol/L) 104 30 2.117 1.211 0.6 7.1 Blood tests AST U/L 116 18 48.621 36.672 14 318 ALT U/L 134 0 61.515 49.304 8 367 Bilirubin umol/L 134 0 11.261 9.398 3 59 Albumin g/L 133 1 44.12 4.624 21 53 Platelet count (x10*9/L) 134 0 229.343 83.631 23 509 INR 98 36 1.052 0.22 0.9 2.5 Fibrosis assessment Enhanced liver fibrosis (ELF) 16 118 9.671 0.754 8.31 11.06 Elastography (kPa) 79 55 10.944 7.049 2.5 39 CAP score 78 56 315.808 59.388 104 400 ConclusionOur study showed that patients with underlying metabolic risk factors were treated in 80% of cases. TE is not performed in all patients due to social isolation limitation imposed by covid-19 infection. In those who had TE;the index diagnosis of cirrhosis was seen in around 20% at the time of TE.

Association between single nucleotide polymorphism of human angiotensin-converting enzyme 2 gene locus and clinical severity of COVID-19

BackgroundCoronavirus disease 2019 (COVID-19) is a devastating pandemic-causing disease with a variable severity among populations. Genetic studies have pinpointed angiotensin-converting enzyme 2 (ACE2), a key enzyme for viral entry, for its possible linkage to the disease progression. The present study aimed to investigate the potential association between single nucleotide polymorphisms (SNPs) of human ACE2 gene with the severity and outcomes of COVID-19 for better patient management. MethodsIn this observational cross-sectional study, COVID-19 confirmed patients were classified into moderate and severe cases according to the “Ain Shams University Hospitals Pocket Guide for COVID-19 Diagnosis.” Genetic analysis of ACE2 SNP rs2048683 was carried out using a TaqMan assay with the real-time polymerase chain reaction (PCR) technique.ResultsAmong 90 confirmed COVID-19 patients, 78.9% (71/90) were classified as severe, and 21.1% (19/90) were classified as moderate. Laboratory biomarkers were significantly (P = 0.000) higher in the severe group than in the moderate group. Similarly, associated comorbidities such as hypertension were significant (P = 0.000) in the severe group, whereas asthma and deep venous thrombosis were significant in the moderate group (P = 0.007 and 0.006, respectively). Elevated serum ferritin level (odds ratio (OR) 162.589, 95% confidence interval (CI) 8.108–3260.293) and ACE2 rs2048683 genotype GG/G (OR 5.852, 95% CI 1.586–21.591) were both considered independent risk factors for severe disease.ConclusionThe findings of the present study provide preliminary evidence of an association between ACE2 rs2048683 SNPs and COVID-19 severity in the Egyptian population, which may inform the need for targeted management.

Angiotensin-converting enzyme-2 and interleukin-12 serum level as indicator to severity between COVID-19 patients

The Coronavirus, one of the most rapidly spreading respiratory viruses, caused a worldwide epidemic that killed about six million people. This led to the fast development of several vaccines and drugs to reduce disease severity and speed patient recovery. This study aimed to identify the serum levels of each of the angiotensin-converting enzyme-2 and interleukin-12 .The severity of infection in coronavirus COVID-19 patients was compared to immune levels of these cytokines and receptors in the different cases of COVID-19 patients. This case-control study included 90 blood samples from COVID-19 patients with ages between 15-80 years. Results revealed that the serum levels of both angiotensin-converting enzyme-2 ( ACE-2) and interleukin-12 (IL-12) were measured in COVID-19 patients and the results were compared using an independent T-test, it was found that their levels for interleukin-12 revealed a significant difference (P ≤0.05) in the serum levels of severe cases when compared with non-severe cases. There was an increase in the serum level of IL-12 in severe cases was 33.340 ng/L, in the serum level and in non-severe cases was 20.913 ng/L. ( P ≤0.000), and for angiotensin-converting enzyme-2 this study revealed a significant difference in ACE-2 serum levels in severe cases (P ≤0.05) when compared with the non-severe cases of patients with COVID 19. The serum level of ACE-2 in severe cases was 11.023 ng/ml, and in non-severe cases, it was 5.443ng/ml ( P ≤0.000). It was concluded that the emerging coronavirus works to create an immune storm represented by raising the serum levels of both ACE-2 and IL-12 that contribute to the damage to the alveoli in severely COV-19 patients.

