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1.
Cells ; 11(9)2022 04 21.
Article in English | MEDLINE | ID: covidwho-1818055

ABSTRACT

Human SARS-CoV-2 and avian infectious bronchitis virus (IBV) are highly contagious and deadly coronaviruses, causing devastating respiratory diseases in humans and chickens. The lack of effective therapeutics exacerbates the impact of outbreaks associated with SARS-CoV-2 and IBV infections. Thus, novel drugs or therapeutic agents are highly in demand for controlling viral transmission and disease progression. Mesenchymal stem cells (MSC) secreted factors (secretome) are safe and efficient alternatives to stem cells in MSC-based therapies. This study aimed to investigate the antiviral potentials of human Wharton's jelly MSC secretome (hWJ-MSC-S) against SARS-CoV-2 and IBV infections in vitro and in ovo. The half-maximal inhibitory concentrations (IC50), cytotoxic concentration (CC50), and selective index (SI) values of hWJ-MSC-S were determined using Vero-E6 cells. The virucidal, anti-adsorption, and anti-replication antiviral mechanisms of hWJ-MSC-S were evaluated. The hWJ-MSC-S significantly inhibited infection of SARS-CoV-2 and IBV, without affecting the viability of cells and embryos. Interestingly, hWJ-MSC-S reduced viral infection by >90%, in vitro. The IC50 and SI of hWJ-MSC secretome against SARS-CoV-2 were 166.6 and 235.29 µg/mL, respectively, while for IBV, IC50 and SI were 439.9 and 89.11 µg/mL, respectively. The virucidal and anti-replication antiviral effects of hWJ-MSC-S were very prominent compared to the anti-adsorption effect. In the in ovo model, hWJ-MSC-S reduced IBV titer by >99%. Liquid chromatography-tandem mass spectrometry (LC/MS-MS) analysis of hWJ-MSC-S revealed a significant enrichment of immunomodulatory and antiviral proteins. Collectively, our results not only uncovered the antiviral potency of hWJ-MSC-S against SARS-CoV-2 and IBV, but also described the mechanism by which hWJ-MSC-S inhibits viral infection. These findings indicate that hWJ-MSC-S could be utilized in future pre-clinical and clinical studies to develop effective therapeutic approaches against human COVID-19 and avian IB respiratory diseases.


Subject(s)
Bronchitis , COVID-19 , Mesenchymal Stem Cells , Wharton Jelly , Animals , Antiviral Agents/metabolism , Antiviral Agents/pharmacology , Bronchitis/metabolism , Chickens , Humans , Immunologic Factors/metabolism , Mesenchymal Stem Cells/metabolism , SARS-CoV-2 , Wharton Jelly/metabolism
2.
PLoS Pathog ; 18(4): e1010468, 2022 04.
Article in English | MEDLINE | ID: covidwho-1779781

ABSTRACT

An overreactive inflammatory response and coagulopathy are observed in patients with severe form of COVID-19. Since increased levels of D-dimer (DD) are associated with coagulopathy in COVID-19, we explored whether DD contributes to the aberrant cytokine responses. Here we show that treatment of healthy human monocytes with DD induced a dose dependent increase in production of pyrogenic mediator, Prostaglandin E2 (PGE2) and inflammatory cytokines, IL-6 and IL-8. The DD-induced PGE2 and inflammatory cytokines were enhanced significantly by co-treatment with immune complexes (IC) of SARS CoV-2 recombinant S protein or of pseudovirus containing SARS CoV-2 S protein (PVCoV-2) coated with spike-specific chimeric monoclonal antibody (MAb) containing mouse variable and human Fc regions. The production of PGE2 and cytokines in monocytes activated with DD and ICs was sensitive to the inhibitors of ß2 integrin and FcγRIIa, and to the inhibitors of calcium signaling, Mitogen-Activated Protein Kinase (MAPK) pathway, and tyrosine-protein kinase. Importantly, strong increase in PGE2 and in IL-6/IL-8/IL-1ß cytokines was observed in monocytes activated with DD in the presence of IC of PVCoV-2 coated with plasma from hospitalized COVID-19 patients but not from healthy donors. The IC of PVCoV-2 with convalescent plasma induced much lower levels of PGE2 and cytokines compared with plasma from hospitalized COVID-19 patients. PGE2 and IL-6/IL-8 cytokines produced in monocytes activated with plasma-containing IC, correlated well with the levels of spike binding antibodies and not with neutralizing antibody titers. Our study suggests that a combination of high levels of DD and high titers of spike-binding antibodies that can form IC with SARS CoV-2 viral particles might accelerate the inflammatory status of lung infiltrating monocytes leading to increased lung pathology in patients with severe form of COVID-19.


