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ARS Home » Southeast Area » Athens, Georgia » U.S. National Poultry Research Center » Exotic & Emerging Avian Viral Diseases Research » Research » Publications at this Location » Publication #342115
Research Project: Intervention Strategies to Prevent and Control Disease Outbreaks Caused by Emerging Strains of Avian Influenza Viruses

Location: Exotic & Emerging Avian Viral Diseases Research

Title: Avian influenza a virus budding morphology: spherical or filamentous?

Author
item CONCEICAO, CARINA LIIETE - University Of Edinburgh
item SMITH, NIKKI - University Of Edinburgh
item MURPHY, LITA - University Of Edinburgh
item JASIM, SEEMA - University Of Edinburgh
item WISE, HELEN - University Of Cambridge
item LYCETT, SAMANTHA - University Of Edinburgh
item MISHARA, ANAMIKA - University Of Edinburgh
item RAUT, ASHWIN - University Of Edinburgh
item BURT, DAVE - University Of Edinburgh
item Kapczynski, Darrell
item IQBAL, MUNIR - The Pirbright Institute
item VERVELDE, LONNEKE - University Of Edinburgh
item DIGARD, PAUL - University Of Edinburgh

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 7/16/2017
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Most strains of influenza A virus (IAV) can produce long (µm length) filamentous virus particles as well as ~100 nm diameter spherical virions. The function of the filamentous particles is unclear but is hypothesized to facilitate transmission within or from the respiratory tract. In mammalian IAVs, virion shape is largely determined by sequence polymorphisms within the matrix (M1) polypeptide. Whether this morphological phenotype and/or transmission hypothesis applies to avian strains of IAV is unknown. Confocal microscopy was used to test a panel of avian virus-derived segment 7s for the ability to produce filamentous virions, as 7:1 reassortants with the non-filamentous PR8 strain and/or in the parental avian virus genetic background. Phylogenetic analysis was used to ensure these strains covered the 11 major clades evident in Eurasian and American M1 genes. Virus fitness and pathogenicity were tested in cell culture, tracheal organ culture (TOC) and embryonated eggs. Several avian M segments induced production of large bundles of 5-10µm filamentous virions when reassorted into PR8. By this criterion, as well as by analysis of non-reassorted viruses, most (13/22), but not all, avian strains of IAV possessed a filamentous phenotype. Budding morphology varied within clades but correlated most strongly with host species, being common in duck viruses (9/13) but rare (1/6) in chicken isolates. In vitro, filamentous budding was strongly associated with a small plaque phenotype, but did not influence overall replication titer. In chick embryos, switches in budding phenotype altered virus pathogenicity but in a strain-dependent manner. However, preliminary analysis of mucous-containing TOCs suggested a growth advantage for filamentous strains. Filamentous budding is a common but not ubiquitous phenotype of avian IAV that can be turned on or off by single amino-acid changes in M1. Consistent with this mutability, budding phenotype did not segregate according to M1 phylogeny (or age of isolate) but may instead correlate with host species. Experiments are ongoing to test the hypothesis that filamentous budding confers a fitness advantage in specific hosts and/or tissues.