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1.
Natural Volatiles & Essential Oils ; 8(5):7309-7325, 2021.
Article in English | GIM | ID: covidwho-1812620

ABSTRACT

Background: Covid 19 is highly contagious. Unfortunately, Dental clinic becomes a high risk center for the potential spread of Covid-19 through the aerosols and droplets generated during dental procedure. Aim: To assess the knowledge, perception, attitude of the general population towards dental treatment during COVID 19 pandemic period.

2.
Infect Genet Evol ; 89: 104712, 2021 04.
Article in English | MEDLINE | ID: covidwho-1196742

ABSTRACT

An immunoinformatics-based approach was used to identify potential multivalent subunit CTL vaccine candidates for SARS-CoV-2. Criteria for computational screening included antigen processing, antigenicity, allergenicity, and toxicity. A total of 2604 epitopes were found to be strong binders to MHC class I molecules when analyzed using IEDB tools. Further testing for antigen processing yielded 826 peptides of which 451 were 9-mers that were analyzed for potential antigenicity. Antigenic properties were predicted for 102 of the 451 peptides. Further assessment for potential allergenicity and toxicity narrowed the number of candidate CTL epitopes to 50 peptide sequences, 45 of which were present in all strains of SARS-CoV-2 that were tested. The predicted CTL epitopes were then tested to eliminate those with MHC class II binding potential, a property that could induce hyperinflammatory responses mediated by TH2 cells in immunized hosts. Eighteen of the 50 epitopes did not show class II binding potential. To our knowledge this is the first comprehensive analysis on the proteome of SARS-CoV-2 for prediction of CTL epitopes lacking binding properties that could stimulate unwanted TH2 responses. Future studies will be needed to assess these epitopes as multivalent subunit vaccine candidates which stimulate protective CTL responses against SARS-COV-2.


Subject(s)
COVID-19 Vaccines/immunology , Epitopes, T-Lymphocyte/immunology , Vaccines, Combined/immunology , Vaccines, Subunit/immunology , Amino Acid Sequence , COVID-19/prevention & control , Epitopes, T-Lymphocyte/chemistry , Histocompatibility Antigens Class I/immunology , Histocompatibility Antigens Class II/immunology , Humans , Immunogenicity, Vaccine/immunology , Molecular Docking Simulation , Proteomics/methods , T-Lymphocytes, Cytotoxic/immunology
3.
3 Biotech ; 10(11): 479, 2020 Nov.
Article in English | MEDLINE | ID: covidwho-885141

ABSTRACT

The complement system is a stakeholder of the innate and adaptive immune system and has evolved as a crucial player of defense with multifaceted biological effects. Activation of three complement pathways leads to consecutive enzyme reactions resulting in complement components (C3 and C5), activation of mast cells and neutrophils by anaphylatoxins (C3a and C5a), the formation of membrane attack complex (MAC) and end up with opsonization. However, the dysregulation of complement cascade leads to unsolicited cytokine storm, inflammation, deterioration of alveolar lining cells, culminating in acquired respiratory destructive syndrome (ARDS). Similar pathogenesis is observed with the middle east respiratory syndrome (MERS), severe acquired respiratory syndrome (SARS), and SARS-CoV-2. Activation of the lectin pathway via mannose-binding lectin associated serine protease 2 (MASP2) is witnessed under discrete viral infections including COVID-19. Consequently, the spontaneous activation and deposits of complement components were traced in animal models and autopsy of COVID-19 patients. Pre-clinical and clinical studies evidence that the inhibition of complement components results in reduced complement deposits on target and non-target tissues, and aid in recovery from the pathological conditions of ARDS. Complement inhibitors (monoclonal antibody, protein, peptide, small molecules, etc.) exhibit great promise in blocking the activity of complement components and its downstream effects under various pathological conditions including SARS-CoV. Therefore, we hypothesize that targeting the potential complement inhibitors and complement cascade to counteract lung inflammation would be a better strategy to treat COVID-19.

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