In vitro methods for testing antiviral drugs

Rumlová, Michaela; Ruml, Tomáš

doi:10.1016/j.biotechadv.2017.12.016

Cited by 40 publications

(36 citation statements)

References 390 publications

(395 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Uncoating is induced by the low pH environment of the endosomes, where the viral proteins enter into a fusion-active state and initiate the merging of the viral envelope with the endosomal membrane, thereby releasing the viral RNA genome into the cytoplasm (Kaufmann and Rossmann, 2011 ; Smit et al, 2011 ). This process requires two steps, the fusion between the viral and endosomal membranes and the uncoating of the protective capsid shell (Rumlová and Ruml, 2018 ). To analyze the fusion event, the lipid composition of the viral membrane of different viruses has been characterized (Brügger et al, 2006 ; Kalvodova et al, 2009 ; Merz et al, 2011 ; Gerl et al, 2012 ; Reddy and Sansom, 2016 ).…”

Section: The Role Of Host Cholesterol During the Flavivirus Life Cyclmentioning

confidence: 99%

The Role of Host Cholesterol During Flavivirus Infection

Osuna-Ramos

Reyes-Ruiz

Ángel

2018

Front. Cell. Infect. Microbiol.

121

View full text Add to dashboard Cite

In recent years the emergence and resurgence of arboviruses have generated a global health alert. Among arboviruses, Dengue (DENV), Zika (ZIKV), Yellow Fever (YFV), and West Nile (WNV) virus, belong to the genus Flavivirus, cause high viremia and occasionally fatal clinical disease in humans. Given the genetic austerity of the virus, they depend on cellular factors and organelles to complete its replication. One of the cellular components required for flavivirus infection is cholesterol. Cholesterol is an abundant lipid in biomembranes of eukaryotes cells and is necessary to maintain the cellular homeostasis. Recently, it has been reported, that cholesterol is fundamental during flavivirus infection in both mammal and insect vector models. During infection with DENV, ZIKV, YFV, and WNV the modulation of levels of host-cholesterol facilitates viral entry, replicative complexes formation, assembly, egress, and control of the interferon type I response. This modulation involves changes in cholesterol uptake with the concomitant regulation of cholesterol receptors as well as changes in cholesterol synthesis related to important modifications in cellular metabolism pathways. In view of the flavivirus dependence of cholesterol and the lack of an effective anti-flaviviral treatment, this cellular lipid has been proposed as a therapeutic target to treat infection using FDA-approved cholesterol-lowering drugs. This review aims to address the dependence of cholesterol by flaviviruses as well as the basis for anti flaviviral therapy using drugs which target is cholesterol synthesis or uptake.

show abstract

Section: The Role Of Host Cholesterol During the Flavivirus Life Cyclmentioning

confidence: 99%

The Role of Host Cholesterol During Flavivirus Infection

Osuna-Ramos

Reyes-Ruiz

Ángel

2018

Front. Cell. Infect. Microbiol.

121

View full text Add to dashboard Cite

show abstract

“…It was successes in preventing of CPV2 replication in puppies as showed in Fig. 2 and virus recovering, which revealed absences of viral particles in fecal swabs, leukopenia, lymphopenia and hypoproteinemia in compared to 2nd group and this supported by Piret et al, who mentioned that the Acyclovir diverges from earlier nucleoside analogues in covering only a partial nucleoside structure: the sugar ring is replaced with an open-chain structure [12,16] It is selectively converted into 9-(2-hydroxyethomethyl)guanine phosphoromonomorpholidate which is far more effective in phosphorylation than cellular thymidine kinase. Subsequently, the monophosphate form is further phosphorylated into the active triphosphate form, 9-(2-hydroxyethomethyl guanine phosphoromonomorpholidate, by cellular kinases.…”

Section: Discussionmentioning

confidence: 66%

Phosphorimidate Derivatives of Acyclovir; Antiviral Activity Against Canine Parvovirus In Vitro

Oak

Mali

Chopade³

et al. 2019

Preprint

View full text Add to dashboard Cite

Canine parvovirosis is a very transmissible, severe and often deadly infectious disease of dogs caused by Type II canine parvovirus (CPV-2). Recently shows that Parvoviruses are very resistant to Acyclovir which is often used for HSV Chemotherapy in humans and various virucidal purposes in animal diseases in veterinary clinics and animal housing facilities. If acquiescence with vaccination programs and with appropriate decontamination plans is guaranteed, there should be no continuous, nor common, CPV-2 outbreaks. However, a continuous spread of CPV-2 infections is observed, even in shelters where an appropriate vaccination program is applied, and this is reason to provide an antiviral drug therapy. The aim of the present study was to Development of antiviral drugs with determination the effect of concentration of new chemical entity and analyze Acyclovir analogous against CPV-2 strains. A sensitive in vitro assay capable of measuring the infectivity of CPV-2 was employed to determine the efficacy of three different concentrations of 9-(2-hydroxyethomethyl)guanine phosphoromonomorpholidate. We successfully show that new compounds inhibit CPV-2 replication with exhibiting 50% inhibitory concentrations (IC 50 s) in the low-micromolar range (50μM ).

show abstract

“…General overviews on methods for determining antiviral efficacy are available in the literature. 116,118 A very comprehensive overview and compilation of the in vitro methods used for testing antivirals is given in the recent review by Rumlová and Ruml. 118 Information on in vivo models for assessing the antiviral efficacy is also given in reviews 15b,119 as well as in the discussion of the compound classes below.…”

Section: Figurementioning

confidence: 99%