Nucleotide sequence of a 55 kbp region from the right end of the genome of a pathogenic African swine fever virus isolate (Malawi LIL20/1)

Dixon, Linda K.; Twigg, Stephen R. F.; Baylis, Sally A.; Vydelingum, Soopayah; Bristow, Christine; Hammond, J. M.; Smith, Geoffrey L.

doi:10.1099/0022-1317-75-7-1655

Cited by 71 publications

(65 citation statements)

References 111 publications

(73 reference statements)

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“…Ba71V has an extra deletion of 3.2 kb in the RVR of its genome, resulting in loss of several ORFs conserved in all natural strains of ASFV sequenced to date (Chapman et al, 2008), and also in the present L60 and NHV -I7L, -I8L, -I9R, -I10L and -I11L. These may have an important role for replication in macrophages and/or virulence, but they are still mostly uncharacterized, except for I10L encoding an extra copy of structural viral protein p22, similar to KP177R present in the LVR (Dixon et al, 1994). Other differences existing between the Ba71V and NHV or OURT88/3 genomes, principally in the LVRs, can cause defective replication: ORFs absent from the Ba71V genome, ORFs with non-conservative aa substitutions or deletions, and ORFs absent from NHV (Table 6).…”

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

112

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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

112

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“…Since IL-6 induces MyD116, HSV may have adopted this cellular response to prevent cell death and facilitate acute infection. The existence of an African swine fever virus virulence-associated gene, termed NL-S, with similarity in its carboxy terminal domain to the MyD116 and the HSV g(1)34.5 protein, has been reported as well (Sussman et al, 1992;Vydelingum et al, 1993;Dixon et al, 1994;Zsak et al, 1996). Whether other viruses harbor similar genes which promote cell survival upon infection remains to be seen.…”

Section: Myd116 ± Viral Homologs and A Protective Role In Apoptosismentioning

confidence: 99%

MyD genes in negative growth control

Liebermann

Hoffman

1998

Oncogene

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“…Although phylogenetic analyses suggest that ASFV gene E296R encodes an APE (23,35), the nuances of enzymatic catalysis, particularly for a multifunctional enzyme (as APEs tend to be), are only accurately understood via empirical analysis of the protein.…”

mentioning

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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Nucleotide sequence of a 55 kbp region from the right end of the genome of a pathogenic African swine fever virus isolate (Malawi LIL20/1)

Cited by 71 publications

References 111 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

MyD genes in negative growth control

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

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