Please use this identifier to cite or link to this item: https://doi.org/10.1186/1743-422X-10-139
Title: The highly pathogenic H7N3 avian influenza strain from July 2012 in Mexico acquired an extended cleavage site through recombination with host 28S rRNA
Authors: Maurer-Stroh, S 
Lee, R.T
Gunalan, V
Eisenhaber, F 
Keywords: RNA 28S
article
gene sequence
host
Influenza virus A H7N3
Mexico
nonhuman
pathogenesis
pathogenicity
phylogeny
poultry
RNA analysis
RNA cleavage
RNA sequence
RNA structure
virus strain
virus transmission
Animals
Chickens
Hemagglutinin Glycoproteins, Influenza Virus
Influenza A Virus, H7N3 Subtype
Influenza in Birds
Mexico
Phylogeny
Recombination, Genetic
RNA, Ribosomal, 28S
RNA, Viral
Sequence Analysis, DNA
Aves
Mammalia
Issue Date: 2013
Citation: Maurer-Stroh, S, Lee, R.T, Gunalan, V, Eisenhaber, F (2013). The highly pathogenic H7N3 avian influenza strain from July 2012 in Mexico acquired an extended cleavage site through recombination with host 28S rRNA. Virology Journal 10 : 139. ScholarBank@NUS Repository. https://doi.org/10.1186/1743-422X-10-139
Abstract: Background: A characteristic difference between highly and non-highly pathogenic avian influenza strains is the presence of an extended, often multibasic, cleavage motif insertion in the hemagglutinin protein. Such motif is found in H7N3 strains from chicken farm outbreaks in 2012 in Mexico. Methods. Through phylogenetic, sequence and structural analysis, we try to shed light on the role, prevalence, likelihood of appearance and origin of the inserted cleavage motifs in these H7N3 avian influenza strains. Results: The H7N3 avian influenza strain which caused outbreaks in chicken farms in June/July 2012 in Mexico has a new extended cleavage site which is the likely reason for its high pathogenicity in these birds. This cleavage site appears to have been naturally acquired and was not present in the closest low pathogenic precursors. Structural modeling shows that insertion of a productive cleavage site is quite flexible to accept insertions of different length and with sequences from different possible origins. Different from recent cleavage site insertions, the origin of the insert here is not from the viral genome but from host 28S ribosomal RNA (rRNA) instead. This is a novelty for a natural acquisition as a similar insertion has so far only been observed in a laboratory strain before. Given the abundance of viral and host RNA in infected cells, the acquisition of a pathogenicity-enhancing extended cleavage site through a similar route by other low-pathogenic avian strains in future does not seem unlikely. Important for surveillance of these H7N3 strains, the structural sites known to enhance mammalian airborne transmission are dominated by the characteristic avian residues and the risk of human to human transmission should currently be low but should be monitored for future changes accordingly. Conclusions: This highly pathogenic H7N3 avian influenza strain acquired a novel extended cleavage site which likely originated from recombination with 28S rRNA from the avian host. Notably, this new virus can infect humans but currently lacks critical host receptor adaptations that would facilitate human to human transmission. © 2013 Maurer-Stroh et al.; licensee BioMed Central Ltd.
Source Title: Virology Journal
URI: https://scholarbank.nus.edu.sg/handle/10635/174175
ISSN: 1743422X
DOI: 10.1186/1743-422X-10-139
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