PMCCPMCCPMCC

Search tips
Search criteria 

Advanced

 
Logo of genannJournal InfoAuthorsPermissionsJournals.ASM.orggenomeA ArticleGenome Announcements
 
Genome Announc. 2013 Jan-Feb; 1(1): e00098-12.
Published online 2013 January 31. doi:  10.1128/genomeA.00098-12
PMCID: PMC3569291

Complete Genome Sequences of Six Avian-Like H1N1 Swine Influenza Viruses from Northwestern China

Abstract

Very little is known about swine influenza in northwestern China. Here, we report the complete genomic sequences of six avian-like H1N1 swine influenza viruses (SIVs) isolated in pigs in northwestern China. Phylogenetic analyses of the sequences of eight genomic segments demonstrated that they are avian-like H1N1 SIVs.

GENOME ANNOUNCEMENT

Three predominant subtypes of swine influenza virus (SIV) circulate worldwide in pigs: classical swine H1N1, avian-like H1N1, and the human-like H3N2. Pigs play an important role in the transmission chain of avian-to-pig-to-human, and SIV can be transmitted to human beings across species (13). New SIV strains can cause economic losses in the pig industry and pose serious threats to human health (4, 5). These avian-like H1N1 viruses emerged in Europe in 1979. In China, the classic SIV was first isolated in 1974, while the avian-like H1N1 virus was first detected in 1993 to 1994 and cocirculated with the classic H1N1 SIVs (6). After that, similar viruses were isolated in many provinces (7, 8). To date, the prevalence of SI in northwestern China remains unclear. The Shaanxi province is located in the northwest of China and is the transportation hub of the northwest provinces. Understanding the prevalence and variations of SIVs in this region is greatly significant to the prevention and control of SI in China.

A total of 500 nasal and tracheal swab samples were collected regularly in slaughterhouses and farms from healthy pigs in the Shaanxi province from 2011 to 2012. The hemagglutination inhibition (HI) antibody positive rate of H1N1 SI reached 16.9 to 36.9%. Six avian-like H1N1 SIVs were isolated in the Shaanxi province. Of these isolates, the full-length sequences of eight genomic segments were amplified by reverse transcription and PCR and were sequenced and compared with published sequences. The homology between the eight genomic segments of these isolates was 98.3% to 99.1%. The hemagglutinin (HA) and neuraminidase (NA) sequences of these isolates were closely related to those of avian-like H1N1 SIVs from other provinces in China, but the homology with those from European countries is low. Three amino acid residue substitutions (V151I, D204V, and Y209H) at the receptor binding sites in HA among these isolates may affect their binding to cell receptors. Sequence analyses also indicated that positions 119 (E), 152 (R), 275 (H), and 295 (N) of NA protein were conserved, suggesting that they are still sensitive to neuraminidase inhibitor drugs (9, 10). In addition, a mutation found at position 44 of NA, a glycosylation site, may affect protein folding and transport (11). The amino acid residue at position 375 of PB1, which is the key to the host characteristics (12), is conserved in these isolates. The virulence is strong when the amino acid residue 627 of PB2 is K, and weak when it is E (13, 14). Interestingly, the position 627 of PB2 is E, rather than K, among these isolates. In addition, since an amino acid substitution at position V27I of M2 was seen in 2 of 6 isolates, these viruses seem to have a certain resistance to amantadine drugs (15). Phylogenetic trees based on eight genomic sequences of these isolates suggested that they are closely related to avian-like HIN1 SIV strains from China and Europe.

Nucleotide sequence accession numbers.

The GenBank accession numbers of these isolates from Shaanxi province are shown in Table 1.

TABLE 1
Nucleotide sequence accession no. of six avian-like H1N1 SIV strains isolated from Shaanxi province of China

ACKNOWLEDGMENTS

This work was supported by grants from the Science and Technology Coordinator Innovation Project in Shaanxi Province, China, and from the National Science Council (NSC 99-2321-B-005-015-MY3), Taiwan.

Footnotes

Citation Wang J-Y, Ren J-J, Qiu Y-H, Liu H-J. 2013. Complete genome sequences of six avian-like H1N1 swine influenza viruses from northwestern China. Genome Announc. 1(1):e00098-12. doi:10.1128/genomeA.00098-12.

