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1.
Clin Infect Dis ; 73(11): e4154-e4165, 2021 12 06.
Article in English | MEDLINE | ID: covidwho-1559099

ABSTRACT

BACKGROUND: Children and older adults with coronavirus disease 2019 (COVID-19) display a distinct spectrum of disease severity yet the risk factors aren't well understood. We sought to examine the expression pattern of angiotensin-converting enzyme 2 (ACE2), the cell-entry receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and the role of lung progenitor cells in children and older patients. METHODS: We retrospectively analyzed clinical features in a cohort of 299 patients with COVID-19. The expression and distribution of ACE2 and lung progenitor cells were systematically examined using a combination of public single-cell RNA-seq data sets, lung biopsies, and ex vivo infection of lung tissues with SARS-CoV-2 pseudovirus in children and older adults. We also followed up patients who had recovered from COVID-19. RESULTS: Compared with children, older patients (>50 years.) were more likely to develop into serious pneumonia with reduced lymphocytes and aberrant inflammatory response (P = .001). The expression level of ACE2 and lung progenitor cell markers were generally decreased in older patients. Notably, ACE2 positive cells were mainly distributed in the alveolar region, including SFTPC positive cells, but rarely in airway regions in the older adults (P < .01). The follow-up of discharged patients revealed a prolonged recovery from pneumonia in the older (P < .025). CONCLUSIONS: Compared to children, ACE2 positive cells are generally decreased in older adults and mainly presented in the lower pulmonary tract. The lung progenitor cells are also decreased. These risk factors may impact disease severity and recovery from pneumonia caused by SARS-Cov-2 infection in older patients.

2.
Preprint in English | EuropePMC | ID: ppcovidwho-296434

ABSTRACT

Background: The onset of various kidney diseases have been reported after COVID-19 vaccination. However, detailed clinical and pathological examination of kidney injury in patients receiving inactivated vaccines are lacking.<br><br>Methods: We screened and analyzed patients with newly diagnosed kidney diseases after inactivated SARS-CoV-2 vaccination in Peking University First Hospital from January 2021 to August 2021. We obtained samples of blood, urine, and renal biopsy tissues. Clinical and laboratory information, as well as light microscopy, immunostaining and ultrastructural observation were described. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Spike protein and Nucleoprotein were stained using immune-fluorescence technique in the kidney biopsy samples. SARS-CoV-2 specific antibodies were tested using magnetic particle chemiluminescence immunoassay.<br><br>Findings: The study group included 17 patients, including immune complex mediated kidney diseases (IgA nephropathy, membranous nephropathy and lupus nephritis), podocytopathy (minimal change disease and focal segmental glomerulosclerosis) and others (antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis, anti-GBM nephritis, acute tubulointerstitial nephritis, and thrombotic microangiopathy). Seven patients (41.18%) developed renal disease after the first dose and 10 (58.82%) after the second dose. We found no definitive evidence of SARS-CoV-2 Spike protein or Nucleoprotein deposition in the kidney biopsy samples. Serological markers implicated abnormal immune responses in predisposed individuals. Treatment and follow-up (median = 86 days) showed that biopsy diagnosis informed treatment and prognosis in all patients.<br><br>Interpretation: We observed various kidney diseases following inactivated SARS-CoV-2 vaccine administration. Our findings provide an evidence against direct vaccine protein deposition as the major pathomechanism, but implicate abnormal immune responses in predisposed individuals. These findings expand our understanding of inactivated SARS-CoV-2 vaccine renal safety.<br><br>Funding: This study was funded by National Natural Science Foundation of China (91742205, 82170711, 81800636, 82070733, 81625004), Clinical Medicine Plus X—Young Scholars Project of Peking University (PKU2021LCXQ017), the Fundamental Research Funds for the Central Universities, CAMS Innovation Fund for Medical Sciences (2019-I2M-5-046), Yunnan Provincial Science and Technology Department (202102AA100051 and 202003AC100010, China), and Beijing Young Scientist Program (BJJWZYJH01201910001006).<br><br>Declaration of Interest: The authors declare no competing interests.<br><br>Ethical Approval: This study was approved by the institutional review board of Peking University First Hospital (2021-352) and the Committee on Human Subject Research and Ethics of Yunnan University (CHSRE2021020). Written Informed Consent Form was obtained from each participant.

