Main Article Content
Novel Coronavirus are very harmful virus. This viruses have positive single stranded RNA genome and enveloped which is called nucleocapsid. The family of this virus is Coronaviridae. This virus originated from species of avian and mammalian. This virus effect on upper respiratory tract in humans. Many species of these novel coronaviruses (HCoVs) are named as HCoV-HKU1, HCoV-NL63. Predominant species of this virus is Middle East respiratory syndrome (MERS-CoV) across the world. In both adults and childrens HCoV-HKU1 sp. is causes for chronic pulmonary disease and HCoV-NL63 species causes for upper and lower respiratory tract disease. Most recent species of this virus is MERS-CoV. This species caused for acute pneumonia and occasional renal failure. The new strain of novel Coronavirus is SARS-CoV-2. This strain causes for the Coronavirus Disease 2019 (COVID-19). This disease named by the World Health Organization. Now world fighting against COVID-19 and according to the recent statistics report of world about the COVID-19 cases approx 22.6M confirmed cases and 792K death cases appeared and recovered 14.5M. COVID-19 disease starts to spread from December 2019 from china. Covid-19 disease is emerged in Wuhan seafood market at Wuhan of South China and then rapidly spread throughout the world. The corona virus outbreak has been declared a public health emergency of International concern by World Health Organization (WHO). In this article we summarize the current clinical characteristics of coronavirus and diagnosis, treatments and prevention of COVID-19 disease. In this review article, we analyze data from various Research Reports like WHO guidelines and other articles. It is very important to the readers that new data of COVID-19 updating nearly every hour of day regarding clinical characteristics, diagnosis, treatment strategies, and outcomes COVID-19 disease. The degree of COVID-19 disease varying throughout the world. COVID-19 affected patient shows various symptoms like fever, cough, sore throat, breathlessness, fatigue, and malaise among others. The COVID-19 disease is being treated through general treatment like symptomatic treatment, by using antiviral drugs, oxygen therapy and by the immune system. There is no vaccine or therapeutic strategies for deal with this disease yet. In this critical situation preventive measures must be require. A very important issue in preventing viral infection is hand hygiene. There are other entities that people can boosting the immune system and help in infection prevention.
Fung TS, Huang M, Liu DX. Coronavirus-induced ER stress response and its involvement in regulation of coronavirus-host interactions. Virus Res. 2014;194: 110–23.
Chen IY, Chang SC, Wu HY, Yu TC, et al. Upregulation of the Chemokine (C-C Motif) Ligand 2 via a Severe Acute Respiratory Syndrome Coronavirus Spike-ACE2 Signaling Pathway. J. Virol. 2010;84:7703–12.
Cui J, Li F, Shi ZL. Origin and evolution of pathogenic coronaviruses. Nat. Rev. Microbiol. 2019;17:181– 92.
Hui DS, Azhar E, Madani TA, Ntoumi F, Kock R, et al. The continuing 2019-nCoV epidemic threat of novel coronaviruses to global health-The latest 2019 novel coronavirus outbreak in Wuhan, China. Int. J. Infect. Dis. 2020;91:264–66.
Fung, TS, Liao Y, Liu DX. The Endoplasmic Reticulum Stress Sensor IRE1α Protects Cells from Apoptosis Induced by the Coronavirus Infectious Bronchitis Virus. J. Virol. 2014;88:12752–64.
Liao Y, Fung TS, Huang M, Fang SG, Zhong Y, et al. Upregulation of CHOP/GADD153 during Coronavirus Infectious Bronchitis Virus Infection Modulates Apoptosis by Restricting Activation of the Extracellular Signal-Regulated Kinase Pathway. J. Virol. 2013; 87:8124–34.
Siu KL, Chan CP, Kok KH, Woo CY, Jin P, et al. Comparative analysis of the activation of unfolded protein response by spike proteins of severe acute respiratory syndrome coronavirus and human coronavirus HKU1. Cell BioSci. 2014;4:1–9.
De-Diego ML, Nieto-Torres JL, Regla-Nava JA, Jimenez-Guardeño JM, Fernandez-Delgado R, et al. Inhibition of NF-κB-Mediated Inflammation in Severe Acute Respiratory Syndrome Coronavirus-Infected Mice Increases Survival. J. Virol. 2014;88:13–24.
Bertram S, Dijkman R, Habjan M, Heurich A, Gierer S, et al. TMPRSS2 Activates the Human Coronavirus 229E for Cathepsin-Independent Host Cell Entry and Is Expressed in Viral Target Cells in the Respiratory Epithelium. J. Virol. 2013;87: 50–60.
Bertram S, Glowacka I, Müller MA, Lavender H, Gnirss K, et al. Cleavage and Activation of the Severe Acute Respiratory Syndrome Coronavirus Spike Protein by Human Airway Trypsin-Like Protease. J. Virol. 2011;85: 63–72.
