Genetic Diversity of African Swine Fever Virus Isolates from Soft Ticks (Ornithodoros moubata) Inhabiting Warthog Burrows in Zambia

Dixon, Linda K.; Wilkinson, Philip

doi:10.1099/0022-1317-69-12-2981

Cited by 62 publications

(60 citation statements)

References 30 publications

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“…Viruses isolated from pigs in Malawi between 1982 and 1989 were also closely related (Sumption et al 1990). In contrast, ASFV isolates from soft ticks collected from warthog burrows over a 2-year period in four areas in Zambia showed considerable variation over the full genome (Dixon & Wilkinson 1988).…”

Section: Molecular Epidemiology Of African Swine Fever Virusmentioning

confidence: 94%

African swine fever: how can global spread be prevented?

Costard

Wieland

Glanville

et al. 2009

Phil. Trans. R. Soc. B

434

407

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African swine fever (ASF) is a devastating haemorrhagic fever of pigs with mortality rates approaching 100 per cent. It causes major economic losses, threatens food security and limits pig production in affected countries. ASF is caused by a large DNA virus, African swine fever virus (ASFV). There is no vaccine against ASFV and this limits the options for disease control. ASF has been confined mainly to sub-Saharan Africa, where it is maintained in a sylvatic cycle and/or among domestic pigs. Wildlife hosts include wild suids and arthropod vectors. The relatively small numbers of incursions to other continents have proven to be very difficult to eradicate. Thus, ASF remained endemic in the Iberian peninsula until the mid-1990s following its introductions in 1957 and 1960 and the disease has remained endemic in Sardinia since its introduction in 1982. ASF has continued to spread within Africa to previously uninfected countries, including recently the Indian Ocean islands of Madagascar and Mauritius. Given the continued occurrence of ASF in sub-Saharan Africa and increasing global movements of people and products, it is not surprising that further transcontinental transmission has occurred. The introduction of ASF to Georgia in the Caucasus in 2007 and dissemination to neighbouring countries emphasizes the global threat posed by ASF and further increases the risks to other countries. We review the mechanisms by which ASFV is maintained within wildlife and domestic pig populations and how it can be transmitted. We then consider the risks for global spread of ASFV and discuss possibilities of how disease can be prevented.

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Section: Molecular Epidemiology Of African Swine Fever Virusmentioning

confidence: 94%

African swine fever: how can global spread be prevented?

Costard

Wieland

Glanville

et al. 2009

Phil. Trans. R. Soc. B

434

407

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“…Specifically, we have suggested that ASFV sequence diversity, corresponding to small insertions/deletions or base substitutions (36), might be, in part, the consequence of an aberrant DNA repair pathway in which chemically damaged nucleotides are replaced with undamaged, although incorrect, nucleotides (30,31,34). However, for the error-proneness of Pol X and the error-tolerance of ASFV DNA ligase to be biologically relevant, they would need to function within the context of a complete DNA repair system in which the other components are capable of tolerating mismatched repair intermediates and products.…”

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confidence: 99%

Contributions of an Endonuclease IV Homologue to DNA Repair in the African Swine Fever Virus

