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Epidemiology, Pharmacology, Diagnosis, and Treatment of COVID-19
Published in Joystu Dutta, Srijan Goswami, Abhijit Mitra, COVID-19 and Emerging Environmental Trends, 2020
Joystu Dutta, Srijan Goswami, Abhijit Mitra
After uncoating, the genomic RNA of coronaviruses act as mRNA for translation of replicase polyproteins 1a and 1ab. Proteolytic cleavage of these polyproteins produces a number of nonstructural proteins including RNA-dependent RNA polymerase (RdRp), helicase, and nonstructural proteins 3, 4, and 6. These nonstructural proteins 3, 4, and 6 are thought to be responsible for anchoring the coronavirus replication transcription complex through recruitment of intracellular endoplasmic reticulum membranes to form double-membrane vesicles abbreviated as DMVs. RdRp and helicase localize to double-membrane vesicles and drive the production of subgenomic mRNAs from which the structural accessory protein is produced in the next phase of translation. Now RdRp is a target for investigational drugs such as remdesivir (Al-Tawfiq et al., 2020) and favipiravir (Qingxian et al., 2020). Preliminary research has shown that both of these agents inhibit RdRp and thus might be useful in the treatment of early and mid-stages of coronavirus disease.
Clinical and epidemiological context of COVID-19
Published in Sanjeeva Srivastava, Multi-Pronged Omics Technologies to Understand COVID-19, 2022
Viswanthram Palanivel, Akanksha Salkar, Radha Yadav, Renuka Bankar, Om Shrivastav, Arup Acharjee
Some of the antiviral therapies which physicians predominantly use are as follows: Targeting viral entry (fusion inhibitors) Baricitinib, a potent Janus kinase (JAK) inhibitor, binds to AP2-associated protein kinase 1. It inhibits both host inflammatory response and viral entry (Zhang et al. 2020).Camostat mesylate is a TMPRSS2 protease inhibitor that blocks the SARS-CoV-2 infection of lung cells (Hoffmann et al. 2021).Targeting virus replication Reverse transcription inhibitors: Remdesivir is an RNA-dependent RNA polymerase (RdRp) inhibitor and is a broad-spectrum antiviral drug against the significant class of single-stranded RNA (ssRNA) viruses (Amirian and Levy 2020).Nucleotide analogs: Favipiravir is a purine (Guanine) analog. It blocks the RdRp to arrest viral RNA synthesis (Furuta, Komeno, and Nakamura 2017). Ribavirin is a guanine derivative analog. It destabilizes viral RNA by inhibiting RNA capping.Protease inhibitors Lopinavir: Lopinavir inhibits the main protease (MPro) of SARSCoV-2. It is used as a lopinavir–ritonavir combination, which shows high efficiency. Primarily, it is an HIV antiviral drug (Nutho et al. 2020).
Epidemiology, virology and clinical aspects of hantavirus infections: an overview
Published in International Journal of Environmental Health Research, 2022
Sima Singh, Arshid Numan, Dinesh Sharma, Rahul Shukla, Amit Alexander, Gaurav Kumar Jain, Farhan Jalees Ahmad, Prashant Kesharwani
Following attachment to a cell surface receptor, the Hantavirus virus is incorporated into the host population. After binding, cell entry is mediated through clathrin-coated pits, and virons are eventually delivered to lysosomes. Virions are uncoated inside the endolysosomal compartment, and three viral capsids are released into the cytoplasm (Jin et al. 2002). This causes the virus to be taken up by a clathrin-coated vesicle (CCV), which is made up of clathrin-coated cellular membrane (Ramanathan and Jonsson 2008). RdRp initiates transcription and produces three mRNAs, one from each S, M, and L section of the viral RNA. The S and L derived mRNAs are translated on free ribosomes. Although M-specific mRNAs are translated on the rough endoplasmic reticulum (ER). Intrinsically, the glycoprotein precursor is cleaved at a closely conserved amino acid motif, yielding two glycoproteins, Gn and Gc (Spiropoulou 2000). The glycoproteins Gn and Gc are transferred to the Golgi complex for glycosylation. Following glycosylation in the ER, Gn and Gc transfer to the Golgi complex. Hanta virions are assumed to form in the Golgi complex. It is accompanied by budding into the Golgi cisternae, migration to the plasma membrane of secretory vesicles, and exocytosis. However, the specifics of virion egress mostly remain unknown (Szabó 2017).