Subject(s)
COVID-19 , Monocytes , Animals , Antigen-Antibody Complex , COVID-19/therapy , Cytokines/metabolism , Dinoprostone/metabolism , Fibrin Fibrinogen Degradation Products , Humans , Immunization, Passive , Immunologic Factors/metabolism , Interleukin-6/metabolism , Interleukin-8/metabolism , Mice , Spike Glycoprotein, Coronavirus/metabolism
3.
Front Immunol ; 12: 769011, 2021.
Article in English | MEDLINE | ID: covidwho-1650341

ABSTRACT

Asthma patients may increase their susceptibility to SARS-CoV-2 infection and the poor prognosis of coronavirus disease 2019 (COVID-19). However, anti-COVID-19/asthma comorbidity approaches are restricted on condition. Existing evidence indicates that luteolin has antiviral, anti-inflammatory, and immune regulation capabilities. We aimed to evaluate the possibility of luteolin evolving into an ideal drug and explore the underlying molecular mechanisms of luteolin against COVID-19/asthma comorbidity. We used system pharmacology and bioinformatics analysis to assess the physicochemical properties and biological activities of luteolin and further analyze the binding activities, targets, biological functions, and mechanisms of luteolin against COVID-19/asthma comorbidity. We found that luteolin may exert ideal physicochemical properties and bioactivity, and molecular docking analysis confirmed that luteolin performed effective binding activities in COVID-19/asthma comorbidity. Furthermore, a protein-protein interaction network of 538 common targets between drug and disease was constructed and 264 hub targets were obtained. Then, the top 6 hub targets of luteolin against COVID-19/asthma comorbidity were identified, namely, TP53, AKT1, ALB, IL-6, TNF, and VEGFA. Furthermore, the enrichment analysis suggested that luteolin may exert effects on virus defense, regulation of inflammation, cell growth and cell replication, and immune responses, reducing oxidative stress and regulating blood circulation through the Toll-like receptor; MAPK, TNF, AGE/RAGE, EGFR, ErbB, HIF-1, and PI3K-AKT signaling pathways; PD-L1 expression; and PD-1 checkpoint pathway in cancer. The possible "dangerous liaison" between COVID-19 and asthma is still a potential threat to world health. This research is the first to explore whether luteolin could evolve into a drug candidate for COVID-19/asthma comorbidity. This study indicated that luteolin with superior drug likeness and bioactivity has great potential to be used for treating COVID-19/asthma comorbidity, but the predicted results still need to be rigorously verified by experiments.


Subject(s)
Anti-Inflammatory Agents/metabolism , Antioxidants/metabolism , Antiviral Agents/metabolism , Asthma/epidemiology , Asthma/metabolism , COVID-19/epidemiology , COVID-19/metabolism , Immunologic Factors/metabolism , Luteolin/metabolism , SARS-CoV-2/metabolism , Anti-Inflammatory Agents/chemistry , Antioxidants/chemistry , Antiviral Agents/chemistry , Comorbidity , Computational Biology/methods , Drug Discovery/methods , Humans , Immunologic Factors/chemistry , Interleukin-6/metabolism , Luteolin/chemistry , Molecular Docking Simulation , Protein Interaction Maps/drug effects , Proto-Oncogene Proteins c-akt/metabolism , Serum Albumin, Human/metabolism , Signal Transduction/drug effects , Tumor Necrosis Factor-alpha/metabolism , Tumor Suppressor Protein p53/metabolism , Vascular Endothelial Growth Factor A/metabolism
4.
PLoS One ; 16(6): e0248479, 2021.
Article in English | MEDLINE | ID: covidwho-1266543