3.
PLoS ONE ; 16(2), 2021.
Article in English | CAB Abstracts | ID: covidwho-1410710

ABSTRACT

Background: Sensitive and high throughput molecular detection assays are essential during the coronavirus disease 2019 (COVID-19) pandemic, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The vast majority of the SARS-CoV-2 molecular assays use nasopharyngeal swab (NPS) or oropharyngeal swab (OPS) specimens collected from suspected individuals. However, using NPS or OPS as specimens has apparent drawbacks, e.g. the collection procedures for NPS or OPS specimens can be uncomfortable to some people and may cause sneezing and coughing which in turn generate droplets and/or aerosol particles that are of risk to healthcare workers, requiring heavy use of personal protective equipment. There have been recent studies indicating that self-collected saliva specimens can be used for molecular detection of SARS-CoV-2 and provides more comfort and ease of use for the patients. Here we report the performance of QuantiVirusTM SARS-CoV-2 test using saliva as the testing specimens with or without pooling. Methods Development and validation studies were conducted following FDA-EUA and molecular assay validation guidelines. Using SeraCare Accuplex SARS-CoV-2 reference panel, the limit of detection (LOD) and clinical performance studies were performed with the QuantiVirusTM SARS-CoV-2 test. For clinical evaluation, 85 known positive and 90 known negative clinical NPS samples were tested. Additionally, twenty paired NPS and saliva samples collected from recovering COVID-19 patients were tested and the results were further compared to that of the Abbott m2000 SARS-CoV-2 PCR assay. Results of community collected 389 saliva samples for COVID-19 screening by QuantiVirusTM SARS-CoV-2 test were also obtained and analyzed. Additionally, testing of pooled saliva samples was evaluated.

4.
Ann Palliat Med ; 10(8): 9233-9238, 2021 08.
Article in English | MEDLINE | ID: covidwho-1399728

ABSTRACT

BACKGROUND: The optimal duration of treatment for intestinal tuberculosis (TB), which remains a common disease worldwide, has not yet been established. The proposed randomized controlled study will aim to compare the efficacy of short-term six-month with nine-month anti-TB therapy for treating intestinal TB. METHODS: This multicenter, open-label, double-blinded, randomized controlled trial conducted in the Affiliated Hangzhou Chest Hospital of Zhejiang University will include a total of 80 patients. Patients who meet the inclusion criteria will be randomly assigned to either the six-month (n=40) or nine-month (n=40) treatment group. The primary outcome will be complete response, which is defined as endoscopy displaying active lesion healing at the end of treatment. Participants will be scheduled for follow-up visits once a month in the first three months, then once every three months until the end of the treatment. The last follow-up will be one year after the treatment. Recurrence will be assessed one year after the end of treatment, which is defined as endoscopy displaying recurrent lesions after complete response. DISCUSSION: In addition to the reports of tuberculous lymphadenitis and spinal TB, there are few appropriate randomized trials for the treatment of extrapulmonary TB with appropriate clinical endpoints. We believe that the proposed randomized controlled trial will provide further data on the efficacy of short-term six-month anti-TB therapy in intestinal TB patients. TRIAL REGISTRATION: This trial will be registered on ClinicalTrial.gov.


Subject(s)
COVID-19 , Tuberculosis, Lymph Node , Humans , Multicenter Studies as Topic , Randomized Controlled Trials as Topic , SARS-CoV-2 , Treatment Outcome
5.
Eur J Med Chem ; 225: 113818, 2021 Dec 05.
Article in English | MEDLINE | ID: covidwho-1385491

ABSTRACT

Cathepsin C, an important lysosomal cysteine protease, mediates the maturation process of neutrophil serine proteases, and participates in the inflammation and immune regulation process associated with polymorphonuclear neutrophils. Therefore, cathepsin C is considered to be an attractive target for treating inflammatory diseases. With INS1007 (trade name: brensocatib) being granted a breakthrough drug designation by FDA for the treatment of Adult Non-cystic Fibrosis Bronchiectasis and Coronavirus Disease 2019, the development of cathepsin C inhibitor will attract attentions from medicinal chemists in the future soon. Here, we summarized the research results of cathepsin C as a therapeutic target, focusing on the development of cathepsin C inhibitor, and provided guidance and reference opinions for the upcoming development boom of cathepsin C inhibitor.


