Genetics, Evolution, and the Zoonotic Capacity of European Swine Influenza Viruses

被引:54
|
作者
Zell, Roland [1 ]
Scholtissek, Christoph [2 ]
Ludwig, Stephan [3 ]
机构
[1] Univ Jena, Jena Univ Hosp, Dept Virol & Antiviral Therapy, D-07740 Jena, Germany
[2] Univ Giessen, Inst Virol, D-35392 Giessen, Germany
[3] Univ Munster, Inst Mol Virol, Ctr Mol Biol Inflammat, D-48161 Munster, Germany
来源
SWINE INFLUENZA | 2013年 / 370卷
关键词
UNUSUAL SUBTYPE H1N7; A-VIRUS; PIG HERDS; AMANTADINE RESISTANCE; SEROLOGICAL EVIDENCE; NUCLEOTIDE-SEQUENCE; HEMAGGLUTININ GENE; PORCINE INFLUENZA; MUTATION-RATES; GREAT-BRITAIN;
D O I
10.1007/82_2012_267
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
The European swine influenza virus lineage differs genetically from the classical swine influenza viruses and the triple reassortants found in North America and Asia. The avian-like swine H1N1 viruses emerged in 1979 after an avian-to-swine transmission and spread to all major European pig-producing countries. Reassortment of these viruses with seasonal H3N2 viruses led to human-like swine H3N2 viruses which appeared in 1984. Finally, human-like swine H1N2 viruses emerged in 1994. These are triple reassortants comprising genes of avian-like H1N1, seasonal H1N1, and seasonal H3N2 viruses. All three subtypes established persistent infection chains and became prevalent in the European pig population. They successively replaced the circulating classical swine H1N1 viruses of that time and gave rise to a number of reassortant viruses including the pandemic (H1N1) 2009 virus. All three European lineages have the capacity to infect humans but zoonotic infections are benign.
引用
收藏
页码:29 / 55
页数:27
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