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Aggregation of Single Nucleotide Polymorphisms in a Human H5N1 Clade 2.2 Hemagglutinin
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- Recombinomics, Inc
- U.S. Naval Medical Research Unit 3 (NAMRU-3)
- Central Laboratory for Veterinary Quality Control, Giza
- Ministry of Health, Arabic Republic of Egypt
- NAMRU-3 Ghana Detachment
- Ghana Veterinary Services
- Noguchi Memorial Institute for Medical Research
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- Document Type:
- Manuscript
- Date:
- Received 16 August 2007 16:24 UTC; Posted 16 August 2007
- Subjects:
- Biotechnology, Ecology, Genetics & Genomics, Immunology, Microbiology, Bioinformatics
- Abstract:
The evolution of H5N1 has attracted significant interest 1-4 due to linkages with avian 5,6 and human infections 7,8. The basic tenets of influenza genetics 9 attribute genetic drift to replication errors caused by a polymerase complex that lacks a proof reading function. However, recent analysis 10 of swine influenza genes identifies regions copied with absolute fidelity for more than 25 years. In addition, polymorphism tracing of clade 2.2 H5N1 single nucleotide polymorphisms identify concurrent acquisition 11 of the same polymorphism onto multiple genetic backgrounds in widely dispersed geographical locations. Here we show the aggregation of regional clade 2.2 polymorphisms from Germany, Egypt, and sub-Sahara Africa onto a human Nigerian H5N1 hemagglutinin (HA), implicating recombination in the dispersal and aggregation of single nucleotide polymorphisms from closely related genomes.
Discussion
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19 votes
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3 comments
These authors (Lebarbenchon C, van der Werf S, Thomas F, Aubin JT, Azebi S, Cuvelier F, Jeannin P, Roca V, Chang CM, Kayser Y, Roche B, Guégan JF, Renaud F, Gauthier-Clerc M) also have another publication: Infect Genet Evol. 2007 May 21; [Epub ahead of print]
“Absence of detection of highly pathogenic H5N1 in migratory waterfowl in southern France in 2005-2006”, which as indicated by the title, fails to detect H5N1 in migratory waterfowl in France. These failures are quite common, and reflect an H5N1 sensitivity problem in the assays used in various surveillance systems.
Although these authors failed to find H5N1, H5N1 was detected and sequenced in France in 2006. Moreover, this summer there have already been three reports of H5N1 in France including two reports in mute swans and one report in wild ducks.
Positive data, supported by clade 2.2 sequence information is far more compelling than repeated negative results generated by assays that have failed to detect H5N1 in live birds in regions where H5N1 has been isolated from dead and dying wild birds.
The recent publication
Hatta M, Hatta Y, Kim JH, Watanabe S, Shinya K, et al. (2007) Growth of H5N1 Influenza A Viruses in the Upper Respiratory Tracts of Mice. PLoS Pathog 3(10): e133 doi:10.1371/journal.ppat.0030133
provides additional positive data for the spread of clade 2.2 (Qinghai) H5N1 by migratory birds in Europe, the Middle East, and Africa. The paper reinforces earlier observations on the role of PB2 E627K and temperature on the replication of clade 2.2 H5N1 in avian and mammalian hosts.
E627K is present in virtually all human isolates of seasonal flu. This change allows seasonal flu to replicate most efficiently at lower (33 C) temperatures, which are found in mammalian noses and throats. This property may contribute to the seasonal aspects of human influenza in northern and southern locations.
However, this also leads to a lowering of the H5N1 level in birds, which have a body temperature of 41 C. Consequently, clade 2.2 circulates undetected in surveillance program that focus on detection in live healthy birds. In contrast, birds that have trouble maintaining body temperature allow the levels to rise, leading to detection of clade 2.2 in dead or dying wild birds, which has been reported in Europe, the Middle East, and Africa. All of the “Asian” H5N1 reported in those regions has been clade 2.2 and almost all isolates have PB2 E627K, one of the markers of clade 2.2 in birds.
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- This document is licensed to the public under the Creative Commons Attribution 2.5 License
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Niman, Henry, Saad, Magdi, Tjaden, Jeffery, Earhart, Kenneth, Monteville, Marshall, Aly, Mona, Mansour, Moustafa, El-Sayed , Nasr, Nayel, Ahmed, Abdelghani, Ahmed, Esmat, Hala, Labib, Emad, Ayoub, Ehab, Arafa, Abdelattar, Raczniak, Gregory, Agyen-Frempong , Mensah, Ampofo, William, and Boynton, Bruce. Aggregation of Single Nucleotide Polymorphisms in a Human H5N1 Clade 2.2 Hemagglutinin. Available from Nature Precedings <http://hdl.handle.net/10101/npre.2007.743.1> (2007)
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Other versions of this document in Nature Precedings
Version number Document title Date v2 Posted 12 September 2007 Other versions of this document elsewhere on the web
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Chris Redfern on 21 August 2007 09:50 UTC
In this manuscript the authors state:
“Infection of long range migratory bird led to a rapid expansion of reported H5N1 infections in wild birds and poultry in Europe, the Middle East, and Africa.”
The view that long range migratory birds are responsible for the rapid expansion has been discredited in a recent review:
Ibis (2007), 149, 202–214: Recent expansion of highly pathogenic avian influenza H5N1: a critical review. M. GAUTHIER-CLERC, C. LEBARBENCHON & F. THOMAS