Subject(s)
Anti-Inflammatory Agents/chemistry , Cathepsin C/antagonists & inhibitors , Drug Discovery , Protease Inhibitors/chemistry , Anti-Inflammatory Agents/therapeutic use , COVID-19/drug therapy , COVID-19/pathology , COVID-19/virology , Cathepsin C/genetics , Cathepsin C/metabolism , Humans , Papillon-Lefevre Disease/genetics , Papillon-Lefevre Disease/pathology , Protease Inhibitors/metabolism , Protease Inhibitors/therapeutic use , Pulmonary Disease, Chronic Obstructive/drug therapy , Pulmonary Disease, Chronic Obstructive/pathology , SARS-CoV-2/isolation & purification , Serine Endopeptidases/metabolism
6.
Cities ; 120: 103404, 2022 Jan.
Article in English | MEDLINE | ID: covidwho-1336326

ABSTRACT

This paper investigates the imppact of COVID-19 travel restrictions on population flow in the People's Republic of China. We discover an "unreasonable" surge in population flow after the Wuhan travel ban. We further find out that such a sure of population flow is attributed to the "spill-over" effect of the Wuhan travel ban. We utilize a logistic regression model to quantify that the spill-over effect linearly decays with the travel distance to the Pandemic center city. Because of the "spill-over" effect of the travel ban policy, government authorities should design redundancy polity to simultaneously implement a travel ban for the pandemic center city and its neighboring cities to restrain human movement and pandemic transmission.

7.
J Chem Inf Model ; 61(8): 3917-3926, 2021 08 23.
Article in English | MEDLINE | ID: covidwho-1317793

ABSTRACT

The continual spread of novel coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), posing a severe threat to the health worldwide. The main protease (Mpro, alias 3CLpro) of SARS-CoV-2 is a crucial enzyme for the maturation of viral particles and is a very attractive target for designing drugs to treat COVID-19. Here, we propose a multiple conformation-based virtual screening strategy to discover inhibitors that can target SARS-CoV-2 Mpro. Based on this strategy, nine Mpro structures and a protein mimetics library with 8960 commercially available compounds were prepared to carry out ensemble docking for the first time. Five of the nine structures are apo forms presented in different conformations, whereas the other four structures are holo forms complexed with different ligands. The surface plasmon resonance assay revealed that 6 out of 49 compounds had the ability to bind to SARS-CoV-2 Mpro. The fluorescence resonance energy transfer experiment showed that the biochemical half-maximal inhibitory concentration (IC50) values of the six compounds could hamper Mpro activities ranged from 0.69 ± 0.05 to 2.05 ± 0.92 µM. Evaluation of antiviral activity using the cell-based assay indicated that two compounds (Z1244904919 and Z1759961356) could strongly inhibit the cytopathic effect and reduce replication of the living virus in Vero E6 cells with the half-maximal effective concentrations (EC50) of 4.98 ± 1.83 and 8.52 ± 0.92 µM, respectively. The mechanism of the action for the two inhibitors were further elucidated at the molecular level by molecular dynamics simulation and subsequent binding free energy analysis. As a result, the discovered noncovalent reversible inhibitors with novel scaffolds are promising antiviral drug candidates, which may be used to develop the treatment of COVID-19.


Subject(s)
COVID-19 , SARS-CoV-2 , Antiviral Agents/pharmacology , Cysteine Endopeptidases , Humans , Molecular Docking Simulation , Protease Inhibitors/pharmacology , Viral Nonstructural Proteins
8.
Pathogens ; 10(7)2021 Jul 12.
Article in English | MEDLINE | ID: covidwho-1308389

