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. 2016 Aug 31;13(1):149.
doi: 10.1186/s12985-016-0607-2.

Suramin is a potent inhibitor of Chikungunya and Ebola virus cell entry

Lisa Henß  1 , Simon Beck  1 , Tatjana Weidner  1 , Nadine Biedenkopf  2   3 , Katja Sliva  1 , Christopher Weber  1 , Stephan Becker  2   3 , Barbara S Schnierle  4
Affiliations

Suramin is a potent inhibitor of Chikungunya and Ebola virus cell entry

Lisa Henß et al. Virol J. .

Abstract

Background: Chikungunya virus (CHIKV) is a mosquito-transmitted alphavirus that causes high fever, rash, and recurrent arthritis in humans. It has efficiently adapted to Aedes albopictus, which also inhabits temperate regions and currently causes large outbreaks in the Caribbean and Latin America. Ebola virus (EBOV) is a member of the filovirus family. It causes the Ebola virus disease (EDV), formerly known as Ebola hemorrhagic fever in humans and has a mortality rate of up to 70 %. The last outbreak in Western Africa was the largest in history and has caused approximately 25,000 cases and 10,000 deaths. For both viral infections no specific treatment or licensed vaccine is currently available. The bis-hexasulfonated naphthylurea, suramin, is used as a treatment for trypanosome-caused African river blindness. As a competitive inhibitor of heparin, suramin has been described to have anti-viral activity.

Methods: We tested the activity of suramin during CHIKV or Ebola virus infection, using CHIKV and Ebola envelope glycoprotein pseudotyped lentiviral vectors and wild-type CHIKV and Ebola virus.

Results: Suramin efficiently inhibited CHIKV and Ebola envelope-mediated gene transfer while vesicular stomatitis virus G protein pseudotyped vectors were only marginally affected. In addition, suramin was able to inhibit wild-type CHIKV and Ebola virus replication in vitro. Inhibition occurred at early time points during CHIKV infection.

Conclusion: Suramin, also known as Germanin or Bayer-205, is a market-authorized drug, however shows significant side effects, which probably prevents its use as a CHIKV drug, but due to the high lethality of Ebola virus infections, suramin might be valuable against Ebola infections.

Keywords: Chikungunya virus; Ebola virus; Suramin.

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Figures

Fig. 1
Fig. 1
Cytotoxicity of suramin treatment. Cytotoxicity of suramin was analyzed by incubation of MCF7, Huh7 and 293 T cells with suramin for 16 h and conducting a MTT assay by following the manufacturer’s instructions (Merck Millipore, Darmstadt). The graph indicates the amount of viable cells as % of the untreated control and values represent the mean data of two independent experiments done in duplicate
Fig. 2
Fig. 2
Neutralization assay with suramin. Suramin dissolved in water was serially diluted, incubated with EBOV GP or VSV-G pseudotyped vector particles (a) or CHIKV and VSV-G pseudotyped vector particles (b) and the mixtures were used for transduction of HEK 293 T cells. Neutralizing activity was determined by detection of relative luciferase units (RLUs). The data represent a typical assay with the mean values of triplicates
Fig. 3
Fig. 3
Suramin inhibits CHIKV infection. Suramin was serially diluted, incubated with CHIKV-luci or VSV-luci for 30 min and added to 293 T cells. Its neutralizing activity was detected after 6 h of incubation as relative luciferase activities. The luciferase activity is shown as a percentage, relative to the untreated control. The data show a representative experiment carried out in triplicate
Fig. 4
Fig. 4
Suramin acts on early steps of CHIKV infections in vitro. HEK 293 T cells were incubated with CHIKV-luci (a) or VSV-luci (b) and suramin (10 μg/ml). The drug was added during the infection (0 h) and then every 30 min after infection up to 2.5 h after infection. After 6 h, infected cells were detected as relative luciferase activities. CHIKV infection without treatment was set to 100 %
Fig. 5
Fig. 5
Suramin inhibits EBOV replication in vitro. Different concentrations of suramin (4.875–300 μg/ml) were incubated with EBOV (multiplicity of infection of 0.1) prior to infection of Huh7 cells. Supernatants were collected 48 h post infection and virus titers were determined in Vero cells by TCID50 analysis (4 replicates). The data represent the mean values of TCID50 titers from 5 independent experiments. The mock value is indicated as a red square
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