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Inhibitors of Viral Protein Synthesis01:30

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Aminoglycosides constitute a highly potent class of bactericidal antibiotics that exert their antimicrobial effects by targeting the bacterial ribosome, specifically disrupting protein synthesis. These polycationic molecules consist of amino-modified sugars linked via glycosidic bonds to an aminocyclitol core such as 2-deoxystreptamine or streptamine. Their strong positive charges facilitate tight binding to the negatively charged phosphate backbone of ribosomal RNA (rRNA), primarily at the 16S...
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Viral meningitis is the most common form of meningitis and is often referred to as aseptic meningitis to indicate the absence of bacterial involvement. It is generally milder than bacterial meningitis, with symptoms including fever, headache, stiff neck, drowsiness, nausea, photophobia, and vomiting. Rarely, more severe manifestations or death may occur. Common causative agents include enteroviruses, particularly coxsackie A and B viruses and echoviruses, all members of the Enterovirus genus...
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Suramin inhibits EV71 infection.

Yaxin Wang1, Jie Qing2, Yuna Sun1

  • 1National Laboratory of Macromolecules, Institute of Biophysics, Chinese Academy of Science, Beijing 100101, China.

Antiviral Research
|December 31, 2013
PubMed
Summary
This summary is machine-generated.

Suramin, a drug used for other diseases, effectively inhibits Enterovirus-71 (EV71) proliferation by blocking viral attachment to host cells. This finding offers a potential new antiviral therapy for EV71 infections, a cause of severe hand-foot-and-mouth disease.

Keywords:
AntiviralEnterovirus 71Suramin

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Area of Science:

  • Virology
  • Infectious Diseases
  • Drug Discovery

Background:

  • Enterovirus-71 (EV71) is a primary cause of hand-foot-and-mouth disease, frequently leading to severe central nervous system infections and fatalities.
  • Current therapeutic options for EV71 are limited, with no specific antiviral agents available despite ongoing vaccine development.

Purpose of the Study:

  • To identify potential antiviral agents against EV71 from a compound library.
  • To investigate the mechanism of action of identified compounds on EV71 infection.

Main Methods:

  • Screening of a compound library to identify EV71 inhibitors.
  • Determination of the IC50 value for identified compounds.
  • Analysis of the effect of compounds on EV71 attachment and other lifecycle stages.

Main Results:

  • Suramin was identified as an inhibitor of EV71 proliferation with an IC50 value of 40 μM.
  • Suramin was shown to inhibit EV71 attachment to host cells, impacting early infection stages.
  • The drug also affected other phases of the EV71 life cycle.

Conclusions:

  • Suramin demonstrates significant antiviral activity against Enterovirus-71.
  • The mechanism involves blocking viral attachment and potentially other steps in the EV71 lifecycle.
  • Suramin, an existing drug, represents a promising candidate for repurposing as an antiviral treatment for EV71 infections.