Differential in vitro inhibition of feline enteric coronavirus and feline infectious peritonitis virus by actinomycin D

Lewis, Evelyn L.; Harbour, D. A.; Beringer, J. E.; Grinsted, J.

doi:10.1099/0022-1317-73-12-3285

Cited by 16 publications

(8 citation statements)

References 24 publications

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“…For MHV, it was shown some time ago that viral replication could occur in enucleated cells or in cells treated with actinomycin D or -amanitin, host RNA polymerase inhibitors (Brayton et al, 1981;Wilhelmsen et al, 1981). By contrast, other studies reported that similar conditions reduced the growth yield of IBV, HCoV-229E, or FCoV (Evans and Simpson, 1980;Kennedy and Johnson-Lussenburg, 1979;Lewis et al, 1992). Even if coronavirus replication does not have an absolute dependence on the nucleus, the possibility remains that some viruses can alter host nuclear functions so as to create an environment more favorable for viral infection.…”

Section: E Nucleocapsid Protein (N)mentioning

confidence: 99%

The Molecular Biology of Coronaviruses

Masters

2006

Advances in Virus Research

1,534

1,677

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Coronaviruses are large, enveloped RNA viruses of both medical and veterinary importance. Interest in this viral family has intensified in the past few years as a result of the identification of a newly emerged coronavirus as the causative agent of severe acute respiratory syndrome (SARS). At the molecular level, coronaviruses employ a variety of unusual strategies to accomplish a complex program of gene expression. Coronavirus replication entails ribosome frameshifting during genome translation, the synthesis of both genomic and multiple subgenomic RNA species, and the assembly of progeny virions by a pathway that is unique among enveloped RNA viruses. Progress in the investigation of these processes has been enhanced by the development of reverse genetic systems, an advance that was heretofore obstructed by the enormous size of the coronavirus genome. This review summarizes both classical and contemporary discoveries in the study of the molecular biology of these infectious agents, with particular emphasis on the nature and recognition of viral receptors, viral RNA synthesis, and the molecular interactions governing virion assembly.

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Section: E Nucleocapsid Protein (N)mentioning

confidence: 99%

The Molecular Biology of Coronaviruses

Masters

2006

Advances in Virus Research

1,534

1,677

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“…Dactinomycin has been shown to inhibit the growth of feline enteric coronavirus strain in feline embryo cells. 110 A recent computational study employing a network-based drug repurposing approach suggested sirolimus and dactinomycin as one of the potential drug combinations which could be effective in treating SARS-CoV-2 infection. 111 It is to be noted that most FDA-approved antiviral agents that target viral proteases are peptidomimetics and macrocyclic compounds.…”

Section: Hits With Support From Available Laboratory and Clinical Datamentioning

confidence: 99%

Repurposing drugs against main protease of SARS-CoV-2: mechanism based insights supported by available laboratory and clinical data

Chakraborti

Bheemireddy²,

Srinivasan³

2020

Preprint

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The ongoing global pandemic of COVID-19 has brought life to almost stand still with implementations of lockdown and social distancing as some of the preventive measures in the absence of any approved specific therapeutic interventions. To combat this crisis, research community world-wide are falling back on the existing repertoire of approved/investigational drugs to probe into their anti-coronavirus properties. In this report, we have described our unique efforts in identifying potential drugs that could be repurposed against main protease of SARS-CoV-2 (SARS-CoV-2 Mpro). To achieve this goal, we have primarily exploited the principles of ‘neighbourhood behaviour’ in protein 3-D (workflow-I) and chemical 2-D structural space (workflow-II) coupled with docking simulations and insights into the possible mode of actions of the selected candidates from available literature. Such an integrative approach culminated in prioritizing 29 potential repurpose-able agents (20 approved drugs and 9 investigational molecules) against SARS-CoV-2 Mpro. Apart from the approved/investigational anti-viral drugs, other notable hits include anti-bacterial, anti-inflammatory, anti-cancer and anti-coagulant drugs. Our analysis suggests that some of these drugs have the potential to simultaneously modulate the functions of viral proteins and host response system. Interestingly, many of these identified candidates (12 molecules from workflow-I and several molecules belonging to the chemical classes of alkaloids, tetracyclines, peptidomimetics from workflow-II) are suggested to possess anti-viral properties which are supported by laboratory and clinical data. Further, this work opens a new avenue of research to probe into the molecular mechanism of action of many drugs which are known to demonstrate anti-viral activity but are so far not known to target viral proteases. Our findings should only be used for research purposes and we strongly urge that no individual should interpret these findings for any self-diagnosis or self-medication without the prior approval from competent international health/medical regulatory agencies.

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“…Actinomycin D (ActD) is a general inhibitor of host RNA synthesis. Viral titers of several cytoplasmic RNA viruses including arenaviruses [115][116][117], measles virus [118], sindbis virus [119], rubella virus [120], polio virus [121,122], coronaviruses [123,124], and lactic dehydrogenase elevating virus [125] could be reduced in the presence of ActD, while the viral RNA synthesis is often unaffected [115,118,123]. We found that expression of NSs protein is essential for the RVFV MP-12 strain to actively synthesize viral proteins and produce high titers of infectious viruses in the presence of ActD [126]; cells infected with recombinant RVFV MP-12 lacking NSs failed to synthesize viral proteins; and while cells infected with MP-12 lacking NSs accumulated phosphorylated eIF2.…”

Section: Role Of Nss Protein In Viral Virulencementioning

confidence: 99%

The Pathogenesis of Rift Valley Fever

Ikegami

Makino

2011

Viruses

309

308

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Rift Valley fever (RVF) is an emerging zoonotic disease distributed in sub-Saharan African countries and the Arabian Peninsula. The disease is caused by the Rift Valley fever virus (RVFV) of the family Bunyaviridae and the genus Phlebovirus. The virus is transmitted by mosquitoes, and virus replication in domestic ruminant results in high rates of mortality and abortion. RVFV infection in humans usually causes a self-limiting, acute and febrile illness; however, a small number of cases progress to neurological disorders, partial or complete blindness, hemorrhagic fever, or thrombosis. This review describes the pathology of RVF in human patients and several animal models, and summarizes the role of viral virulence factors and host factors that affect RVFV pathogenesis.

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Differential in vitro inhibition of feline enteric coronavirus and feline infectious peritonitis virus by actinomycin D

Cited by 16 publications

References 24 publications

The Molecular Biology of Coronaviruses

The Molecular Biology of Coronaviruses

Repurposing drugs against main protease of SARS-CoV-2: mechanism based insights supported by available laboratory and clinical data

The Pathogenesis of Rift Valley Fever

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