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ShareSep. 30, 2008 — Researchers from the University of Warwick, Coventry, United Kingdom have developed a new antiviral using naturally occurring influenza virus "protecting virus" that may defend against any influenza A virus in any animal host.
Human influenza virus A is not only responsible for seasonal disease in humans, it is also the cause of worldwide pandemics of which the last three resulted in millions of deaths all over the globe. Currently, live and killed vaccines countering specific strains of the flu are available, however a vaccine for a new pandemic strain would take months to develop. Also, increased resistance to antivirals currently on the market has emphasized the need for a new effective prophylactic and therapeutic treatment method.
The "protecting virus" contains an altered gene that makes it harmless and prevents it from reproducing in a cell. If another influenza virus invades the cell it still remains harmless, but rapidly reproduces and prevents infection by literally crowding out the new influenza strain.
In the study researchers used a "protecting virus" (known as 244) as an influenza A antiviral therapy and tested it in mice. A 120-ng intranasal dose completely protected mice simultaneously challenged with 10 50% lethal doses of influenza A/WSN (H1N1) virus. The 244 protecting virus also protected mice against strong doses of H2N2, H3N2, and H3N8.
Prophylactic activity was maintained in mice at least 1 week prior to challenge and a clear therapeutic benefit was observed when administered 24 to 48 hours following a lethal challenge. Finally, the 244 protecting virus was noted to be 10- to 100-fold more active than previous defective influenza A viruses.
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The above story is reprinted from materials provided by American Society for Microbiology.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Dimmock et al. Influenza Virus Protecting RNA: an Effective Prophylactic and Therapeutic Antiviral. Journal of Virology, 2008; 82 (17): 8570 DOI: 10.1128/JVI.00743-08
Note: If no author is given, the source is cited instead.
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