scholarly journals Insights into the Acquisition of Virulence of Avian Influenza Viruses during a Single Passage in Ferrets

Viruses ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 915
Author(s):  
Butler ◽  
Middleton ◽  
Haining ◽  
Layton ◽  
Rockman ◽  
...  
Keyword(s):  
Avian Influenza ◽  
Respiratory Tract ◽  
Severe Disease ◽  
Influenza Viruses ◽  
Mammalian Host ◽  
Upper Respiratory Tract ◽  
Avian Influenza Viruses ◽  
Single Passage ◽  
H5n1 Isolate ◽  
High Pathogenicity

Circulating avian influenza viruses pose a significant threat, with human infections occurring infrequently but with potentially severe consequences. To examine the dynamics and locale of the adaptation process of avian influenza viruses when introduced to a mammalian host, we infected ferrets with H5N1 viruses. As expected, all ferrets infected with the human H5N1 isolate A/Vietnam/1203/2004 showed severe disease and virus replication outside the respiratory tract in multiple organs including the brain. In contrast infection of ferrets with the avian H5N1 virus A/Chicken/Laos/Xaythiani26/2006 showed a different collective pattern of infection; many ferrets developed and cleared a mild respiratory infection but a subset (25–50%), showed extended replication in the upper respiratory tract and developed infection in distal sites. Virus from these severely infected ferrets was commonly found in tissues that included liver and small intestine. In most instances the virus had acquired the common virulence substitution PB2 E627K but, in one case, a previously unidentified combination of two amino acid substitutions at PB2 S489P and NP V408I, which enhanced polymerase activity, was found. We noted that virus with high pathogenicity adaptations could be dominant in an extra-respiratory site without being equally represented in the nasal wash. Further ferret passage of these mutated viruses resulted in high pathogenicity in all ferrets. These findings illustrate the remarkable ability of avian influenza viruses that avoid clearance in the respiratory tract, to mutate towards a high pathogenicity phenotype during just a single passage in ferrets and also indicate a window of less than 5 days in which treatment may curtail systemic infection.

scholarly journals Seasonal and Pandemic Human Influenza Viruses Attach Better to Human Upper Respiratory Tract Epithelium than Avian Influenza Viruses

2010 ◽  
Vol 176 (4) ◽  
pp. 1614-1618 ◽  
Author(s):  
Debby van Riel ◽  
Michael A. den Bakker ◽  
Lonneke M.E. Leijten ◽  
Salin Chutinimitkul ◽  
Vincent J. Munster ◽  
...  
Keyword(s):  
Avian Influenza ◽  
Respiratory Tract ◽  
Influenza Viruses ◽  
Upper Respiratory Tract ◽  
Human Influenza ◽  
Avian Influenza Viruses ◽  
Upper Respiratory

scholarly journals Amino Acid Residue 217 in the Hemagglutinin Glycoprotein Is a Key Mediator of Avian Influenza H7N9 Virus Antigenicity

2018 ◽  
Vol 93 (1) ◽  
Author(s):  
Pengxiang Chang ◽  
Joshua E. Sealy ◽  
Jean-Remy Sadeyen ◽  
Munir Iqbal
Keyword(s):  
Amino Acid ◽  
Avian Influenza ◽  
Immune Escape ◽  
Influenza Viruses ◽  
Single Mutation ◽  
H7n9 Virus ◽  
Avian Influenza Viruses ◽  
Antigenic Analysis ◽  
Neutralizing Capacity ◽  
High Pathogenicity

ABSTRACTAvian influenza viruses continue to evolve and acquire mutations that facilitate antigenic drift and virulence change. In 2017, low-pathogenicity H7N9 avian influenza viruses evolved to a high-pathogenicity phenotype in China. Comparative antigenic analysis of the low- and high-pathogenicity virus strains showed marked variability. In order to identify residues that may be linked to the antigenic change among the H7N9 viruses, we serially passaged the viruses in the presence of homologous ferret antiserum. Progeny viruses able to overcome the neutralizing capacity of the antiserum were sequenced. The analysis showed that the emergent immune escape viruses contained mutations A125T, A151T, and L217Q in the hemagglutinin (HA) glycoprotein as early as passage 5 and that these mutations persisted until passage 10. The results revealed that a single mutation, L217Q, in the HA of H7N9 virus led to 23- and 8-fold reductions in hemagglutination inhibition (HI) titer with ferret and chicken antisera, respectively. Further analysis showed that this change also contributed to antigenic differences between the low- and high-pathogenicity H7N9 viruses, thus playing a major role in their antigenic diversification. Therefore, evolutionary changes at amino acid position 217 in the H7N9 viruses can serve as a genetic marker for virus antigenic diversity during vaccine seed matching and selection. Thein vitroimmune escape mutant selection method used in this study could also aid in the prediction of emerging antigenic variants in naturally infected or immunized animals.IMPORTANCEAvian influenza H7N9 viruses circulating in poultry and wild birds continue to evolve and acquire important phenotypic changes. Mutations to the virus hemagglutinin (HA) glycoprotein can modulate virus antigenicity and facilitate virus escape from natural or vaccine-induced immunity. The focus of this study was to identify evolutionary markers in the HA of H7N9 that drive escape from antibody-based immunity. To achieve this, we propagated low-pathogenicity H7N9 virus in the presence of polyclonal antiserum derived from ferrets infected with the same strain of virus (homologous antiserum). This selection process was repeated 10 times. The HA gene sequences of viruses recovered after the fifth passage showed that the viruses readily acquired mutations at three different amino acid positions (A125T, A151T, and L217Q). Further functional analysis of these mutations confirmed that the mutation at residue 217 in the HA was responsible for mediating changes to the immunological properties of the H7N9 virus.