ABSTRACT

The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become a global concern. Immunoglobin A (IgA) contributes to virus neutralization at the early stage of infection. Longitudinal studies are needed to assess whether SARS-CoV-2-specific IgA production persists for a longer time in patients recovered from severe COVID-19 and its lasting symptoms that can have disabling consequences should also be alerted to susceptible hosts. Here, we tracked the anti-SARS-CoV-2 spike protein receptor-binding domain (RBD) antibody levels in a cohort of 88 COVID-19 patients. We found that 52.3% of the patients produced more anti-SARS-CoV-2 RBD IgA than IgG or IgM, and the levels of IgA remained stable during 4-41 days of infection. One of these IgA-dominant COVID-19 patients, concurrently with IgA nephropathy (IgAN), presented with elevated serum creatinine and worse proteinuria during the infection, which continued until seven months post-infection. The serum levels of anti-SARS-CoV-2 RBD and total IgA were higher in this patient than in healthy controls. Changes in the composition of the intestinal microbiota, increased IgA highly coated bacteria, and elevated concentration of the proinflammatory cytokine IL-18 were indicative of potential involvement of intestinal dysbiosis and inflammation to the systemic IgA level and, consequently, the disease progression. Collectively, our work highlighted the potential adverse effect of the mucosal immune response to SARS-CoV-2 infection, and that additional care should be taken with COVID-19 patients presenting with chronic diseases such as IgAN.

10.
Synth Syst Biotechnol ; 6(3): 135-143, 2021 Sep.
Article in English | MEDLINE | ID: covidwho-1267929

ABSTRACT

SARS-CoV-2, the causative agent for COVID-19, infect human mainly via respiratory tract, which is heavily inhabited by local microbiota. However, the interaction between SARS-CoV-2 and nasopharyngeal microbiota, and the association with metabolome has not been well characterized. Here, metabolomic analysis of blood, urine, and nasopharyngeal swabs from a group of COVID-19 and non-COVID-19 patients, and metagenomic analysis of pharyngeal samples were used to identify the key features of COVID-19. Results showed lactic acid, l-proline, and chlorogenic acid methyl ester (CME) were significantly reduced in the sera of COVID-19 patients compared with non-COVID-19 ones. Nasopharyngeal commensal bacteria including Gemella morbillorum, Gemella haemolysans and Leptotrichia hofstadii were notably depleted in the pharynges of COVID-19 patients, while Prevotella histicola, Streptococcus sanguinis, and Veillonella dispar were relatively increased. The abundance of G. haemolysans and L. hofstadii were significantly positively associated with serum CME, which might be an anti-SARS-CoV-2 bacterial metabolite. This study provides important information to explore the linkage between nasopharyngeal microbiota and disease susceptibility. The findings were based on a very limited number of patients enrolled in this study; a larger size of cohort will be appreciated for further investigation.

11.
Chem Biol Drug Des ; 98(1): 1-18, 2021 07.
Article in English | MEDLINE | ID: covidwho-1201241

ABSTRACT

The ongoing pandemic of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become a global health concern and pose a serious threat to humanity. There is an urgent need for developing therapeutic drugs and (or) biologics to prevent the spread of the virus. The life cycle of SARS-CoV-2 shows that the virus enters host cells by first binding to angiotensin-converting enzyme 2 (ACE2) through its spike protein receptor-binding domain (RBD). Therefore, blocking the binding between of ACE2 and SARS-CoV-2 RBD can inhibit the virus infection in the host cells. In this study, by grafting the complementarity-determining regions (CDRs) of developed SARS-CoV, MERS-CoVs specific neutralizing antibodies (nAbs) include monoclonal antibodies (mAbs) as well as SARS-CoV-2 mAbs onto a known stable nanobody (Nb) scaffold, and a total of 16 Nbs sequences were designed. Five Nbs, namely CS01, CS02, CS03, CS10, and CS16, were selected based on the free energy landscape of protein docking verified by the recently reported Nb-RBD cocrystal structures. CS01, CS02, and CS03 occupied the ACE2 binding site of RBD, while CS10 and CS16 were proposed to inhibit the interaction between RBD and ACE2 through an allosteric mechanism. Based on the structures of the five Nbs in complex with RBD, seven brand-new Nbs with enhanced binding affinities (CS02_RD01, CS03_RD01, CS03_RD02, CS03_RD03, CS03_RD04, CS16_RD01, and CS16_RD02) were generated by redesign of residues on the interface of the five Nbs contact with SARS-CoV-2 RBD. In addition, the identified "hot spots" on the interface of each complex provide useful information to understand the binding mechanism of designed Nbs to SARS-CoV-2 RBD. In sum, the predicted stabilities and high binding affinities of the 11 (re)designed Nbs indicating the potential of the developed computational framework in this work to design effective agents to block the infection of SARS-CoV-2.


