ABSTRACT
The pandemic of the severe acute respiratory syndrome coronavirus (SARS-CoV)-2 at the end of 2019 marked the third outbreak of a highly pathogenic coronavirus affecting the human population in the past twenty years. Cross-species zoonotic transmission of SARS-CoV-2 has caused severe pathogenicity and led to more than 655,000 fatalities worldwide until July 28, 2020. Outbursts of this virus underlined the importance of controlling infectious pathogens across international frontiers. Unfortunately, there is currently no clinically approved antiviral drug or vaccine against SARS-CoV-2, although several broad-spectrum antiviral drugs targeting multiple RNA viruses have shown a positive response and improved recovery in patients. In this review, we compile our current knowledge of the emergence, transmission, and pathogenesis of SARS-CoV-2 and explore several features of SARS-CoV-2. We emphasize the current therapeutic approaches used to treat infected patients. We also highlight the results of in vitro and in vivo data from several studies, which have broadened our knowledge of potential drug candidates for the successful treatment of patients infected with and discuss possible virus and host-based treatment options against SARS-CoV-2.
Subject(s)
Betacoronavirus , Coronavirus Infections , Pandemics , Pneumonia, Viral , Animals , Antiviral Agents/pharmacology , Antiviral Agents/therapeutic use , Betacoronavirus/drug effects , Betacoronavirus/genetics , Betacoronavirus/physiology , COVID-19 , COVID-19 Vaccines , Coronaviridae/pathogenicity , Coronaviridae Infections/epidemiology , Coronaviridae Infections/virology , Coronavirus Infections/drug therapy , Coronavirus Infections/epidemiology , Coronavirus Infections/prevention & control , Coronavirus Infections/therapy , Coronavirus Infections/transmission , Cytokine Release Syndrome/etiology , Cytokine Release Syndrome/prevention & control , Cytokines/antagonists & inhibitors , Drug Delivery Systems , Endocytosis/drug effects , Forecasting , Genome, Viral , Global Health , Humans , Immunity, Herd , Immunization, Passive , Pandemics/prevention & control , Peptide Hydrolases/pharmacology , Peptide Hydrolases/therapeutic use , Pneumonia, Viral/drug therapy , Pneumonia, Viral/epidemiology , Pneumonia, Viral/prevention & control , Pneumonia, Viral/transmission , RNA, Viral/genetics , Receptors, Coronavirus , Receptors, Virus/antagonists & inhibitors , Receptors, Virus/metabolism , SARS-CoV-2 , Spike Glycoprotein, Coronavirus/antagonists & inhibitors , Spike Glycoprotein, Coronavirus/metabolism , Viral Vaccines , Virus Internalization/drug effects , Virus Replication/drug effects , Zoonoses , COVID-19 Drug Treatment , COVID-19 SerotherapyABSTRACT
Dysfunction of CD8+ T cells can lead to the development of chronic viral infection. Identifying mechanisms responsible for such T cell dysfunction is therefore of great importance to understand how to prevent persistent viral infection. Here we show using lymphocytic choriomeningitis virus (LCMV) infection that carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is fundamental for recruiting lymphocyte-specific protein kinase (Lck) into the T cell receptor complex to form an efficient immunological synapse. CEACAM1 is essential for activation of CD8+ T cells, and the absence of CEACAM1 on virus-specific CD8+ T cells limits the antiviral CD8+ T cell response. Treatment with anti-CEACAM1 antibody stabilizes Lck in the immunological synapse, prevents CD8+ T cell exhaustion, and improves control of virus infection in vivo. Treatment of human virus-specific CD8+ T cells with anti-CEACAM1 antibody similarly enhances their proliferation. We conclude that CEACAM1 is an important regulator of virus-specific CD8+ T cell functions in mice and humans and represents a promising therapeutic target for modulating CD8+ T cells.
Subject(s)
Antigens, CD/metabolism , CD8-Positive T-Lymphocytes/immunology , Carcinoembryonic Antigen/metabolism , Cell Adhesion Molecules/metabolism , Lymphocytic Choriomeningitis/immunology , Lymphocytic choriomeningitis virus/immunology , Adoptive Transfer , Animals , Bone Marrow Transplantation , CD8-Positive T-Lymphocytes/metabolism , Carcinoembryonic Antigen/genetics , Chimera , Chronic Disease , Female , Humans , Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/metabolism , Lymphocytic Choriomeningitis/virology , Lymphocytic choriomeningitis virus/pathogenicity , Male , Mice , Mice, Inbred C57BL , Mice, TransgenicABSTRACT
Abfraction or Theory of Abfraction is a theory explaining the non-carious cervical lesions (NCCL). It suggests that they are caused by flexural forces, usually from cyclic loading; the enamel, especially at the cementoenamel junction (CEJ), undergoes this pattern of destruction by separating the enamel rods. Clinical aspect importance of these ineart lesions are at most important to be detected for early intervention and treatment modalities as options during the progression of the disease. How to cite this article: Shetty SM, Shetty RG, Mattigatti S, Managoli NA, Rairam SG, Patil AM. No Carious Cervical Lesions: Abfraction. J Int Oral Health 2013; 5(5):142-5.
