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Emergence of truncated PB1-F2 protein of H3N2 influenza virus during its epidemic period in Jiangsu Province, China.

AbstractBACKGROUND:
PB1-F2 protein has been proven to increase the pathogenicity of influenza A virus (IAV) strains in primary infection and in secondary bacterial infection. It can also regulate the activity of viral polymerase. However, it was shown in another retrospective study that a portion of IAVs do not express full-length PB1-F2 protein during virus development; different kinds of stop codons cause exits in the open reading frames and form PB1-F2 gene products with the corresponding genotypes. Truncated PB1-F2 in human H3N2 IAVs has long been detected in North America but its evolution in China is still unclear.
METHODS:
Influenza-like illnesses (ILIs) from the whole of Jiangsu Province were collected and inspected to determine the type and subtype of the viruses. A portion of isolates collected in the epidemic period were selected as samples for later whole-genome sequencing, and the exact sequences were determined and analyzed.
RESULTS:
H3N2 influenza virus was one of the epidemical strains which had been prevalent during 2009-2010, in Jiangsu. Five H3N2 isolates with truncated PB1-F2 protein (25aa) were detected in influenza samples from Nanjing and Xuzhou, while seven similar H3N2 isolates were also reported in Niigata, Japan.
CONCLUSION:
This emergence indicates the possibility that there has been transmission of the H3N2 virus between the two countries.
AuthorsPingmin Wei, Pengfei Luo, Wei Li, Hairong Zi, Xian Qi, Fei Deng, Yuanfang Qin, Bin Wu, Fenyang Tang
JournalChinese medical journal (Chin Med J (Engl)) Vol. 127 Issue 8 Pg. 1487-92 ( 2014) ISSN: 2542-5641 [Electronic] China
PMID24762594 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • PB1-F2 protein, Influenza A virus
  • Viral Proteins
Topics
  • China (epidemiology)
  • Humans
  • Influenza A Virus, H3N2 Subtype (genetics, metabolism)
  • Influenza, Human (virology)
  • Viral Proteins (chemistry, genetics, metabolism)

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