ABSTRACT

The Coronavirus disease (COVID-19) caused by the virus SARS-CoV-2 has become a global pandemic in a very short time span. Currently, there is no specific treatment or vaccine to counter this highly contagious disease. There is an urgent need to find a specific cure for the disease and global efforts are directed at developing SARS-CoV-2 specific antivirals and immunomodulators. Ayurvedic Rasayana therapy has been traditionally used in India for its immunomodulatory and adaptogenic effects, and more recently has been included as therapeutic adjuvant for several maladies. Amongst several others, Withania somnifera (Ashwagandha), Tinospora cordifolia (Guduchi) and Asparagus racemosus (Shatavari) play an important role in Rasayana therapy. The objective of this study was to explore the immunomodulatory and anti SARS-CoV2 potential of phytoconstituents from Ashwagandha, Guduchi and Shatavari using network pharmacology and docking. The plant extracts were prepared as per ayurvedic procedures and a total of 31 phytoconstituents were identified using UHPLC-PDA and mass spectrometry studies. To assess the immunomodulatory potential of these phytoconstituents an in-silico network pharmacology model was constructed. The model predicts that the phytoconstituents possess the potential to modulate several targets in immune pathways potentially providing a protective role. To explore if these phytoconstituents also possess antiviral activity, docking was performed with the Spike protein, Main Protease and RNA dependent RNA polymerase of the virus. Interestingly, several phytoconstituents are predicted to possess good affinity for the three targets, suggesting their application for the termination of viral life cycle. Further, predictive tools indicate that there would not be adverse herb-drug pharmacokinetic-pharmacodynamic interactions with concomitantly administered drug therapy. We thus make a compelling case to evaluate the potential of these Rasayana botanicals as therapeutic adjuvants in the management of COVID-19 following rigorous experimental validation.


Subject(s)
Antiviral Agents/metabolism , Asparagus Plant/chemistry , COVID-19/metabolism , Immunologic Factors/metabolism , Molecular Docking Simulation/methods , Plant Extracts/metabolism , SARS-CoV-2/enzymology , Tinospora/chemistry , Withania/chemistry , Antiviral Agents/pharmacokinetics , Binding Sites , COVID-19/drug therapy , COVID-19/virology , Coronavirus 3C Proteases/metabolism , Coronavirus RNA-Dependent RNA Polymerase/metabolism , Herb-Drug Interactions , Humans , Immunologic Factors/pharmacokinetics , India , Medicine, Ayurvedic/methods , Phytotherapy/methods , Plant Extracts/pharmacokinetics , Protein Binding , Spike Glycoprotein, Coronavirus/metabolism
6.
Biomolecules ; 11(3)2021 03 15.
Article in English | MEDLINE | ID: covidwho-1167410

ABSTRACT

Galectin-9 (Gal-9) is a ß-galactoside-binding lectin capable of promoting or suppressing the progression of infectious diseases. This protein is susceptible to cleavage of its linker-peptides by several proteases, and the resulting cleaved forms, N-terminal carbohydrate recognition domain (CRD) and C-terminal CRD, bind to various glycans. It has been suggested that full-length (FL)-Gal-9 and the truncated (Tr)-Gal-9s could exert different functions from one another via their different glycan-binding activities. We propose that FL-Gal-9 regulates the pathogenesis of infectious diseases, including human immunodeficiency virus (HIV) infection, HIV co-infected with opportunistic infection (HIV/OI), dengue, malaria, leptospirosis, and tuberculosis (TB). We also suggest that the blood levels of FL-Gal-9 reflect the severity of dengue, malaria, and HIV/OI, and those of Tr-Gal-9 markedly reflect the severity of HIV/OI. Recently, matrix metallopeptidase-9 (MMP-9) was suggested to be an indicator of respiratory failure from coronavirus disease 2019 (COVID-19) as well as useful for differentiating pulmonary from extrapulmonary TB. The protease cleavage of FL-Gal-9 may lead to uncontrolled hyper-immune activation, including a cytokine storm. In summary, Gal-9 has potential to reflect the disease severity for the acute and chronic infectious diseases.


