Epitopic diversity of African swine fever virus

Pan, I. C.; Whyard, Terry; Hess, W. R.; Yuasa, N.; Shimizu, M.

doi:10.1016/0168-1702(88)90025-1

Cited by 20 publications

(15 citation statements)

References 14 publications

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“…pigs or in porcine macrophages (39,40), and since it has been shown that the ASFV APE is essential for viral viability in macrophages but not in Vero cells (41), we suggest that damage to the ASFV genome is more extensive in macrophage cells than it is in Vero cells, and that this in turn affords the ASFV DNA "repair" system greater opportunity to introduce point mutations. Importantly, this is consistent with the fact that ASFV field isolates passaged in porcine macrophages display greater antigenic diversification than does the Vero cell-adapted BA71V isolate after passage in Vero cells (40).…”

Section: The Big Picturementioning

confidence: 77%

ASFV DNA Polymerase X Is Extremely Error-Prone under Diverse Assay Conditions and within Multiple DNA Sequence Contexts

2006

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We previously demonstrated that the DNA repair system encoded by the African swine fever virus (ASFV) is both extremely error-prone during the single-nucleotide gap-filling step (catalyzed by ASFV DNA Polymerase X) and extremely error-tolerant during the nick-sealing step (catalyzed by ASFV DNA ligase). On the basis of these findings we have suggested that at least some of the diversity known to exist among ASFV isolates may be a consequence of mutagenic DNA repairwherein damaged nucleotides are replaced with undamaged but incorrect nucleotides by Pol X and the resultant mismatched nicks are sealed by ASFV DNA ligase. Recently, this hypothesis appeared to be discredited by Salas and coworkers [J. Mol. Biol. 2003, 326, 1403-1412 who reported the fidelity of Pol X to be, on average, two orders of magnitude higher than what we previously published. In an effort to address this discrepancy and provide a definitive conclusion about the fidelity of Pol X, herein we examine the fidelity of Pol X-catalyzed single-nucleotide gap-filling in both the steady state and the pre-steady state under a diverse array of assay conditions (varying pH and ionic strength) and within different DNA sequence contexts. These studies corroborate our previously published data (demonstrating the low-fidelity of Pol X to be independent of assay condition/sequence context), do not reproduce the data of Salas et al., and therefore confirm Pol X to be one of the most errorprone polymerases known. These results are discussed in light of ASFV biology and the mutagenic DNA repair hypothesis described above.ASFV 1 causes a disease of varying mortality [depending on the particular isolate (1)] in domestic pigs in Africa, the Iberian Peninsula, and the Caribbean (2). Possessing a large [168-189 kb (3)] double-stranded DNA genome encoding 151 proteins (4), ASFV is one of the most complex viruses known. In its target cells, marcrophages and monocytes (5), ASFV utilizes the host cell nucleus during an early phase of viral DNA synthesis but appears to complete the replication/assembly of its genome in cytoplasmic/perinuclear viral factories (6 -8). Consistent with the latter intracellular location, ASFV encodes its own replicative polymerase in addition to a minimalist DNA repair system consisting of an AP endonuclease (APE), a repair polymerase (Pol X), and an ATP-dependent DNA ligase (4). While this tripartite repair system would appear to have been retained for the purpose of processing spontaneously 2 generated apurinic/apyrimidinic (AP) sites and/or reactive oxygen species (ROS)-induced singlestrand † This work was supported by NIH Grant GM43268. B.J.L. was supported in part by a predoctoral NIH CBIP fellowship (2T32 GM08512).*To whom correspondence should be addressed at the Department of Chemistry [phone: (614) breaks in the viral genome (9), the unique substrate specificities of both Pol X and ASFV DNA ligase have led us to hypothesize that this "repair" system may have subsequently evolved a secondary function, that of viral genome muta...

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Section: The Big Picturementioning

confidence: 77%

ASFV DNA Polymerase X Is Extremely Error-Prone under Diverse Assay Conditions and within Multiple DNA Sequence Contexts

2006

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“…The sequence changes in the viral DNA from different ASFV isolates have not yet been related to a particular phenotype alteration. However, differences in biologieM properties [20], DNA structure [36] antigenic [9] and phenotypie differences [7] have been reported in several ASFV strains. It is important to control accurately the passage history of any particular strain or isolate before attempting studies on the phenotypic characteristics of the virus.…”

Section: Discussionmentioning

confidence: 99%

African swine fever virus DNA: deletions and additions during adaptation to growth in monkey kidney cells

Tabarés

Olivares

Santurde

et al. 1987

Archives of Virology

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Restriction enzyme cleavage maps for the fragments produced by Cla I, Sal I and Sma I have been constructed for African swine fever virus (ASFV) DNA grown in pig leukocytes (strain E70 L6) and after adaptation to growth in MS monkey kidney cells (strain E70MS14). The mapping data revealed that before adaptation to growth in MS cells, the size of the DNA from ASFV strain E70 L6 was l73 Kbp and after adaptation it was only l56 Kbp. The decrease in size was produced by deletions and additions mainly in the terminal regions of the genome. These genetic variations were located between 0.0 to 0.01 m.u. (Cla I-M1 fragment), 0.04 to 0.14 m.u. (Sma I-B1, Sal I-A1 fragments), 0.51 to 0.52 m.u. (Cla I-O fragment), 0.84 to 0.86 m.u. (Sma I-H1), 0.95 to 0.97 m.u. (Cla I-A1, Cla I-G1 fragments) and 0.99 to 1.0 m.u. (Cla I-G1) on viral genome of ASFV grown in pig leukocytes.

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“…Virus clones differing in various properties including antigenic determinants, virulence, plaque size, haemadsorption characteristics and genome restriction enzyme profiles have been isolated from uncloned ASF virus isolates (Garcia-Barreno et al, 1986;Pan & Hess, 1985;Pan et al, 1988;Santurde et al, 1988;Wesley & Pan, 1982). In the present study our analysis was carried out on uncloned ASF virus isolated originally from ticks but subsequently grown in domestic pigs.…”

Section: Discussionmentioning

confidence: 99%

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

Dixon

Wilkinson

1988

Journal of General Virology

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Epitopic diversity of African swine fever virus

Cited by 20 publications

References 14 publications

ASFV DNA Polymerase X Is Extremely Error-Prone under Diverse Assay Conditions and within Multiple DNA Sequence Contexts

ASFV DNA Polymerase X Is Extremely Error-Prone under Diverse Assay Conditions and within Multiple DNA Sequence Contexts

African swine fever virus DNA: deletions and additions during adaptation to growth in monkey kidney cells

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

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