Lamarche

Tsai

2006

Biochemistry

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: We recently demonstrated that African swine fever virus DNA polymerase X (Pol X) is extremely error-prone during single-nucleotide gap-filling and that the downstream ASFV DNA ligase seals 3′ mismatched nicks with high efficiency. To further assess the credence of our hypothesis that these proteins may promote viral diversification by functioning within the context of an aberrant DNA repair pathway, herein we characterize the third protein expected to function in this system, a putative AP endonuclease (APE). Assays of the purified protein using oligonucleotide substrates unequivocally establish canonical APE activity, 3′-phosphatase and 3′-phosphodiesterase activities (in the context of a singlenucleotide gap), 3′ f 5′ exonuclease activity (in the context of a nick), and nucleotide incision repair activity against 5,6-dihydrothymine. The 3′ f 5′ exonuclease activity is shown to be highly dependent upon the identity of the nascent 3′ base pair and to be inhibited when 2-deoxyribose-5-phosphate, rather than phosphate, constitutes the 5′ moiety of the nick. ASFV APE retains activity when assayed in the presence of EDTA but is inactivated by incubation with 1,10-phenanthroline in the absence of a substrate, suggesting that it is an endonuclease IV homologue possessing intrinsic metal cofactors. The activities of ASFV APE, when considered alongside those of Pol X and ASFV DNA ligase, provide an enhanced understanding of (i) the types of damage that are likely to be sustained by the viral genome and (ii) the mechanisms by which the minimalist ASFV DNA repair pathway, consisting of just these three proteins, contributes to the fitness of the virus.Apurinic/apyrimidinic (AP) 1 sites, generated either by DNA glycosylase-mediated or spontaneous base loss, can be both mutagenic (1, 2) and cytotoxic (3) and are among the most abundant types of damage found in DNA (4). Although they can be processed by AP lyases, which cleave 3′ to the lesion by a -elimination mechanism to generate a single-nucleotide gap flanked by 5′-phosphate and a 3′-polymerase-blocking R, -unsaturated aldehyde (5-7), AP sites are likely to be processed predominantly by AP endonucleases (8), which catalyze hydrolysis of the sugarphosphate backbone 5′ of the lesion to generate a singlenucleotide gap flanked by a polymerase-usable 3′-hydroxyl and 5′-2-deoxyribose-5-phosphate (5′-dRP) (7). Two families of APEs have been identified to date; these consist of proteins with homology to Escherichia coli exonuclease III 2 and proteins with homology to E. coli endonuclease IV. While the reaction that these proteins catalyze is identical, they differ dramatically in both tertiary structure and mechanisms of catalysis (9). Whereas exonuclease III displays a fourlayered R, -sandwich fold and employs a single readily dissociatable magnesium ion (9, 10), endonuclease IV is an R 8 8 TIM barrel that utilizes three tightly bound zinc ions (9,11).In addition to their APE activities, both exonuclease III and endonuclease IV (and their respective homologues) pos...

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“…Achieving this requires the availability of historical isolates and techniques capable of differentiating between strains. For ASF, studies of this nature have been impeded by the lack of discernible serotypes and could previously only be achieved by costly and time-consuming genomic characterisation methods such as restriction fragment length polymorphism (RFLP) analysis (Wesley and Tuthill, 1984, Dixon and Wilkinson, 1988and Blasco et al, 1989.…”

Section: Introductionmentioning

confidence: 99%

Genetic characterisation of African swine fever viruses from outbreaks in southern Africa (1973–1999)

Boshoff

Bastos

Gerber

et al. 2007

Veterinary Microbiology

172

200

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African swine fever (ASF) is a highly lethal and economically significant disease of domestic pigs in the southern African sub-region, where outbreaks regularly occur. There is anecdotal evidence suggesting that trans-boundary movement of infected animals may have played a role in precipitating widespread outbreaks in the past, however, since the 1970s outbreaks have generally been more localised, particularly in those countries where control of animal movement is strictly regulated. The origin and relatedness of regional ASF outbreaks was investigated here by means of a two-step genetic characterisation approach whereby p72 gene sequencing was used to delineate genotypes, prior to intra- were considered novel. Eight of these were country-specific with the remaining six having a trans-boundary distribution. CVR products were heterogeneous in size ranging from 377 bp to 533 bp across the 14 southern African genotypes. Within-genotype CVR comparisons revealed the presence of a genotype XIX virus with an extended field presence in South Africa (1985)(1986)(1987)(1988)(1989)(1990)(1991)(1992)(1993)(1994)(1995)(1996) and permitted discrimination between three genotype VII viruses that were identical across the p72 gene.

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Genetic Diversity of African Swine Fever Virus Isolates from Soft Ticks (Ornithodoros moubata) Inhabiting Warthog Burrows in Zambia

Cited by 62 publications

References 30 publications

African swine fever: how can global spread be prevented?

African swine fever: how can global spread be prevented?

Contributions of an Endonuclease IV Homologue to DNA Repair in the African Swine Fever Virus

Genetic characterisation of African swine fever viruses from outbreaks in southern Africa (1973–1999)

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