Subject(s)
Communicable Diseases/blood , Galectins/blood , Acute Disease , Amino Acid Sequence , COVID-19/blood , COVID-19/physiopathology , Chronic Disease , Communicable Diseases/immunology , Communicable Diseases/physiopathology , Dengue/blood , Dengue/physiopathology , Galectins/genetics , Galectins/metabolism , HIV Infections/blood , HIV Infections/physiopathology , Humans , Immunologic Factors/metabolism , Leptospirosis/blood , Leptospirosis/physiopathology , Malaria/blood , Malaria/physiopathology , Tuberculosis/blood , Tuberculosis/physiopathology
7.
Sci Adv ; 7(6)2021 02.
Article in English | MEDLINE | ID: covidwho-1066791

ABSTRACT

Dysregulations in the inflammatory response of the body to pathogens could progress toward a hyperinflammatory condition amplified by positive feedback loops and associated with increased severity and mortality. Hence, there is a need for identifying therapeutic targets to modulate this pathological immune response. Here, we propose a single cell-based computational methodology for predicting proteins to modulate the dysregulated inflammatory response based on the reconstruction and analysis of functional cell-cell communication networks of physiological and pathological conditions. We validated the proposed method in 12 human disease datasets and performed an in-depth study of patients with mild and severe symptomatology of the coronavirus disease 2019 for predicting novel therapeutic targets. As a result, we identified the extracellular matrix protein versican and Toll-like receptor 2 as potential targets for modulating the inflammatory response. In summary, the proposed method can be of great utility in systematically identifying therapeutic targets for modulating pathological immune responses.


Subject(s)
COVID-19/pathology , Immunologic Factors/metabolism , Inflammation/pathology , Systems Biology/methods , COVID-19/immunology , COVID-19/virology , Cell Communication , Cytokines/genetics , Cytokines/metabolism , Humans , Immunity, Innate , Lymphocytes/cytology , Lymphocytes/immunology , Lymphocytes/metabolism , Receptors, Chemokine/genetics , Receptors, Chemokine/metabolism , SARS-CoV-2/isolation & purification , Severity of Illness Index , Toll-Like Receptor 2/antagonists & inhibitors , Toll-Like Receptor 2/metabolism , Versicans/antagonists & inhibitors , Versicans/metabolism
8.
Trends Immunol ; 42(1): 31-44, 2021 01.
Article in English | MEDLINE | ID: covidwho-1065238

ABSTRACT

The majority of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-infected individuals remain paucisymptomatic, contrasting with a minority of infected individuals in danger of death. Here, we speculate that the robust disease resistance of most individuals is due to a swift production of type I interferon (IFNα/ß), presumably sufficient to lower the viremia. A minority of infected individuals with a preexisting chronic inflammatory state fail to mount this early efficient response, leading to a delayed harmful inflammatory response. To improve the epidemiological scenario, we propose combining: (i) the development of efficient antivirals administered early enough to assist in the production of endogenous IFNα/ß; (ii) potentiating early IFN responses; (iii) administering anti-inflammatory treatments when needed, but not too early to interfere with endogenous antiviral responses.


Subject(s)
Antiviral Agents/immunology , COVID-19/immunology , Immunologic Factors/immunology , Interferon Type I/immunology , SARS-CoV-2/immunology , Angiotensin-Converting Enzyme 2/immunology , Angiotensin-Converting Enzyme 2/metabolism , Antiviral Agents/metabolism , Antiviral Agents/therapeutic use , COVID-19/drug therapy , COVID-19/virology , Cytokines/immunology , Cytokines/metabolism , Humans , Immunologic Factors/metabolism , Immunologic Factors/therapeutic use , Interferon Type I/metabolism , SARS-CoV-2/drug effects , SARS-CoV-2/metabolism , Serine Endopeptidases/immunology , Serine Endopeptidases/metabolism , Virus Replication/drug effects , Virus Replication/immunology
9.
J Neuroimmune Pharmacol ; 16(2): 270-288, 2021 06.
Article in English | MEDLINE | ID: covidwho-1064584

ABSTRACT

Extracellular vesicles (EVs) are the common designation for ectosomes, microparticles and microvesicles serving dominant roles in intercellular communication. Both viable and dying cells release EVs to the extracellular environment for transfer of cell, immune and infectious materials. Defined morphologically as lipid bi-layered structures EVs show molecular, biochemical, distribution, and entry mechanisms similar to viruses within cells and tissues. In recent years their functional capacities have been harnessed to deliver biomolecules and drugs and immunological agents to specific cells and organs of interest or disease. Interest in EVs as putative vaccines or drug delivery vehicles are substantial. The vesicles have properties of receptors nanoassembly on their surface. EVs can interact with specific immunocytes that include antigen presenting cells (dendritic cells and other mononuclear phagocytes) to elicit immune responses or affect tissue and cellular homeostasis or disease. Due to potential advantages like biocompatibility, biodegradation and efficient immune activation, EVs have gained attraction for the development of treatment or a vaccine system against the severe acute respiratory syndrome coronavirus 2 (SARS CoV-2) infection. In this review efforts to use EVs to contain SARS CoV-2 and affect the current viral pandemic are discussed. An emphasis is made on mesenchymal stem cell derived EVs' as a vaccine candidate delivery system.