PREVIOUS SARS-COV2 INFECTION, AGE AND FRAILTY PREDICT 6-MONTH BNT162B2 VACCINE-INDUCED ANTIBODY TITRE IN NURSING HOME RESIDENTS

Introduction Older nursing home residents are the population at greatest risk of morbidity and mortality from SARS-CoV-2 infection. No studies have examined the determinants of long-term antibody responses post-vaccination in this group. Method Longitudinal cohort study in residents of 5 nursing homes assessed prior to vaccination and at both 5-weeks and 6-months post SARS-CoV2 vaccine (BNT162b2). Comprehensive clinical assessment was performed, including assessment for comorbidity, frailty (NH-FRAIL) and SARS-CoV-2 infection history. Serum Nucleocapsid and Anti-Spike Receptor Binding Domain (RBD) antibodies were analysed at all timepoints and an in vitro Angiotensin Converting Enzyme (ACE2) Receptor-Spike RBD neutralisation assay used to assess serum neutralisation capacity. Results Of 86 participants (81.1 ± 10.8 years;65% female), just-under half (45.4%;39/86) had evidence of previous SARS-CoV-2 infection. All participants demonstrated a significant antibody response to vaccination at 5-weeks and a significant decline in this response by 6-months. SARS-CoV-2 infection history was the strongest predictor of antibody titre (log-transformed) at both 5-weeks (β: 3.00;95% CI [Confidence Interval]: 2.32, 3.70;p < 0.001) and 6-months (β: 3.59;95% CI: 2.89, 4.28;p < 0.001). Independent of SARS-CoV-2 infection history, both age in years (β: -0.05;95% CI: −0.08, −0.02;p < 0.001) and frailty (β: -0.22;95% CI: −0.33, −0.11;p < 0.001) were associated with a lower antibody titre at 6-months. Antibody titres at both 5-weeks and 6-months significantly correlated with in vitro neutralisation capacity. Conclusion and Implications In older nursing home residents, SARS-CoV-2 infection history was the strongest predictor of anti-spike antibody titres at 6-months, whilst age and frailty were independently associated with lower titres at 6-months. Antibody titres significantly correlated with in vitro neutralisation capacity. Whilst older SARS-CoV-2 naïve nursing home residents may be particularly vulnerable to breakthrough SARS-CoV-2 infection, the relationship between antibody titres, SARS-CoV-2 infection and clinical outcomes remains to be fully elucidated in this cohort.

Computational simulations reveal the binding dynamics between human ACE2 and the receptor binding domain of SARS-CoV-2 spike protein

Background: A novel coronavirus (the SARS-CoV-2) has been identified in January 2020 as the causal pathogen for COVID-19 , a pandemic started near the end of 2019. The Angiotensin converting enzyme 2 protein (ACE2) utilized by the SARS-CoV as a receptor was found to facilitate the infection of SARS-CoV-2, initiated by the binding of the spike protein to human ACE2. Methods: Using homology modeling and molecular dynamics (MD) simulation methods, we report here the detailed structure and dynamics of the ACE2 in complex with the receptor binding domain (RBD) of the SARS-CoV-2 spike protein. Results: The predicted model is highly consistent with the experimentally determined structures, validating the homology modeling results. Besides the binding interface reported in the crystal structures, novel binding poses are revealed from all-atom MD simulations. The simulation data are used to identify critical residues at the complex interface and provide more details about the interactions between the SARS-CoV-2 RBD and human ACE2. Conclusion: Simulations reveal that RBD binds to both open and closed state of ACE2. Two human ACE2 mutants and rat ACE2 are modeled to study the mutation effects on RBD binding to ACE2. The simulations show that the N-terminal helix and the K353 are very important for the tight binding of the complex, the mutants are found to alter the binding modes of the CoV2-RBD to ACE2.

