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Published on: April 28, 2019
Epizootic hemorrhagic disease virus infection of type I interferon receptor deficient mice
Michael Eschbaumer1, Markus Keller, Martin Beer
1Institute of Diagnostic Virology, Friedrich-Loeffler-Institut, Südufer 10, 17493 Greifswald - Insel Riems, Germany. michael.eschbaumer@fli.bund.de
Abstract:
Type I interferon receptor deficient (IFNAR(-/-)) mice were infected with an Israeli isolate of serotype 7 of epizootic hemorrhagic disease virus (EHDV; Orbivirus, Reoviridae). Two out of two mice that received 5×10(5) 50% tissue culture infectious doses (TCID(50)) by intraperitoneal injection died or were euthanized in a moribund state on day 5 after infection. One mouse out of three that had been inoculated with 5×10(2) TCID(50) died on day 7 while the remaining mice did not show any clinical signs and survived until the end of the experiment. Spleens of all dead mice were highly positive in an EHDV real-time RT-PCR (quantification cycle values ≤15) and contained ≥10(5.8) TCID(50) of virus per ml of homogenate. The viral RNA content and virus titer in the spleens of the two surviving mice, on the other hand, were over 100-fold lower. Different from data reported for BTV, the outcome of EHDV infection of IFNAR(-/-) mice is dose-dependent and subclinical infections can occur.
Insights
Type I interferon receptor deficient mice infected with epizootic hemorrhagic disease virus (EHDV) showed a dose-dependent outcome. High doses were lethal, while lower doses resulted in subclinical infections, unlike Bluetongue virus (BTV) models.
Area of Science:
- Virology
- Immunology
- Infectious Diseases
Background:
- Epizootic hemorrhagic disease virus (EHDV) is an Orbivirus causing significant veterinary concern.
- Type I interferon signaling is crucial for controlling viral infections.
- Previous studies on Bluetongue virus (BTV) in similar models provide a comparative context.
Purpose of the Study:
- To investigate the susceptibility of Type I interferon receptor deficient (IFNAR(-/-)) mice to EHDV infection.
- To determine the dose-dependency and clinical outcomes of EHDV infection in IFNAR(-/-) mice.
- To compare the EHDV infection profile with that of BTV in the same model.
Main Methods:
- Infection of IFNAR(-/-) mice with EHDV (serotype 7) via intraperitoneal injection using different doses (5×10^5 TCID50 and 5×10^2 TCID50).
- Clinical monitoring of mice for signs of disease and survival.
- Quantification of viral RNA and infectious virus titers in spleen homogenates using real-time RT-PCR and TCID50 assays.
Main Results:
- High dose (5×10^5 TCID50) EHDV infection led to mortality in all mice by day 5.
- Lower dose (5×10^2 TCID50) infection resulted in one fatality by day 7, with remaining mice showing no clinical signs.
- Dead mice had high viral loads (≥10^5.8 TCID50/ml) in spleens, while survivors had over 100-fold lower viral RNA and titers.
Conclusions:
- EHDV infection in IFNAR(-/-) mice is dose-dependent.
- Subclinical EHDV infections are possible in this model, contrasting with some BTV findings.
- IFNAR signaling plays a critical role in controlling EHDV pathogenesis.
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