Millet JK, Whittaker GR, Host cell entry of Middle East respiratory syndrome coronavirus after twostep, furin-mediated activation of the spike protein. Proc. Natl. Acad. Sci. USA. 2014;111:14–19.
Huang IC, Bailey CC, Weyer JL, Radoshitzky SR, Becker MM, et al. Distinct Patterns of IFITMMediated Restriction of Filoviruses, SARS Coronavirus, and Influenza A Virus. PLoS Pathog. 2011;7: e1001258.
Li K, Markosyan RM, Zheng YM, Golfetto O. Bungart B, et al. IFITM Proteins Restrict Viral Membrane Hemifusion. PLoSPathog. 2013;9:e1003124.
Wu CH, Chen PJ, Yeh SH. Nucleocapsid Phosphorylation and RNA Helicase DDX1 Recruitment Enables Coronavirus Transition from Discontinuous to Continuous Transcription. Cell Host Microb. 2014;16:462–72.
Tan YW, Hong W, Liu DX. Binding of the 51untranslated region of coronavirus RNA to zinc finger CCHC-type and RNA-binding motif 1 enhances viral replication and transcription. Nucleic Acids Res. 2012;40: 5065–77.
Neuman BW, Kiss G, Kunding AH, Bhella D, Baksh MF, et al. A structural analysis of M protein in coronavirus assembly and morphology. J. Struct. Biol. 2011;174:11–22
Wong HH, Kumar P, Tay FPL, Moreau D, Liu DX, et al. Genome-Wide Screen Reveals Valosin-Containing Protein Requirement for Coronavirus Exit from Endosomes. J. Virol. 2015;89:11116–28.
Segawa K, Kurata S, Yanagihashi Y, Brummelkamp TR, Matsuda ,et al. Caspase-mediated cleavage of phospholipid flippase for apoptotic phosphatidyl serine exposure. Sci. 2014;344:1164–68.
Pearce AF, Lyles DS. Vesicular Stomatitis Virus Induces Apoptosis Primarily through Bak Rather than Bax by Inactivating Mcl-1 and Bcl-XL. J. Virol. 2009;83:9102–12.
Tamura R, Kanda T, Imazeki F, Wu S, Nakamoto S, et al. Hepatitis C Virus Nonstructural 5A Protein Inhibits Lipopolysaccharide-Mediated Apoptosis of Hepatocytes by Decreasing Expression of Toll-Like Receptor 4. J. Infect. Dis. 2011; 204:793–801.
Aweya JJ, Sze CW, Bayega A, Mohd-Ismail NK, Deng L, et al. NS5B induces up-regulation of the BH3-only protein, BIK, essential for the hepatitis C virus RNA replication and viral release. Virol. 2015;474:41–51.
Nakamura-Lopez Y, Villegas-Sepúlveda N, Gomez B. RSV P-protein impairs extrinsic apoptosis pathway in a macrophage-like cell line persistently infected with respiratory syncytial virus. Virus Res. 2015;204:82–87.
Mocarski ES, Upton JW, Kaiser WJ. Viral infection and the evolution of caspase 8-regulated apoptotic and necrotic death pathways. Nat. Rev. Immunol. 2012;12: 79–88.
Tao X, Hill TE, Morimoto C, Peters CJ, Ksiazek TG, et al. Bilateral Entry and Release of Middle East Respiratory Syndrome Coronavirus Induces Profound Apoptosis of Human Bronchial Epithelial Cells. J. Virol. 2013;87:9953–58.
Yeung ML, Yao Y, Jia L, Chan JFW, Chan KH, et al. MERS coronavirus induces apoptosis in kidney and lung by upregulating Smad7 and FGF2. Nat. Microbiol. 2016;1:16004.
Desforges M, Le Coupanec A, Stodola JK, Meessen Pinard M, Talbot PJ. Human coronaviruses: Viral and cellular factors involved in neuro invasiveness and neuro pathogenesis. Virus Res. 2014;194:145–58.
Favreau DJ, Meessen-Pinard M, Desforges M, et al. Human Coronavirus-Induced Neuronal Programmed Cell Death Is Cyclophilin D Dependent and Potentially Caspase Dispensable. J. Virol. 2012;86: 81–93.
Krähling V, Stein DA, Spiegel M, Weber F, Mühlberger E. Severe Acute Respiratory Syndrome Coronavirus Triggers Apoptosis via Protein Kinase R but Is Resistant to Its Antiviral Activity. J. Virol. 2009;83:2298–309.
Ben HN, Leghmari K, Planès R, Thieblemont N, et al. HIV-1 Tat protein binds to TLR4-MD2 and signals to induce TNF-α and IL-10. Retrovirol. 2013;10:1–12.
Kumar H, Kawai T, Akira S. Toll-like receptors and innate immunity. Biochem. Biophys. Res. Commun. 2009;388:621–25.
Brown J, Wang H, Hajishengallis GN, Martin M. TL. Rsignaling Networks: An Integration of Adaptor Molecules, Kinases, and Cross-talk. J. Dent. Res. 2011;90: 417–27