Molecular characterization of African swine fever virus isolates originating from outbreaks in the Russian Federation between 2007 and 2011

被引:43
|
作者
Malogolovkin, Alexander [1 ]
Yelsukova, Alexandra [1 ]
Gallardo, Carmina [2 ]
Tsybanov, Sodnom [1 ]
Kolbasov, Denis [1 ]
机构
[1] Russian Acad Agr Sci, SRI Natl Res Inst Vet Virol & Microbiol NRIVVaM, Pokrov 601120, Russia
[2] Ctr Invest Sanidad Anim CISA INIA, Madrid, Spain
关键词
African swine fever virus; Genotyping; Phylogenetic analysis; Amplified fragment length polymorphism; EPIDEMIOLOGY; P72; P54;
D O I
10.1016/j.vetmic.2012.03.002
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
African swine fever is one of the most important viral diseases of pigs and which caused significant economic damage on the pig production worldwide. Nowadays, it is still present on the African continent, in Transcaucasus countries (TCC), on Island of Sardinia and in Russia. Outbreaks of the disease have been reported in Russia for the last four years, affected especially the Southern Federal District of the country. Since 2010, a new outbreak area has been observed in the Northwestern Federal District. In order to study the evolution of African swine fever virus (ASFV) isolates, strains were collected in the Russian Federation from 2007 to 2011 and investigated by means of partial sequencing and fragment length polymorphism. In detail, 7 variable regions, namely B646L, E183L, I196L, B602L, I73R/I329R, I78R/I215L and KP86R were investigated. Phylogenetic analyses revealed 100% nucleotide identity of B646L and E183L gene sequences of all examined isolates. All isolates formed one genetic cluster within genotype II. Moreover, no amplified fragment length polymorphism (AFLP) was observed for B602L, I196L, I73R/I329R, and I78R/I215L genes. The flanking primers used to amplify the KP86R gene failed to amplify a product in all the isolates. The obtained data strongly suggests that only one ASFV virus variant caused the outbreaks from 2007 to 2011 in the territory of the Russian Federation. (C) 2012 Elsevier B.V. All rights reserved.
引用
收藏
页码:415 / 419
页数:5
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