Novel Swine Virulence Determinant in the Left Variable Region of the African Swine Fever Virus Genome

Neilan, John G.; Zsák, László; Lu, Zhiqiang; Kutish, G. F.; Afonso, Claudio L.; Rock, Daniel L.

doi:10.1128/jvi.76.7.3095-3104.2002

Cited by 73 publications

(74 citation statements)

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“…On the other hand, significant differences exist in pMGF 110-2L, -9L and, to a esser extent, p86R, which could lead to lower virulence. A study with isolates lacking all MGF 110 members suggested that these may neither be essential for replication nor have a role in virulence (Agüero et al, 1990 Burrage et al, 2004;Neilan et al, 2002;Zsak et al, 2001). In Vero cell-adapted Ba71V, also with a deletion of 8.2 kb in this area of the genome, replication in macrophages was restored after the introduction of consecutive 3CL, 3DL and 3EL (MGF 360-9L, -10L and -11L, respectively); 3FR (MGF 505-1R); and 3HL, 3IL and 3LL (MGF 360-12L, -13L and -14L, respectively) (Zsak et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Related strains of African swine fever virus with different virulence: genome comparison and analysis

Portugal

Coelho

Höper

et al. 2015

Journal of General Virology

110

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Section: Discussionmentioning

confidence: 99%

Related strains of African swine fever virus with different virulence: genome comparison and analysis

Portugal

Coelho

Höper

et al. 2015

Journal of General Virology

110

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“…The N-terminal regions of members of MGFs 300, 360 and 505/530 share significant similarity with each other (Yozawa et al, 1994). Several genes in MGF 360 and 505/530 determine host range and virulence (Afonso et al, 2004;Neilan et al, 2002;Tulman & Rock, 2001). It has also been observed that repeated passage of field isolates of ASFV through tissue culture results in the loss of members of the MGF 110 family (Almendral et al, 1990;de la Vega et al, 1990;Pires et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Comparison of the genome sequences of non-pathogenic and pathogenic African swine fever virus isolates

Chapman

Tcherepanov

Upton

et al. 2008

Journal of General Virology

257

256

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The genomic coding sequences, apart from the inverted terminal repeats and cross-links, have been determined for two African swine fever virus (ASFV) isolates from the same virus genotype, a non-pathogenic isolate from Portugal, OURT88/3, and a highly pathogenic isolate from West Africa, Benin 97/1. These genome sequences were annotated and compared with that of a tissue culture-adapted isolate, BA71V. The genomes range in length between 170 and 182 kbp and encode between 151 and 157 open reading frames (ORFs). Compared to the Benin 97/1 isolate, the OURT88/3 and BA71V isolates have deletions of 8–10 kbp that encode six copies of the multigene family (MGF) 360 and either one MGF 505/530 copy in the BA71V or two copies in the OURT88/3 isolate. The BA71V isolate has a deletion, close to the right end of the genome, of 3 kbp compared with the other isolates. The five ORFs in this region include an additional copy of an ORF similar to that encoding the p22 virus structural protein. The OURT88/3 isolate has interruptions in ORFs that encode a CD2-like and a C-type lectin protein. Variation between the genomes is observed in the number of copies of five different MGFs. The 109 non-duplicated ORFs conserved in the three genomes encode proteins involved in virus replication, virus assembly and modulation of the host's defences. These results provide information concerning the genetic variability of African swine fever virus isolates that differ in pathogenicity.

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“…Using restriction endonuclease digestion, the authors demonstrated the existence of different lengths of SmA1 and EcoR-I restriction fragment patterns as a probable consequence of deletion or genetic rearrangement of the virus genome. Furthermore, it was demonstrated that variation in length of restriction fragments can be associated with virulence (NEILAN et al, 2002). A high level of variability in the virulence of ASFV field isolates from inside and outside Africa was demonstrated by restriction length fragment polymorphism (RFLP).…”

Section: Asfv Population Virulence Heterogeneity In Brazilian Outbreaksmentioning

confidence: 99%

“…The ASFV genome is a DNA molecule which contains a central conserved region and variable terminal regions composed of internal inverted complementary repetitions arranged in tandem, including the five multigene families (MGF 100, 110, 300, 360 and 505/530) where genetic variation mainly occurs (CHAPMAN et al, 2008). The genetic variability of several genes associated with virulence and host range suggested that low virulence could be associated with a decrease in the number of genes in families 360 and 505/530 following mutations with large deletions (CHAPMAN et al, 2008;NEILAN et al, 2002;TULMAN;ROCK, 2001). …”