Subject(s)
Angiotensin-Converting Enzyme 2/chemistry , Antibodies, Neutralizing/chemistry , Antibodies, Viral/chemistry , COVID-19 , Molecular Dynamics Simulation , SARS-CoV-2/chemistry , Single-Domain Antibodies/chemistry , Angiotensin-Converting Enzyme 2/immunology , Antibodies, Neutralizing/immunology , Antibodies, Viral/immunology , Humans , Protein Domains , SARS-CoV-2/immunology , Single-Domain Antibodies/immunology
12.
Mol Phylogenet Evol ; 157: 107017, 2021 04.
Article in English | MEDLINE | ID: covidwho-1127076

ABSTRACT

The COVID-19 pandemic is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) whose origin is still shed in mystery. In this study, we developed a method to search the basal SARS-CoV-2 clade among collected SARS-CoV-2 genome sequences. We first identified the mutation sites in the SARS-CoV-2 whole genome sequence alignment. Then by the pairwise comparison of the numbers of mutation sites among all SARS-CoV-2s, the least mutated clade was identified, which is the basal clade under parsimony principle. In our first analysis, we used 168 SARS-CoV-2 sequences (GISAID dataset till 2020/03/04) to identify the basal clade which contains 33 identical viral sequences from seven countries. To our surprise, in our second analysis with 367 SARS-CoV-2 sequences (GISAID dataset till 2020/03/17), the basal clade has 51 viral sequences, 18 more sequences added. The much larger NCBI dataset shows that this clade has expanded with 85 unique sequences by 2020/04/04. The expanding basal clade tells a chilling fact that the least mutated SARS-CoV-2 sequence was replicating and spreading for at least four months. It is known that coronaviruses have the RNA proofreading capability to ensure their genome replication fidelity. Interestingly, we found that the SARS-CoV-2 without its nonstructural proteins 13 to 16 (Nsp13-Nsp16) exhibits an unusually high mutation rate. Our result suggests that SARS-CoV-2 has an unprecedented RNA proofreading capability which can intactly preserve its genome even after a long period of transmission. Our selection analyses also indicate that the positive selection event enabling SARS-CoV-2 to cross species and adapt to human hosts might have been achieved before its outbreak.


Subject(s)
COVID-19/virology , Genome, Viral , Phylogeny , SARS-CoV-2/genetics , Evolution, Molecular , Humans , Mutation , Mutation Rate , Pandemics , Point Mutation , SARS-CoV-2/classification , Selection, Genetic , Viral Nonstructural Proteins/genetics , Viral Nonstructural Proteins/metabolism
13.
Theranostics ; 11(5): 2170-2181, 2021.
Article in English | MEDLINE | ID: covidwho-1016389

ABSTRACT

Introduction: An increasing number of children with severe coronavirus disease 2019 (COVID-19) is being reported, yet the spectrum of disease severity and expression patterns of angiotensin-converting enzyme 2 (ACE2) in children at different developmental stages are largely unknow. Methods: We analysed clinical features in a cohort of 173 children with COVID-19 (0-15 yrs.-old) between January 22, 2020 and March 15, 2020. We systematically examined the expression and distribution of ACE2 in different developmental stages of children by using a combination of children's lung biopsies, pluripotent stem cell-derived lung cells, RNA-sequencing profiles, and ex vivo SARS-CoV-2 pseudoviral infections. Results: It revealed that infants (< 1yrs.-old), with a weaker potency of immune response, are more vulnerable to develop pneumonia whereas older children (> 1 yrs.-old) are more resistant to lung injury. The expression levels of ACE2 however do not vary by age in children's lung. ACE2 is notably expressed not only in Alveolar Type II (AT II) cells, but also in SOX9 positive lung progenitor cells detected in both pluripotent stem cell derivatives and infants' lungs. The ACE2+SOX9+ cells are readily infected by SARS-CoV-2 pseudovirus and the numbers of the double positive cells are significantly decreased in older children. Conclusions: Infants (< 1 yrs.-old) with SARS-CoV-2 infection are more vulnerable to lung injuries. ACE2 expression in multiple types of lung cells including SOX9 positive progenitor cells, in cooperation with an unestablished immune system, could be risk factors contributing to vulnerability of infants with COVID-19. There is a need to continue monitoring lung development in young children who have recovered from SARS-CoV-2 infection.


