tetano
Editor, Senior Moderator
Published ahead of print 26 December 2013, doi: 10.1128/JVI.01840-13 JVI.01840-13
H1N1, but not H3N2, influenza A virus infection protects ferrets from H5N1 encephalitis
Stephanie J. Bissel1⇑,
Guoji Wang1,
Donald M. Carter2,
Corey J. Crevar2,
Ted M. Ross2,3 and
Clayton A. Wiley1
+ Author Affiliations
1Department of Pathology, University of Pittsburgh, 200 Lothrop St. Pittsburgh, PA 15213
2Center for Vaccine Research, University of Pittsburgh, 3501 Fifth Avenue, Pittsburgh, PA 15261
3Department of Microbiology and Molecular Genetics, University of Pittsburgh, 3501 Fifth Avenue, Pittsburgh, PA 15261
ABSTRACT
Seasonal influenza causes substantial morbidity and mortality because of efficient human-to-human spread. Rarely, zoonotic strains of influenza virus spread to humans, where they have the potential to mediate new pandemics with high mortality. We studied systemic viral spread after intranasal infection with highly pathogenic avian influenza virus (H5N1 (A/Viet Nam/1203/2004)) in ferrets with or without prior pandemic H1N1pdm09 (A/Mexico/4108/2009) or H3N2 (A/Victoria/361/2011) infection. After intranasal challenge with H5N1 influenza virus, na?ve ferrets rapidly succumbed to systemic infection. Animals challenged with H5N1 influenza virus greater than 3 months after recovering from an initial H1N1pdm09 infection survived H5N1 virus challenge and cleared virus from the respiratory tract 4 days after infection. However, a prolonged low-level infection of hematopoietic elements in the small bowel lamina propria, liver and spleen was present for greater than 2 weeks post-infection, raising the potential for reassortment of influenza genes in a host infected with multiple strains of influenza. Animals previously infected with an H3N2 influenza virus succumbed to systemic disease and encephalitis after H5N1 virus challenge. These results indicate prior infection with different seasonal influenza strains leads to radically different protection from H5N1 challenge and fatal encephalitis.
http://jvi.asm.org/content/early/2013/12/20/JVI.01840-13.abstract
H1N1, but not H3N2, influenza A virus infection protects ferrets from H5N1 encephalitis
Stephanie J. Bissel1⇑,
Guoji Wang1,
Donald M. Carter2,
Corey J. Crevar2,
Ted M. Ross2,3 and
Clayton A. Wiley1
+ Author Affiliations
1Department of Pathology, University of Pittsburgh, 200 Lothrop St. Pittsburgh, PA 15213
2Center for Vaccine Research, University of Pittsburgh, 3501 Fifth Avenue, Pittsburgh, PA 15261
3Department of Microbiology and Molecular Genetics, University of Pittsburgh, 3501 Fifth Avenue, Pittsburgh, PA 15261
ABSTRACT
Seasonal influenza causes substantial morbidity and mortality because of efficient human-to-human spread. Rarely, zoonotic strains of influenza virus spread to humans, where they have the potential to mediate new pandemics with high mortality. We studied systemic viral spread after intranasal infection with highly pathogenic avian influenza virus (H5N1 (A/Viet Nam/1203/2004)) in ferrets with or without prior pandemic H1N1pdm09 (A/Mexico/4108/2009) or H3N2 (A/Victoria/361/2011) infection. After intranasal challenge with H5N1 influenza virus, na?ve ferrets rapidly succumbed to systemic infection. Animals challenged with H5N1 influenza virus greater than 3 months after recovering from an initial H1N1pdm09 infection survived H5N1 virus challenge and cleared virus from the respiratory tract 4 days after infection. However, a prolonged low-level infection of hematopoietic elements in the small bowel lamina propria, liver and spleen was present for greater than 2 weeks post-infection, raising the potential for reassortment of influenza genes in a host infected with multiple strains of influenza. Animals previously infected with an H3N2 influenza virus succumbed to systemic disease and encephalitis after H5N1 virus challenge. These results indicate prior infection with different seasonal influenza strains leads to radically different protection from H5N1 challenge and fatal encephalitis.
http://jvi.asm.org/content/early/2013/12/20/JVI.01840-13.abstract