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It seems that seals can do an excellent job of passing influenza to birds.
http://www.pubmedcentral.gov/article...z&artid=249560
J Virol. 1990 July; 64(7): 3297?3303.
Generation of seal influenza virus variants pathogenic for chickens, because of hemagglutinin cleavage site changes.
S Q Li, M Orlich, and R Rott
Institut f?r Virologie, Justus-Liebig-Universit?t Giessen, Federal Republic of Germany.
This article has been cited by other articles in PMC.
Abstract
Influenza virus A/seal/Mass/1/80 (H7N7) was adapted to grow in MDCK cells and chicken embryo cells (CEC) in the absence of exogenous protease. The biological properties of the virus variants obtained coincided with intracellular activation of the hemagglutinin (HA) by posttranslational proteolytic cleavage and depended on the cell type used for adaptation. MDCK cell-adapted variants contained point mutations in regions of the HA more distant from the cleavage site. It is proposed that these mutations are probably responsible, through an unknown mechanism, for enhanced cleavability of HA in MDCK cells. Such virus variants were apathogenic in chickens. CEC-adapted variants, on the other hand, contained an insertion of basic amino acids at the HA cleavage site, in addition to scattered point mutations. The insertions converted the cleavage sites in the variant virus HAs so that they came to resemble the cleavage site found in highly pathogenic avian influenza viruses. CEC variants with such cleavage site modifications were highly pathogenic for chickens.
The lethal outcome of the infection in chickens demonstrated for the first time that an influenza virus derived from a mammalian species can be modified during adaptation to a new cell type to such an extent that the resulting virus variant becomes pathogenic for an avian species.
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Someone more knowledgeable than me should read the details of this reports. (it's .pdf, so I can't do a copy) As I gather......the cleavage site between HA1 and HA2 of the H7 seal influenza contains a single arginine. The lack of multiple basic amino acids, means it is normally apathogenic to chickens.
They grew the seal H7 virus in both MDCK and CEC and learned that the CEC (chicken) adapted cells obtained mutations nearer the cleavage site which increased in pathogenicity to chickens, where the MDCK grown cells obtained mutations further away from the HA cleavage site, hence less pathogencity for chickens.
I was looking for info in the binding sites, and once again ran into data on the importance of other mutations. So the a2,3 a2,6 binding mutations open the door for other highly significant mutations to come into play.
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http://www.pubmedcentral.gov/article...z&artid=249560
J Virol. 1990 July; 64(7): 3297?3303.
Generation of seal influenza virus variants pathogenic for chickens, because of hemagglutinin cleavage site changes.
S Q Li, M Orlich, and R Rott
Institut f?r Virologie, Justus-Liebig-Universit?t Giessen, Federal Republic of Germany.
This article has been cited by other articles in PMC.Abstract
Influenza virus A/seal/Mass/1/80 (H7N7) was adapted to grow in MDCK cells and chicken embryo cells (CEC) in the absence of exogenous protease. The biological properties of the virus variants obtained coincided with intracellular activation of the hemagglutinin (HA) by posttranslational proteolytic cleavage and depended on the cell type used for adaptation. MDCK cell-adapted variants contained point mutations in regions of the HA more distant from the cleavage site. It is proposed that these mutations are probably responsible, through an unknown mechanism, for enhanced cleavability of HA in MDCK cells. Such virus variants were apathogenic in chickens. CEC-adapted variants, on the other hand, contained an insertion of basic amino acids at the HA cleavage site, in addition to scattered point mutations. The insertions converted the cleavage sites in the variant virus HAs so that they came to resemble the cleavage site found in highly pathogenic avian influenza viruses. CEC variants with such cleavage site modifications were highly pathogenic for chickens.
The lethal outcome of the infection in chickens demonstrated for the first time that an influenza virus derived from a mammalian species can be modified during adaptation to a new cell type to such an extent that the resulting virus variant becomes pathogenic for an avian species.
----------------------------------------------
Someone more knowledgeable than me should read the details of this reports. (it's .pdf, so I can't do a copy) As I gather......the cleavage site between HA1 and HA2 of the H7 seal influenza contains a single arginine. The lack of multiple basic amino acids, means it is normally apathogenic to chickens.
They grew the seal H7 virus in both MDCK and CEC and learned that the CEC (chicken) adapted cells obtained mutations nearer the cleavage site which increased in pathogenicity to chickens, where the MDCK grown cells obtained mutations further away from the HA cleavage site, hence less pathogencity for chickens.
I was looking for info in the binding sites, and once again ran into data on the importance of other mutations. So the a2,3 a2,6 binding mutations open the door for other highly significant mutations to come into play.
.
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