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Medicinal Plants Against COVID-19
Published in Hanadi Talal Ahmedah, Muhammad Riaz, Sagheer Ahmed, Marius Alexandru Moga, The Covid-19 Pandemic, 2023
Binish Khaliq, Naila Ali, Ahmed Akrem, M. Yasin Ashraf, Arif Malik, Arifa Tahir, M. Zia-Ul-Haq
In addition to, a flavonoid such as quercetin and saponin was isolated from the T. sinensis leaf extract and liquor ice roots, respectively [80, 81] showed strong antiviral activity against the SARS coronavirus. These compounds stop the cellular attachment and prevent the entry of virus to the human cell. More than 10,000 different compounds like drugs, natural, and synthetic are screened, and these compounds showed the effect results against the SARS coronavirus [82]. Indole alkaloids and were isolated from eucalyptus, L. japonica and Rauwolfia and from chestnut tree, respectively inhibited aescin the SARS coronavirus replication [82]. RNA dependent RNA polymerase is the major enzyme in the replication of SARS coronavirus, which synthesized the positive and negative strand of coronavirus RNA. A toxic steroid-like cardenolides were obtained from the plant and swine testicular cells inhibited the gastro entry of coronavirus [83]. These results showed that toxic cardenolide reduce the 50% RNA copies and suppress the viral replication [83].
The Viruses
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
The neuraminidase enables influenza virus to penetrate mucous secretions by virtue of its enzymatic activity. Neuraminidase also promotes the release of the virions as they bud from the cell surface. The envelope hemagglutinin serves to attach the virus to cells by binding to cell receptors. The virus then enters the cell in an endosomal vesicle. As the pH of the vesicle becomes acidic, the hemagglutinin changes conformation and allows fusion of the viral envelope with the endosomal membrane, resulting in uncoating and release of the viral nucleocapsid into the cell cytoplasm. Influenza viruses, unlike most RNA viruses, replicate in the cell nucleus rather than in the cytoplasm. The influenza virus has a negative stranded RNA, which is not translated directly by the host cell. Initiation of replication is possible because the virus encodes and packages its own RNA-dependent RNA polymerase. The viral RNA consists of eight different single-stranded segments, each coding for at least one of the major viral proteins. If two strains of influenza A virus infect the same cell, an interchange of entire genomic segments can occur (reassortment). Unlike classical genetic recombination, splicing and rejoining of the nucleic acid is not required in this process. Related influenza A viruses also infect animals of a variety of species, including pigs and many types of birds. These viral strains represent potential pools of genetic material for pathogenic human influenza strains by reassortment of genomic segments between animal and human influenza strains that infect a common host.
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
Coronaviruses utilise RNA dependent RNA synthesis to generate mRNAs to be transcribed by host cell machinery. The RNA dependent RNA polymerase is synthesised from sense RNA (original genomic RNA). This viral polymerase is attached to the 3' end of the original viral genomic RNA (+ssRNA) and initiates the transcription process. During this transcription process, the RNA dependent RNA polymerase synthesises a series of positive-sense subgenomic mRNAs that vary in their length. This occurs by discontinuous transcription.
Drugs repurposing for SARS-CoV-2: new insight of COVID-19 druggability
Published in Expert Review of Anti-infective Therapy, 2022
Sujit Kumar Debnath, Monalisha Debnath, Rohit Srivastava, Abdelwahab Omri
Remdesivir is a nucleoside analog that inhibits coronaviruses’ RNA-dependent RNA polymerase (RdRp). Remdesivir is a phosphoramidite prodrug metabolized in cells to produce an active NTP analog known as remdesivir triphosphate. RdRp attributes the conversion from this triphosphate to monophosphate. This RdRp also extends RNA by nucleotides before exerting stalling mechanism to specific CoVs. It was observed that RdRp-RNA complexes were formed after adding remdesivir with RNA product 3’-end. Studies showed remdesivir monophosphate mimics adenosine monophosphate and forms standard [86]. This drug is effective against many viruses, like coronaviruses, pneumoviruses, paramyxoviruses, filoviruses, Ebola virus, etc. A placebo-controlled, randomized, double-blind trial was conducted with remdesivir [87]. The adverse effects were reported in 66% of patients, and an early stop of treatment was reported in 12% of patients. This study did not support the statistically significant improvement of clinical benefits.
Considerations of the effects of commonly investigated drugs for COVID-19 in the cholesterol synthesis pathway
Published in Expert Opinion on Pharmacotherapy, 2021
Juan Luis Gomez Marti, Adam M. Brufsky
Inhibition of the RNA-dependent RNA polymerase (RdRp) has been tried with suboptimal results. Reverse transcriptase inhibitors such as remdesivir have modest efficacy in the treatment of hospitalized patients, it does not clearly result in an increased survival rate [37]. The viral replication machinery of SARS-CoV-2 contains exonuclease-based proofreading, which promotes replication and removal of exogenous nucleotide analogs. Deoxyribose-containing RdRp nucleotide analogs have been shown to be more resistant to the exonuclease proofreading complex than those containing ribose rings such as remdesivir. In this regard, sofosbuvir contains a deoxyribose that exhibits more resistance to this proofreading complex, providing more stability than remdesivir [38]. Trial results evaluating sofosbuvir efficacy against COVID-19 are encouraging. A meta-analysis showed that sofosbuvir in combination with daclatasvir improved time to clinical recovery (HR = 2.04), as well as all-cause mortality compared to control arms (risk ratio = 0.31) [39]. Another trial reported a half-reduction in duration of hospital stay compared to ribavirin (5 vs 9 days, respectively), relative risk of death of 0.17, and a number needed-to-treat for benefit of 3.6 [40].
Ravaging SARS-CoV-2: rudimentary diagnosis and puzzling immunological responses
Published in Current Medical Research and Opinion, 2021
Tapan Kumar Mukherjee, Parth Malik, Radhashree Maitra, John R. Hoidal
It is further noted that RNA viruses are notorious for high mutation rates which can occur a million times faster than that of their hosts. This feature is a primary reason why we need an influenza vaccine every year. The mutagenic capability of a virus depends upon several factors, including the fidelity of viral enzymes that replicate nucleic acids. In the case of SARS-CoV-2, the fidelity of the RNA dependent RNA polymerase (RdRp) is critical. Mutation rates drive viral evolution and genome variability, thereby enabling the virus to escape host immunity and develop drug resistance20. Pachetti et al. reported that the viral genomes present different point mutations, distinguishable within different geographic areas. Three recurrent mutations were identified in Europe (in positions 3036, 14,408 and 23,403) and three different mutations were identified in North America (in positions 17,746, 17,857 and 18,060). These mutations are yet to be detected in Asia. However, the number and occurrence, as well as the median value of virus point mutations identified in Asia, is ever increasing.