Section: Asfv Population Virulence Heterogeneity In Brazilian Outbreaksmentioning

confidence: 99%

“…The high morbidity and mortality rates associated with ASF and the lack of preventive vaccines make the disease one of the major causes of economic losses to pig farmers, and a central issue for global food security (ARZT et al, 2010). ASF infection of domestic pigs can occur in peracute, acute, chronic and subclinical forms, depending on viral strain virulence and host factors (NEILAN et al, 2002). Initially endemic to sub-Saharan African countries, the ASF virus (ASFV) has spread rapidly into countries never before infected (BASTOS et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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Epizootiology, laboratory and virulence analyses during the emergency phase of the African swine fever eradication program in Brazil in 1978: a historic account

Lyra

Freitas²

2015

Sem. Ci. Agr.

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After the first African swine fever (ASF) outbreak occurred in Brazil in 1978, an official laboratory for ASF diagnosis (ASFDL) was established. The current work reviews the efforts of the laboratory team to define an ASF diagnosis during the emergency phase of the ASF Eradication Program. From June to December 1978, 3,803 samples of pig tissue, blood and serum were analyzed. ASFDL first isolated the ASF virus (ASFV) from pig tissue samples from the Teresópolis municipality in the Brazilian state of Rio de Janeiro. During the first two months, ASFV was isolated from 130 of 320 (40.62%) pig samples analyzed by haemadsorption (HAD), indicating that the outbreak had reached 96 of 214 municipalities surveyed throughout the country in that period. The distribution of positive ASFV samples indicated the potential route of virus dispersal. Because of the rapidity of the actions implemented against ASF, the number of ASFV positive samples decreased from 48.36% in June to 33.53% in July, and then to 0% in August 1978. In parallel, ASFV antibody detection increased from 17.89% in June to 52.04% in August 1978. In the state of Paraná, a comparison of ASFV isolates with descriptions of the disease, and a rapid decrease in mortality rates suggested the occurrence of a low or moderate virulence ASFV strain. Establishment of ASFDL was crucial for the program, which eradicated ASFV from the country within six years of the first outbreak. Advances in cellular and molecular biology corroborated pioneer studies regarding ASFV virulence, and have highlighted the importance of establishing and maintaining secure measures to prevent ASFV reintroduction to the country. Information on virulence heterogeneity in ASFV populations during outbreaks provided a paramount tool for the adoption of eradication best practices. país, nos primeiros dois meses, de 320 amostras analisadas, 130 (40.62%) foram positivas pelo teste de hemadsorção o que sugere que a infecção com VPSA alcançou suínos em 96 dos 214 municípios analisados no período. A distribuição dos isolamentos do vírus no país mostrou uma possível rota de dispersão viral. Devido à rapidez das ações de eliminação dos focos, o número de amostras positivas caiu de 48,36% em Junho para 33,53% em Julho até nenhuma em Agosto, de 1978. Paralelamente, a detecção de anticorpos aumentou de 17,89% a 52,04% de Junho para Agosto de 1978. Os isolamentos do vírus pela técnica de hemadsorção (HAD) quando comparados com a descrição da doença e o forte declínio na taxa de mortalidade no Estado do Paraná sugeriram a ocorrência de cepas virais de VPSA de baixa a moderada virulência. A implantação do LDPSA foi crucial para o programa que assegurou a erradicação do VPSA em todo país após seis anos do primeiro surto. Os avanços na biologia celular e molecular corroboraram as suposições dos estudos pioneiros sobre a virulência viral e alertam para a importância de se estabelecer e manter medidas de segurança para prevenir a reintrodução do VPSA no país. A informação sobre heterogeneidade na virulência...

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Novel Swine Virulence Determinant in the Left Variable Region of the African Swine Fever Virus Genome

Cited by 73 publications

References 50 publications

Related strains of African swine fever virus with different virulence: genome comparison and analysis

Related strains of African swine fever virus with different virulence: genome comparison and analysis

Comparison of the genome sequences of non-pathogenic and pathogenic African swine fever virus isolates

Epizootiology, laboratory and virulence analyses during the emergency phase of the African swine fever eradication program in Brazil in 1978: a historic account

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