Giuseppe
Emeritus
[Source: Journal of Infectious Diseases, full page: (LINK). Abstract, edited.]
An investigational antiviral drug fludase effectively inhibits replication of zoonotic A(H7N9) influenza viruses and protects mice from lethality
Henju Marjuki 1,?, Vasiliy P. Mishin 1,?, Anton P. Chesnokov 1,2, Juan A. De La Cruz 1,2, Alicia M. Fry 1, Julie Villanueva 1 and Larisa V. Gubareva 1,*
Author Affiliations: <SUP>1</SUP>Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention <SUP>2</SUP>Battelle Memorial Institute, Atlanta, Georgia, USA
*Corresponding author: Larisa V. Gubareva, Phone: +1 404 639 3204, E-mail: lgubareva@cdc.gov
? Equally contributed to this work
<CITE><ABBR>J Infect Dis.</ABBR> (2014) doi: 10.1093/infdis/jiu105 / Fi</CITE>rst published online: February 25, 2014 / This article is Open Access
Abstract
Human infections caused by the avian influenza A(H7N9) virus have been associated with substantial morbidity and mortality. Emergence of virus variants, carrying markers of decreased susceptibility to neuraminidase inhibitors, was reported. Here we showed that fludase, an antiviral drug with sialidase activity, potently inhibited replication of wild-type H7N9 viruses and their oseltamivir-resistant R292 K variants in mice. A once-daily administration initiated early after lethal infection, hampered body weight loss and completely protected mice from lethality. We observed a time-dependent effect for 24−72-hour delayed fludase treatments on morbidity and mortality. The results warrant further investigation of fludase for influenza treatment.
Received November 20, 2013. Revision received February 7, 2014. Accepted February 13, 2014.
? The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America.
This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (http://creativecommons.org/licenses/by-nc-nd/3.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited.
For commercial re-use, please contact journals.permissions@oup.com.
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An investigational antiviral drug fludase effectively inhibits replication of zoonotic A(H7N9) influenza viruses and protects mice from lethality
Henju Marjuki 1,?, Vasiliy P. Mishin 1,?, Anton P. Chesnokov 1,2, Juan A. De La Cruz 1,2, Alicia M. Fry 1, Julie Villanueva 1 and Larisa V. Gubareva 1,*
Author Affiliations: <SUP>1</SUP>Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention <SUP>2</SUP>Battelle Memorial Institute, Atlanta, Georgia, USA
*Corresponding author: Larisa V. Gubareva, Phone: +1 404 639 3204, E-mail: lgubareva@cdc.gov
? Equally contributed to this work
<CITE><ABBR>J Infect Dis.</ABBR> (2014) doi: 10.1093/infdis/jiu105 / Fi</CITE>rst published online: February 25, 2014 / This article is Open Access
Abstract
Human infections caused by the avian influenza A(H7N9) virus have been associated with substantial morbidity and mortality. Emergence of virus variants, carrying markers of decreased susceptibility to neuraminidase inhibitors, was reported. Here we showed that fludase, an antiviral drug with sialidase activity, potently inhibited replication of wild-type H7N9 viruses and their oseltamivir-resistant R292 K variants in mice. A once-daily administration initiated early after lethal infection, hampered body weight loss and completely protected mice from lethality. We observed a time-dependent effect for 24−72-hour delayed fludase treatments on morbidity and mortality. The results warrant further investigation of fludase for influenza treatment.
Received November 20, 2013. Revision received February 7, 2014. Accepted February 13, 2014.
? The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America.
This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (http://creativecommons.org/licenses/by-nc-nd/3.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited.
For commercial re-use, please contact journals.permissions@oup.com.
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