Subject(s)
Angiotensin-Converting Enzyme 2/metabolism , COVID-19/pathology , Lung/cytology , Stem Cells/metabolism , Adolescent , Biopsy , Child , Child, Preschool , Female , Humans , Immune System , Infant , Infant, Newborn , Lung/virology , Male , RNA-Seq , Risk Factors , SARS-CoV-2 , SOX9 Transcription Factor/metabolism , Single-Cell Analysis , Stem Cells/virology
14.
Sci Rep ; 10(1): 22048, 2020 12 16.
Article in English | MEDLINE | ID: covidwho-983660

ABSTRACT

Although several cases of family clusters with SARS-Cov-2 infection have been reported, there are still limited data preventing conclusions from being drawn regarding the characteristics and laboratory findings in the COVID-19 population within family clusters. In the present study, we retrospectively collected five family clusters with COVID-19 and summarized the dynamic profiles of the clinical characteristics, laboratory findings, immune markers, treatment and prognosis of this population. Furthermore, we also compared clinical and laboratory data between the SARS-Cov-2 infection with family cluster (n = 21) and those without family cluster (n = 16). We demonstrated that the duration of SARS-Cov-2 replication might be varied based on the different family clusters due to their different genetic backgrounds. The onset improved lung radiology might start at the end of the SARS-Cov-2 positive period. Furthermore, the obtained results demonstrated that similar basic characteristics and clinical findings seem to exist between the cases with SARS-Cov-2 and without family clusters. The serum level of ferritin might have a different biological function and be a new biomarker for the family cluster. Further studies with larger numbers of patients are required.


Subject(s)
COVID-19/transmission , Adolescent , Adult , Aged , Antiviral Agents/therapeutic use , COVID-19/diagnosis , COVID-19/epidemiology , COVID-19/virology , Child, Preschool , China/epidemiology , Family , Female , Humans , Infant , Male , Middle Aged , Pandemics , Prognosis , Retrospective Studies , SARS-CoV-2/isolation & purification
16.
Res Sq ; 2020 Aug 20.
Article in English | MEDLINE | ID: covidwho-729814

ABSTRACT

Dysfunctional immune responses contribute critically to the progression of Coronavirus Disease-2019 (COVID-19) from mild to severe stages including fatality, with pro-inflammatory macrophages as one of the main mediators of lung hyper-inflammation. Therefore, there is an urgent need to better understand the interactions among SARS-CoV-2 permissive cells, macrophage, and the SARS-CoV-2 virus, thereby offering important insights into new therapeutic strategies. Here, we used directed differentiation of human pluripotent stem cells (hPSCs) to establish a lung and macrophage co-culture system and model the host-pathogen interaction and immune response caused by SARS-CoV-2 infection. Among the hPSC-derived lung cells, alveolar type II and ciliated cells are the major cell populations expressing the viral receptor ACE2 and co-effector TMPRSS2, and both were highly permissive to viral infection. We found that alternatively polarized macrophages (M2) and classically polarized macrophages (M1) had similar inhibitory effects on SARS-CoV-2 infection. However, only M1 macrophages significantly up-regulated inflammatory factors including IL-6 and IL-18, inhibiting growth and enhancing apoptosis of lung cells. Inhibiting viral entry into target cells using an ACE2 blocking antibody enhanced the activity of M2 macrophages, resulting in nearly complete clearance of virus and protection of lung cells. These results suggest a potential therapeutic strategy, in that by blocking viral entrance to target cells while boosting anti-inflammatory action of macrophages at an early stage of infection, M2 macrophages can eliminate SARS-CoV-2, while sparing lung cells and suppressing the dysfunctional hyper-inflammatory response mediated by M1 macrophages.

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