Insilico Screening of Bioactive Phytochemicals against Spike Protein of COVID-19

Coronavirus disease 2019 (COVID-19) is a pandemic and this disease has infected millions of people globally now. COVID-19 is caused by a novel beta coronavirus strain known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Once SARS-CoV-2 manages to enter the body, it identifies and binds to the angiotensin converting enzyme 2 (ACE2) receptors through the binding receptor of Spike Protein (S-protein). The present study aimed to investigate the phytochemicals as potential inhibitors of the binding domain of S protein so that the binding of COVID-19 with ACE2 receptors could be restrained. For this purpose, the library of 2113 phytochemicals was docked against the binding domain of the S-protein. Top ten compounds with maximum binding affinity to the active sites of target protein were further screened for ADMET properties by adopting SwissADME and ADMETsar online servers. The compounds namely Morin, Curcumin, Apigenin, Cedronolactone A and Matairesinol showed acceptable drug-like properties therefore these compounds can be proposed as effective inhibitors, disrupting the S-protein-ACE2 interaction. This study might help in the development of a natural and cost-effective drug against COVID-19. Further, in vivo and in vitro examinations are required to validate our results.

Renin–Angiotensin–Aldosterone System Inhibitors in Covid-19

To the Editor: In their Special Report, Vaduganathan and colleagues (April 23 issue)1 describe the use of renin–angiotensin–aldosterone system (RAAS) inhibitors in patients with coronavirus disease 2019 (Covid-19). We would like to add the following points. First, it is worthwhile noting that studies involving in vitro human and animal cell cultures have shown that the effector peptide product of angiotensin-converting enzyme 2 (ACE2), angiotensin-(1–7), is degraded by the dipeptidase ACE into angiotensin-(1–5), and ACE inhibitors increase circulating levels of angiotensin-(1–7) in patients with chronic heart failure.2 This action provides a plausible mechanism for the increase in levels of angiotensin-(1–7) mediated . . .

Expression of ACE2 in the Intact and Acutely Injured Kidney.

Background: The actions of angiotensin-converting enzyme 2 (ACE2) oppose those of the renin-angiotensin-aldosterone system. ACE2 may be a cytoprotectant in some tissues. This study examined ACE2 expression in models of AKI. Methods: ACE2 mRNA and protein expression and ACE2 activity were assessed in murine ischemic AKI. Renal ACE2 mRNA expression was evaluated in LPS-induced AKI in wild-type (C57BL/6J) mice, in heme oxygenase-1+/+ and heme oxygenase-1-/- mice, and after unilateral ureteral obstruction (UUO) in wild-type mice. The effect of sex and age on renal ACE2 protein expression was also assessed. Results: In ischemic AKI, ACE2 mRNA and protein expression and ACE2 activity were reduced as compared with such indices in the intact kidney. In ischemic AKI, ACE2, which, in health, is prominently expressed in the tubular epithelium, especially proximal tubules, is decreased in expression in these segments. Decreased ACE2 expression in AKI did not reflect reduced GFR, because ACE2 mRNA expression was unaltered after UUO. LPS induced renal ACE2 mRNA expression in wild-type mice, but this effect did not occur in heme oxygenase-1-deficient mice. In ischemic and LPS-induced AKI, renal expression of the Mas receptor was increased. In the intact kidney, renal ACE2 protein expression decreased in female mice as compared with male mice, but was unaltered with age. Conclusion: We conclude that renal ACE2 expression is decreased in ischemic AKI, characterized by decreased GFR and abundant cell death, but is upregulated in LPS-induced AKI, an effect requiring heme oxygenase-1. Determining the significance of ACE2 expression in experimental AKI merits further study. We suggest that understanding the mechanism underlying ACE2 downregulation in AKI may offer insights relevant to COVID-19: ACE2 expression is downregulated after ACE2 mediates SARS-CoV-2 cellular entry; such downregulation is proinflammatory; and AKI commonly occurs and determines outcomes in COVID-19.