Subject(s)
COVID-19/drug therapy , Drug Delivery Systems/trends , Extracellular Vesicles , SARS-CoV-2/drug effects , Animals , Antiviral Agents/administration & dosage , Antiviral Agents/metabolism , COVID-19/immunology , COVID-19/metabolism , Drug Delivery Systems/methods , Extracellular Vesicles/immunology , Extracellular Vesicles/metabolism , Humans , Immunity, Cellular/drug effects , Immunity, Cellular/physiology , Immunologic Factors/administration & dosage , Immunologic Factors/metabolism , SARS-CoV-2/immunology , SARS-CoV-2/metabolism
10.
Adv Drug Deliv Rev ; 169: 100-117, 2021 02.
Article in English | MEDLINE | ID: covidwho-966180

ABSTRACT

To address the COVID-19 pandemic, there has been an unprecedented global effort to advance potent neutralizing mAbs against SARS-CoV-2 as therapeutics. However, historical efforts to advance antiviral monoclonal antibodies (mAbs) for the treatment of other respiratory infections have been met with categorical failures in the clinic. By investigating the mechanism by which SARS-CoV-2 and similar viruses spread within the lung, along with available biodistribution data for systemically injected mAb, we highlight the challenges faced by current antiviral mAbs for COVID-19. We summarize some of the leading mAbs currently in development, and present the evidence supporting inhaled delivery of antiviral mAb as an early intervention against COVID-19 that could prevent important pulmonary morbidities associated with the infection.


Subject(s)
Antibodies, Monoclonal/therapeutic use , Antiviral Agents/therapeutic use , COVID-19/therapy , Immunologic Factors/therapeutic use , SARS-CoV-2/drug effects , Angiotensin-Converting Enzyme 2/antagonists & inhibitors , Angiotensin-Converting Enzyme 2/metabolism , Animals , Antibodies, Monoclonal/chemistry , Antibodies, Monoclonal/metabolism , Antiviral Agents/chemistry , Antiviral Agents/metabolism , COVID-19/diagnosis , COVID-19/metabolism , Humans , Immunization, Passive , Immunologic Factors/chemistry , Immunologic Factors/metabolism , Protein Structure, Secondary , Protein Structure, Tertiary , SARS-CoV-2/chemistry , SARS-CoV-2/metabolism , Virus Shedding/drug effects , Virus Shedding/physiology
11.
Drug Resist Updat ; 53: 100733, 2020 12.
Article in English | MEDLINE | ID: covidwho-915413

ABSTRACT

The COVID-19 pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), represents an unprecedented challenge to global public health. At the time of this review, COVID-19 has been diagnosed in over 40 million cases and associated with 1.1 million deaths worldwide. Current management strategies for COVID-19 are largely supportive, and while there are more than 2000 interventional clinical trials registered with the U.S. National Library of Medicine (clinicaltrials.gov), results that can clarify benefits and risks of candidate therapies are only gradually becoming available. We herein describe recent advances in understanding SARS-CoV-2 pathobiology and potential therapeutic targets that are involved in viral entry into host cells, viral spread in the body, and the subsequent COVID-19 progression. We highlight two major lines of therapeutic strategies for COVID-19 treatment: 1) repurposing the existing drugs for use in COVID-19 patients, such as antiviral medications (e.g., remdesivir) and immunomodulators (e.g., dexamethasone) which were previously approved for other disease conditions, and 2) novel biological products that are designed to target specific molecules that are involved in SARS-CoV-2 viral entry, including neutralizing antibodies against the spike protein of SARS-CoV-2, such as REGN-COV2 (an antibody cocktail), as well as recombinant human soluble ACE2 protein to counteract SARS-CoV-2 binding to the transmembrane ACE2 receptor in target cells. Finally, we discuss potential drug resistance mechanisms and provide thoughts regarding clinical trial design to address the diversity in COVID-19 clinical manifestation. Of note, preventive vaccines, cell and gene therapies are not within the scope of the current review.


