African Swine Fever Virus

Tulman, E. R.; Delhon, G.; Ku, Bok Kyung; Rock, Daniel L.

doi:10.1007/978-3-540-68618-7_2

Cited by 134 publications

(129 citation statements)

References 300 publications

(360 reference statements)

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“…Literature on wild pigs and AFS is however dispersed and scattered, and information sources amalgamating the epidemiological role of different species are presently lacking. In contrast, virus pathogenesis in the Ornithodoros tick has been extensively studied (reviewed by Kleiboeker and Scoles, 2001), as has the viral genome (reviewed by Viñuela, 1985) and genetic basis of virus virulence (reviewed by Tulman et al, 2009). Variation in clinical disease and virus genome length and composition is known to occur, with infections in domestic swine ranging from sub-clinical to lethal and field strains having genomes up to 20 kbp longer than laboratoryadapted strains (Tulman et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

“…In contrast, virus pathogenesis in the Ornithodoros tick has been extensively studied (reviewed by Kleiboeker and Scoles, 2001), as has the viral genome (reviewed by Viñuela, 1985) and genetic basis of virus virulence (reviewed by Tulman et al, 2009). Variation in clinical disease and virus genome length and composition is known to occur, with infections in domestic swine ranging from sub-clinical to lethal and field strains having genomes up to 20 kbp longer than laboratoryadapted strains (Tulman et al, 2009). Recent molecular epidemiological studies have also uncovered substantial field heterogeneity with at least 22 genotypes being identified to date on the basis of C-terminus p72 gene sequencing (Bastos et al, 2003;Lubisi et al, 2005;Boshoff et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

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Role of Wild Suids in the Epidemiology of African Swine Fever

2009

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There is presently no vaccine to combat African swine fever (ASF), a viral hemorrhagic fever of domestic pigs that causes up to 100% morbidity and mortality in naive, commercial pig populations. In its endemic setting, ASF virus cycles between asymptomatic warthogs and soft ticks, with persistence in exotic locations being ascribed to the almost global distribution of susceptible soft tick and suid hosts. An understanding of the role played by diverse hosts in the epidemiology of this multi-host disease is crucial for effective disease control. Unlike the intensively studied Ornithodoros tick vector, the role of many wild suids remains obscure, despite growing recognition for suid-exclusive virus cycling, without the agency of the argasid tick, at some localities. Because the four wild suid genera, Phacochoerus, Potamochoerus, Hylochoerus, and Sus differ from each other in taxonomy, distribution, ecology, reservoir host potential, virus shedding, ASF symptomology, and domestic-pig contact potential, their role in disease epidemiology is also varied. This first consolidated summary of ASF epidemiology in relation to wild suids summarizes current knowledge and identifies information gaps and future research priorities crucial for formulating effective disease control strategies.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Role of Wild Suids in the Epidemiology of African Swine Fever

2009

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“…The disease is classified as notifiable by the World Organization for Animal Health (OIE) and is caused by a DNA arbovirus belonging to the genus Asfivirus and family Asfarviridae [1]. ASF virus (ASFV) has a double-stranded DNA genome of between 170 and 190 kb in size, which is variable due to deletions and insertions occurring within the terminal regions of the genome and within a coding gene region within the central region of the genome [1][2][3], termed the central variable region (CVR).…”

Section: Introductionmentioning

confidence: 99%

“…ASF virus (ASFV) has a double-stranded DNA genome of between 170 and 190 kb in size, which is variable due to deletions and insertions occurring within the terminal regions of the genome and within a coding gene region within the central region of the genome [1][2][3], termed the central variable region (CVR).…”

Section: Introductionmentioning

confidence: 99%

Molecular characterisation of African swine fever viruses from Nigeria (2003–2006) recovers multiple virus variants and reaffirms CVR epidemiological utility

et al. 2010

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“…ASFV infection of domestic pigs can induce a spectrum of disease severity, from highly lethal to subclinical, depending on host characteristics and the particular circulating virus strain (1).…”

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The Progressive Adaptation of a Georgian Isolate of African Swine Fever Virus to Vero Cells Leads to a Gradual Attenuation of Virulence in Swine Corresponding to Major Modifications of the Viral Genome

Krug

Holinka

O’Donnell

et al. 2015

J Virol

149

159

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African swine fever virus (ASFV) causes a contagious and often lethal disease of feral and domestic swine. Experimental vaccines derived from naturally occurring, genetically modified, or cell culture-adapted ASFV have been evaluated, but no commercial vaccine is available to control African swine fever (ASF). We report here the genotypic and phenotypic analysis of viruses obtained at different passages during the process of adaptation of a virulent ASFV field isolate from the Republic of Georgia (ASFV-G) to grow in cultured cell lines. ASFV-G was successively passaged 110 times in Vero cells. Viruses obtained at passages 30, 60, 80, and 110 were evaluated in vitro for the ability to replicate in Vero cells and primary swine macrophages cultures and in vivo for assessing virulence in swine. Replication of ASFV-G in Vero cells increased with successive passages, corresponding to a decreased replication in primary swine macrophages cultures. In vivo, progressive loss of virus virulence was observed with increased passages in Vero cells, and complete attenuation of ASFV-G was observed at passage 110. Infection of swine with the fully attenuated virus did not confer protection against challenge with virulent parental ASFV-G. Full-length sequence analysis of each of these viruses revealed significant deletions that gradually accumulated in specific areas at the right and left variable ends of the genome. Mutations that result in amino acid substitutions and frameshift mutations were also observed, though in a rather limited number of genes. The potential importance of these genetic changes in virus adaptation/attenuation is discussed. IMPORTANCEThe main problem in controlling ASF is the lack of vaccines. Attempts to produce vaccines by adaptation of ASFV to cultured cell lines have been made. These attempts led to the production of attenuated viruses that conferred only homologous protection. Specifics regarding adaptation of these isolates to cell cultures have been insufficiently described. Details like the numbers of passages required to obtain attenuated viruses, genetic modifications introduced into the virus genomes along passages, and the extent of attenuation and induced protective efficacy are not readily available. In this study, we assessed the changes that lead to decreased growth in swine macrophages and to attenuation in swine. Loss of virulence, probably associated with limited replication in vivo, may lead to the lack of protective immunity in swine observed after challenge. This report provides valuable information that can be used to further the understanding of ASFV gene function, virus attenuation, and protection against infection.A frican swine fever (ASF) is a contagious disease of swine caused by ASF virus (ASFV), an enveloped virus containing a large (190-kbp) double-stranded DNA (dsDNA) genome. ASFV infection of domestic pigs can induce a spectrum of disease severity, from highly lethal to subclinical, depending on host characteristics and the particular circulating virus strain (1).A...

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African Swine Fever Virus

Cited by 134 publications

References 300 publications

Role of Wild Suids in the Epidemiology of African Swine Fever

Role of Wild Suids in the Epidemiology of African Swine Fever

Molecular characterisation of African swine fever viruses from Nigeria (2003–2006) recovers multiple virus variants and reaffirms CVR epidemiological utility

The Progressive Adaptation of a Georgian Isolate of African Swine Fever Virus to Vero Cells Leads to a Gradual Attenuation of Virulence in Swine Corresponding to Major Modifications of the Viral Genome

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