SYSTEMATIC REVIEW ON MECHANISM OF ACTION, MORTALITIES, MORBIDITIES, AND PREVENTION FROM COVID-19

: Coronaviruses are enveloped, positive-sense, single-stranded RNA viruses which belong to family Coronaviridae. These viruses are responsible for mild to severe respiratory ailments such as common cold to SARS, MERS and COVID-19. Pandemic COVID-19 is an ongoing issue of 2020. It starts from Wuhan city of China that later extended to the whole world (203 countries). However, according to another report of World Health Organization (WHO) the virus may start from some other part of the world rather than Wuhan city of China. The major structural components of COVID-19 are spike, envelope and nucleocapsid proteins. It enters the cell via cellular receptors angiotensin-converting enzyme 2 (ACE-2). Its symptoms are high fever, dry cough, fatigue, dyspnea, tiredness, headache, body-aches, pneumonia, and difficult breathing. Its man to man transmission is extraordinarily high and has ability to infect all age groups however, morbidity cases are noticed higher in elderly group of people. It can be transferred by the carriers via cough, sneeze or when they touched the surfaces or any object. It is concluded that there are more chances for the spread of disease in casual and workplaces. To control pandemic COVID-19 there is need to spread awareness about its structure, way of transmission and prevention. The present review discusses structure, mechanism of action, incubation period, most affected age groups, symptoms, transmission, and precautions to stop its progress.

A new lens for success

In March 2020, for example, Qiang Zhou, a Westlake structural biologist, used cryo-electron microscopy to solve the structure of the human angiotensin-converting enzyme 2 (ACE2), and to show how the SARS-CoV-2 spike protein binds with ACE2 to infect human cells (R. Yan et al. [...]the university's cryo-electron microscopy centre opened in late 2018 with two high-end 300 kV instruments, and a plan to become the biggest such centre in China by installing a further four. Unlike the Austrian research establishment, which is "very traditional, with the emphasis on big professorial chairs", says Henzinger, IST, like Westlake, operates more along Anglo-American lines, based on tenure-track appointments (which are rare in continental Europe) and relatively small, independent research groups.

Progress in drug development for treatment of coronavirus disease 2019 (COVID-19)

Since the outbreak of the novel coronavirus (SARS-CoV-2), the number of people infected worldwide has been increasing, and the medical situation is very severe. In emergency situations, the development of innovative drugs and the treatment of new coronavirus pneumonia (COVID-19) new adaptations on the market The development of the certificate has become the only way to find specific therapeutic drugs and the best treatment plan for COVID-19. The mechanism of angiotensin-converting enzyme 2 (ACE2) that mediates the invasion of host cells by SARS-CoV-2 has been discovered and is based on SARS-CoV- 2. Potential therapeutic targets of host and host, mainly including RNA-dependent RNA polymerase, 3CL protease, papain-like protease, Janus kinase, interleukin 6 and immunomodulators, etc. According to the above-mentioned pharmacological mechanism of action, the treatment of marketed drugs Great progress has been made in the development of new indications for COVID-19 and the clinical research and development of innovative drugs, but no specific drugs have been found. Some traditional Chinese medicines in China can block the SARS-CoV-2 replication cycle, regulate the body's immune response, and treat COVID-19. Biopharmaceuticals are currently undergoing phase I clinical studies in the world for the treatment of COVID-19. Biopharmaceuticals are progressing rapidly, accounting for 67%. At present, the research and development of drugs for the treatment of COVID-19 in China is facing severe challenges and biosafety The number of protection laboratories is small, the research on the mechanism of SARS-CoV-2 infection and the body's response mechanism is not in-depth, the resources of non-clinical cells and animal models are scarce, and the professional quantitative pharmacology research platform and professional talent training system are not perfect to treat COVID-19 The informatization of drug clinical trials and sample testing capabilities are in urgent need of improvement. If China can use this to improve its ability to develop new drugs in emergency situations, it will be able to better protect people's health.

Study on the potential mechanism of Fufang Yinhua Jiedu granules based on network pharmacology in the treatment of novel coronavirus

Objective To explore the potential effect and mechanism of Fufang Yinhua Jiedu Granules against the coronavirus disease 19 (COVID-19) by means of network pharmacology, and then to verify its anti-coronavirus effect through in vitro models.