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SARS-CoV-2 Morphology, Genomic Organisation and Lifecycle
Published in Srijan Goswami, Chiranjeeb Dey, COVID-19 and SARS-CoV-2, 2022
Srijan Goswami, Ushmita Gupta Bakshi
The RNA dependent RNA polymerase copies the +ssRNA starting from the 3' end up until it reaches the first transcription regulatory sequence (TRS), for example, the gene for nucleocapsid designated as N in Figure 2.13. From that TRS (corresponding to N gene), the viral polymerase jumps to the 5' end and copies the leader sequence, yielding a small negative mRNA (of N gene). Again, the viral polymerase starts copying from the 3' end of +ssRNA, and this time it ignores the first TRS (i.e., the N gene) and instead recognises the second TRS, for example, the gene for membrane protein designated as M. From that TRS (corresponding to the M gene), the viral polymerase jumps to the 5' end and again copies the leader sequence, yielding another small negative mRNA (of M gene). That means everything in between the TRS and leader sequence (L) is completely omitted. This discontinuous transcription process continues until all the different types of negative subgenomic mRNAs are synthesised that are important for the viral lifecycle. All these newly synthesised negative mRNAs of varying size come from the same strand of original RNA, therefore, they are called subgenomic. The negative subgenomic mRNAs are then converted back to respective positive subgenomic mRNAs, and these are an actual form of subgenomic mRNA that encodes viral structural proteins. These viral structural proteins are combined with original genomic sense genomic RNA to make progeny.
Order Hepelivirales
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
The Benyviridae genomes are linear and consist of four to five segments of 1.3 to 6.7 kb in size. The genomic RNAs are capped, polyadenylated, and serve as messenger RNAs, while subgenomic RNAs are synthesized during replication for segments 2.
Torovirus
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Ziton Abdulrida Ighewish Al-Khafaji, Ghanim Aboud Al-Mola
For many positive-stranded RNA virus, subgenomic RNAs are transcribed, often encoding for structural proteins. The dsRNA genome is transcribed or replicated, thereby providing viral mRNAs and new ssRNA(+) genomes. Structural proteins encoded by subgenomic mRNAs are synthesized. Assembly and budding take place at membranes of the endoplasmic reticulum (ER), the intermediate compartments, or the Golgi complex, or at all three.
COVID-19: a wreak havoc across the globe
Published in Archives of Physiology and Biochemistry, 2023
Heena Rehman, Md Iftekhar Ahmad
There are two types of RNA which are synthesised by the virus, namely genomic and subgenomic RNAs. The sub-genomic RNAs act as mRNA for the structural and accessory genes. These genes are present downstream of the replicase polyprotein. The genomic and subgenomic RNAs are produced from negative RNA strand intermediate. There are certain cis-acting sequences which play a significant role in the replication of RNA. One of the cis-acting sequences is present within the 5′ UTR region. A seven looped structure is present in 5′ UTR region, which may stretch into replicase 1a (Raman et al. 2003, Brown et al. 2007, Liu et al. 2009, Guan et al. 2011). Another cis-acting sequence is present in the 3′ UTR region which is a bulged stem-loop, hypervariable region and a pseudoknot (Hsue and Masters 1997, Williams et al. 1999, Liu et al. 2001, Goebel et al. 2007). However, the stem loop structure and pseudoknot in the 3′ UTR region overlap each other; hence, they cannot form together (Hsue and Masters 1997, Williams et al. 1999, Hsue et al.2000, Goebel et al. 2007). All of these structures control alternate phases of synthesis of RNA. During the production of subgenomic RNAs, the body TRS and leader sequences fuse together. It is speculated that it occurs during the synthesis of positive strand of RNA (Sawicki et al. 2007). RNA dependent RNA polymerase (RdRp) halts at any of the TRS sequence. After this halt, the RdRp either continues elongation to next TRS or switches to multiply leader sequence at 5′ endguided by complementarity of TRS to leader TRS.
Ligand-based discovery of coronavirus main protease inhibitors using MACAW molecular embeddings
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
Jie Dong, Mihayl Varbanov, Stéphanie Philippot, Fanny Vreken, Wen-bin Zeng, Vincent Blay
A variety of medicinal targets to fight infection by SARS-CoV-2 are being investigated8,9, and the main viral protease Mpro is particularly promising. After the virus infects and enters a human host cell, the two main ORF1a/b of its RNA genome first translate and express two polyprotein precursors (pp1a and pp1ab) with the help of the host cell machinery10–14. The polyprotein precursor undergoes intramolecular cleavage under the action of the main protease of SARS-CoV-2, Mpro (also known as 3C-like protease or 3CLpro), and the papain-like protease, PLpro, to produce multiple non-structural proteins (Nsps), Nsp1 to Nsp16. Some of the non-structural proteins produced participate in the production of viral subgenomic RNA encoding the four major structural proteins (Envelope/E protein, Membrane/M protein, Spike/S protein, and Nucleocapsid/N protein), which are needed to complete the reproduction and release of progeny viruses10–14.
Understanding host responses to equine encephalitis virus infection: implications for therapeutic development
Published in Expert Review of Anti-infective Therapy, 2022
Kylene Kehn-Hall, Steven B. Bradfute
There is little known about host factors needed for subgenomic RNA translation. However, a recent study found that Src kinase facilitates subgenomic RNA translation [89]. Inhibitors of Src family kinases, namely Torin 1 and Dasatinib, decreased CHIKV infectious titers and reduced CHIKV and VEEV structural protein synthesis, with no impact on viral RNA levels. Torin 1 and Dasatinib treatment had a broad impact on alphaviruses, reducing production of CHIKV, VEEV, o’nyong’nyong virus (ONNV), Ross River virus (RRV), and MAYV. Sorafenib, traditionally defined as a Raf kinase inhibitor, was also found to inhibit VEEV production through inhibition of subgenomic protein translation [90]. However, sorafenib’s activity was not dependent on c-Raf and b-Raf, but rather on its suppression of phosphorylation of multiple translational proteins, including eukaryotic initiation factor 4E (eIF4E), 70-kDa ribosomal protein S6 kinase (p70S6K), and ribosomal S6. siRNA studies confirmed the importance of the cap-binding protein eIF4E for VEEV replication. Sorafenib had broad alphavirus activity inhibiting replication of VEEV, EEEV, SINV, and CHIKV.