REFERENCES

1. Ito T, Couceiro JN, Kelm S, Baum LG, Krauss S, Castrucci MR, Donatelli I, Kida H, Paulson JC, Webster RG, Kawaoka Y. 1998. Molecular basis for the generation in pigs of influenza A viruses with pandemic potential. J. Virol. 72:7367–7373. [PMC free article] [PubMed]
2. Karasin AI, Carman S, Olsen CW. 2006. Identification of human H1N2 and human-swine reassortant H1N2 and H1N1 influenza A viruses among pigs in Ontario, Canada (2003 to 2005). J. Clin. Microbiol. 44:1123–1126. [PMC free article] [PubMed]
3. Naffakh N, van der Werf S. 2009. April 2009: an outbreak of swine-origin influenza A(H1N1) virus with evidence for human-to-human transmission. Microbes Infect. 11:725–728. [PubMed]
4. Dacso CC, Couch RB, Six HR, Young JF, Quarles JM, Kasel JA. 1984. Sporadic occurrence of zoonotic swine influenza virus infections. J. Clin. Microbiol. 20:833–835. [PMC free article] [PubMed]
5. Wentworth DE, Thompson BL, Xu X, Regnery HL, Cooley AJ, McGregor MW, Cox NJ, Hinshaw VS. 1994. An influenza A (H1N1) virus, closely related to swine influenza virus, responsible for a fatal case of human influenza. J. Virol. 68:2051–2058. [PMC free article] [PubMed]
6. Guan Y, Shortridge KF, Krauss S, Li PH, Kawaoka Y, Webster RG. 1996. Emergence of avian H1N1 influenza viruses in pigs in China. J. Virol. 70:8041–8046. [PMC free article] [PubMed]
7. Liu J, Bi Y, Qin K, Fu G, Yang J, Peng J, Ma G, Liu Q, Pu J, Tian F. 2009. Emergence of European avian influenza virus-like H1N1 swine influenza A viruses in China. J. Clin. Microbiol. 47:2643–2646. [PMC free article] [PubMed]
8. Yu H, Zhang PC, Zhou YJ, Li GX, Pan J, Yan LP, Shi XX, Liu HL, Tong GZ. 2009. Isolation and genetic characterization of avian-like H1N1 and novel ressortant H1N2 influenza viruses from pigs in China. Biochem. Biophys. Res. Commun. 386:278–283. [PubMed]
9. Scholtissek C, Rohde W, Von Hoyningen V, Rott R. 1978. On the origin of the human influenza virus subtypes H2N2 and H3N2. Virology 87:13–20. [PubMed]
10. Suzuki H, Saito R, Masuda H, Oshitani H, Sato M, Sato I. 2003. Emergence of amantadine-resistant influenza A viruses: epidemiological study. J. Infect. Chemother. 9:195–200. [PubMed]
11. Igarashi M, Ito K, Kida H, Takada A. 2008. Genetically destined potentials for N-linked glycosylation of influenza virus hemagglutinin. Virology 376:323–329. [PubMed]
12. Peiris JS, de Jong MD, Guan Y. 2007. Avian influenza virus (H5N1): a threat to human health. Clin. Microbiol. Rev. 20:243–267. [PMC free article] [PubMed]
13. Gabriel G, Abram M, Keiner B, Wagner R, Klenk HD, Stech J. 2007. Differential polymerase activity in avian and mammalian cells determines host range of influenza virus. J. Virol. 81:9601–9604. [PMC free article] [PubMed]
14. Labadie K, Dos Santos Afonso E, Rameix-Welti MA, van der Werf S, Naffakh N. 2007. Host-range determinants on the PB2 protein of influenza A viruses control the interaction between the viral polymerase and nucleoprotein in human cells. Virology 362:271–282. [PubMed]
15. Saito R, Sakai T, Sato I, Sano Y, Oshitani H, Sato M, Suzuki H. 2003. Frequency of amantadine-resistant influenza A viruses during two seasons featuring cocirculation of H1N1 and H3N2. J. Clin. Microbiol. 41:2164–2165. [PMC free article] [PubMed]

Articles from Genome Announcements are provided here courtesy of American Society for Microbiology (ASM)