Subject(s)
Antiviral Agents/administration & dosage , COVID-19/drug therapy , Drug Development/methods , Animals , Antibodies, Monoclonal/administration & dosage , Antibodies, Monoclonal/immunology , Antibodies, Monoclonal/metabolism , Antiviral Agents/immunology , Antiviral Agents/metabolism , COVID-19/immunology , COVID-19/metabolism , Drug Development/trends , Humans , Immunologic Factors/administration & dosage , Immunologic Factors/immunology , Immunologic Factors/metabolism , Time Factors , Virus Internalization/drug effects
12.
Prostaglandins Leukot Essent Fatty Acids ; 161: 102177, 2020 10.
Article in English | MEDLINE | ID: covidwho-796199

ABSTRACT

As the infected cases of COVID-19 reach more than 20 million with more than 778,000 deaths globally, an increase in psychiatric disorders including anxiety and depression has been reported. Scientists globally have been searching for novel therapies and vaccines to fight against COVID-19. Improving innate immunity has been suggested to block progression of COVID-19 at early stages, while omega-3 polyunsaturated fatty acids (n-3 PUFAs) have been shown to have immunomodulation effects. Moreover, n-3 PUFAs have also been shown to improve mood disorders, thus, future research is warranted to test if n-3 PUFAs may have the potential to improve our immunity to counteract both physical and mental impact of COVID-19.


Subject(s)
Anxiety/prevention & control , Coronavirus Infections/prevention & control , Depression/prevention & control , Dietary Supplements , Fatty Acids, Omega-3/administration & dosage , Immunologic Factors/administration & dosage , Pandemics/prevention & control , Pneumonia, Viral/prevention & control , Anxiety/immunology , Anxiety/metabolism , Anxiety/virology , Betacoronavirus/immunology , Betacoronavirus/pathogenicity , COVID-19 , Coronavirus Infections/immunology , Coronavirus Infections/metabolism , Coronavirus Infections/virology , Cytokines/biosynthesis , Cytokines/immunology , Dendritic Cells/drug effects , Dendritic Cells/immunology , Dendritic Cells/virology , Depression/immunology , Depression/metabolism , Depression/virology , Epithelial Cells/drug effects , Epithelial Cells/immunology , Epithelial Cells/virology , Fatty Acids, Omega-3/immunology , Fatty Acids, Omega-3/metabolism , Host-Pathogen Interactions/drug effects , Host-Pathogen Interactions/immunology , Humans , Immunity, Innate/drug effects , Immunologic Factors/immunology , Immunologic Factors/metabolism , Lymphocytes/drug effects , Lymphocytes/immunology , Lymphocytes/virology , Macrophages/drug effects , Macrophages/immunology , Macrophages/virology , Pneumonia, Viral/immunology , Pneumonia, Viral/metabolism , Pneumonia, Viral/virology , SARS-CoV-2
13.
Int J Mol Sci ; 21(18)2020 Sep 17.
Article in English | MEDLINE | ID: covidwho-789462

ABSTRACT

At present, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection has quickly become a health emergency because no specifics vaccines or drugs, at this moment, are available. Recent studies have shown that the transplantation of mesenchymal stem cells (MSCs) into Coronavirus Disease 2019 (COVID-19) patients could represent a promising strategy for the development of new therapeutic methods. We speculate and suggest that the secretome of human Oral Tissue Stem Cells (hOTSCs), for their immunomodulatory and anti-inflammatory specific properties, could exert beneficial effects on the COVID-19 patients through an innovative aerosolisation technique. This non-invasive technique can offer multiple advantages in prophylaxis, as well as the prevention and treatment of severe epidemic respiratory syndrome with minimum risk and optimal therapeutic effects. This has the potential to create a novel pathway towards immunomodulatory therapy for the treatment of COVID-19 positive patients.


Subject(s)
Coronavirus Infections/drug therapy , Immunologic Factors/therapeutic use , Mesenchymal Stem Cells/metabolism , Mouth Mucosa/cytology , Pneumonia, Viral/drug therapy , Proteome/therapeutic use , COVID-19 , Humans , Immunologic Factors/metabolism , Pandemics , Proteome/metabolism , Secretory Pathway
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