scholarly journals Pathogenicity and Transmissibility of North American H7 Low Pathogenic Avian Influenza Viruses in Chickens and Turkeys

Viruses ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 163 ◽  
Author(s):  
Ishita Roy Chowdhury ◽  
Sai Yeddula ◽  
Shin-Hee Kim
Keyword(s):  
Avian Influenza ◽  
Respiratory Tract ◽  
Broiler Chickens ◽  
Influenza Viruses ◽  
Upper Respiratory Tract ◽  
Pathogenic Avian Influenza ◽  
Recent Emergence ◽  
Specific Pathogen ◽  
Upper Respiratory ◽  
Low Pathogenic Avian Influenza

Low pathogenic avian influenza (LPAI) viruses can silently circulate in poultry and wild aquatic birds and potentially mutate into highly pathogenic avian influenza (HPAI) viruses. In the U.S., recent emergence and spread of H7N8 and H7N9 HPAI viruses not only caused devastating losses to domestic poultry but also underscored the capability of LPAI viruses to mutate into HPAI viruses. Therefore, in this study, we evaluated pathogenicity and transmissibility of H7N8 and H7N9 LPAI viruses (the progenitors of HPAI viruses) in chickens and turkeys. We also included H7N2 isolated from an outbreak of LPAI in commercial chickens. H7 viruses replicated more efficiently in the respiratory tract than in the gastrointestinal tract, suggesting that their replication is restricted to the upper respiratory tract. Specifically, H7N2 replicated most efficiently in two-week-old chickens and turkeys. In contrast, H7N8 replicated least efficiently in those birds. Further, replication of H7N2 and H7N9 was restricted in the upper respiratory tract of four-week-old specific-pathogen-free (SPF) and broiler chickens. Despite their restricted replication, the two viruses efficiently transmitted from infected to naïve birds by direct contact, leading to seroconversion of contacted chickens. Our findings suggest the importance of continuous monitoring and surveillance of LPAI viruses in the fields.

scholarly journals Genesis and spread of multiple reassortants during the 2016/2017 H5 avian influenza epidemic in Eurasia

2020 ◽  
Vol 117 (34) ◽  
pp. 20814-20825 ◽  
Author(s):  
Samantha J. Lycett ◽  
Anne Pohlmann ◽  
Christoph Staubach ◽  
Valentina Caliendo ◽  
Mark Woolhouse ◽  
...  
Keyword(s):  
Avian Influenza ◽  
Severe Disease ◽  
Wild Birds ◽  
Influenza Viruses ◽  
Avian Influenza Viruses ◽  
Highly Pathogenic ◽  
Time Resolved ◽  
Bird Populations ◽  
Pathogenic Avian Influenza ◽  
Reassortant Viruses

Highly pathogenic avian influenza (HPAI) viruses of the H5 A/goose/Guangdong/1/96 lineage can cause severe disease in poultry and wild birds, and occasionally in humans. In recent years, H5 HPAI viruses of this lineage infecting poultry in Asia have spilled over into wild birds and spread via bird migration to countries in Europe, Africa, and North America. In 2016/2017, this spillover resulted in the largest HPAI epidemic on record in Europe and was associated with an unusually high frequency of reassortments between H5 HPAI viruses and cocirculating low-pathogenic avian influenza viruses. Here, we show that the seven main H5 reassortant viruses had various combinations of gene segments 1, 2, 3, 5, and 6. Using detailed time-resolved phylogenetic analysis, most of these gene segments likely originated from wild birds and at dates and locations that corresponded to their hosts’ migratory cycles. However, some gene segments in two reassortant viruses likely originated from domestic anseriforms, either in spring 2016 in east China or in autumn 2016 in central Europe. Our results demonstrate that, in addition to domestic anseriforms in Asia, both migratory wild birds and domestic anseriforms in Europe are relevant sources of gene segments for recent reassortant H5 HPAI viruses. The ease with which these H5 HPAI viruses reassort, in combination with repeated spillovers of H5 HPAI viruses into wild birds, increases the risk of emergence of a reassortant virus that persists in wild bird populations yet remains highly pathogenic for poultry.

From low to high pathogenicity-Characterization of H7N7 avian influenza viruses in two epidemiologically linked outbreaks

2018 ◽  
Vol 65 (6) ◽  
pp. 1576-1587 ◽  
Author(s):  
Klaas Dietze ◽  
Annika Graaf ◽  
Timo Homeier-Bachmann ◽  
Christian Grund ◽  
Leonie Forth ◽  
...  
Keyword(s):  
Avian Influenza ◽  
Influenza Viruses ◽  
Avian Influenza Viruses ◽  
High Pathogenicity
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