ライフサイエンスコーパス: ASFV

1 ASFV APE retains activity when assayed in the presence o

2 ASFV carries a gene (Ba71V D250R/Malawi g5R) that encode

3 ASFV DNA ligase (AsfvLIG) is one of the most error-prone

4 ASFV DNA Polymerase X (AsfvPolX) is the most distinctive

5 ASFV has a large, double-stranded DNA genome that encode

6 ASFV infection led to a reduction in the levels of PP-In

7 ASFV is a viral agent with significant economic impact d

8 ASFV-DP also interacted with viral and cellular RNAs in

9 ASFV-DP was capable of interaction with poly(A) RNA in c

10 ASFV-G was successively passaged 110 times in Vero cells

11 ASFV-G-Delta8DR inoculated intramuscularly or intranasal

12 ASFV-G-Delta9GL/DeltaUK is the first rationally designed

13 ASFV-G-DeltaI177L is one of the few experimental vaccine

14 ASFV-G-DeltaMGF replicates as efficiently in primary swi

15 ASFV-specific antibodies were first detected from day 10

16 ASFVs can, however, be adapted to grow in monkey cell li

17 Our results show that virulent Armenia/07 ASFV controls the cGAS-STING pathway, but these mechanis

18 ainst challenge with the virulent Benin 97/1 ASFV genotype I isolate at day 130 postimmunization.

19 s were created within the ASFV Georgia 2007 (ASFV-G) genome, attenuation was achieved but the protect

20 a highly virulent virus, ASFV Georgia 2007 (ASFV-G), has caused an epizootic that spread rapidly int

21 enetically modified, or cell culture-adapted ASFV have been evaluated, but no commercial vaccine is a

22 s porcinus was observed for three additional ASFV tick isolates in their associated ticks.

23 Additionally, ASFV-G-DeltaMGF is the first experimental vaccine report

24 thesis of viral DNA and proteins early after ASFV infection, altered transcription of apoptosis-relat

25 The protection against ASFV-G is highly effective after 28 days postvaccination

26 The protection against ASFV-G is highly effective by 28 days postvaccination.

27 ttempts toward experimental vaccines against ASFV-G.

28 ed by the unavailability of vaccines against ASFV.

29 All ASFV-G-DeltaI177L-infected animals had low viremia titer

30 h nucleotide and amino acid levels among all ASFV field isolates examined.

31 t some of the diversity known to exist among ASFV isolates may be a consequence of mutagenic DNA repa

32 ns were found in both proteins, mostly among ASFV strains from East Africa, where multiple virus tran

33 An ASFV-G-Delta9GL HAD50 of 10(3) conferred partial and com

34 In this study, we constructed an ASFV 8-DR gene deletion mutant (delta8-DR) and its rever

35 mutant (Pr4Delta35) was constructed from an ASFV isolate of tick origin, Pr4.

36 SFV through homologous recombination with an ASFV p72 promoter-beta-glucuronidase indicator cassette

37 Here, we analyzed ASFV serotype-specific locus (C-type lectin (EP153R) and

38 ationship between the cGAS-STING pathway and ASFV virulence, contributing to uncover the molecular me

39 when considered alongside those of Pol X and ASFV DNA ligase, provide an enhanced understanding of (i

40 correlates with the appearance of serum anti-ASFV antibodies, but not with virus-specific circulating

41 As ASFV Pol X has no 5'-dRP lyase domain, it is reasonable

42 ted, or genetically modified live attenuated ASFV.

43 d using genetically modified live attenuated ASFVs where viral genes involved in virus virulence were

44 Interactions between ASFV and MxA were similar to those seen between MxA and

45 k on characterizing the interactions between ASFV and sncRNAs.

46 standing of the complex interactions between ASFV and the host cell.

47 To investigate the interplay between ASFV and sncRNAs, a study of host and viral small RNAs e

48 catalytic efficiency of nick sealing by both ASFV DNA ligase and bacteriophage T4 DNA ligase was dete

49 t during the nick-sealing step (catalyzed by ASFV DNA ligase).

50 le-nucleotide gap-filling step (catalyzed by ASFV DNA polymerase X) and extremely error-tolerant duri

51 aled 3 potential novel small RNAs encoded by ASFV, ASFVsRNA1-3.

52 idase indicator cassette (p72GUS) flanked by ASFV sequences targeting the TK region.

53 nes whose cellular functions are required by ASFV.

54 the resultant mismatched nicks are sealed by ASFV DNA ligase.

55 e data suggest that disruption of the TGN by ASFV can slow membrane traffic during viral infection.

56 ies, but not with virus-specific circulating ASFV-specific gamma interferon (IFN-gamma)-producing cel

57 tion for rational drug design to help combat ASFV in the future.

58 of ticks orally exposed to a tick-competent ASFV isolate, Pretoriuskop/96/4/1 (Pr4), increased 10-fo

59 Complete ASFV genome sequences were generated from cell culture i

60 report the cryo-EM structure of the complete ASFV virion, comprising a viral particle of multiple lay

61 ASFV isolates, did not attenuate completely ASFV-G.

62 In contrast, ASFV replication in cells expressing MxB protein or a mu

63 re available or under development to control ASFV-G.

64 Upon ASFV DNA binding, the Cas12a/crRNA/ASFV DNA complex becomes activated and degrades a fluore

65 In addition, the ternary Cas12a/crRNA/ASFV DNA complex is highly stable at physiological tempe

66 nducing sterile immunity against the current ASFV strain responsible for recent outbreaks.IMPORTANCE

67 Like Malawi-Lil-20/1-Delta9GL, ASFV-G-Delta9GL showed limited replication in primary sw

68 with a CRISPR RNA (crRNA) is used to detect ASFV target DNA.

69 ction potential between evolutionary distant ASFV strains and strongly suggest that C-type lectin and

70 cleotide gap-filling and that the downstream ASFV DNA ligase seals 3' mismatched nicks with high effi

71 l of these may be substrates for g5Rp during ASFV infection.

72 Decrease of cellular mRNA is observed during ASFV infection, suggesting that inhibition of cellular p

73 e may be exploited to develop more effective ASFV vaccines that take advantage of the sncRNA system.

74 s the first rationally designed experimental ASFV vaccine that protects against the highly virulent A

75 completely attenuate a highly virulent field ASFV isolate.

76 unctional implications of these findings for ASFV pol X activities are discussed.

77 e progression in swine, the natural host for ASFV.

78 enes previously not known to be required for ASFV infection.

79 The significance of these results for ASFV pol X activity in the recognition of damaged DNA is

80 asfarvirus family but highly divergent from ASFV.

81 of host and viral small RNAs extracted from ASFV-infected primary porcine macrophages (PAMs) was und

82 f rapid and real-time resolution of the full ASFV genome from a diagnostic sample.

83 covered and characterized a novel functional ASFV-encoded sncRNA.

84 larly with the virus lacking the I177L gene, ASFV-G-DeltaI177L, at a dose range of 10(2) to 10(6) 50%

85 tigene family 360 (MGF360) and MGF505 genes (ASFV-G-DeltaMGF).

86 field isolate from the Republic of Georgia (ASFV-G) to grow in cultured cell lines.

87 ed from highly virulent ASFV strain Georgia (ASFV-G) lacking only six of the multigene family 360 (MG

88 A complex, while the latter demonstrates how ASFV Pol X binds DNA in the absence of DNA-binding motif

89 2007 Georgia isolate (ASFV-G), a genotype II ASFV.

90 tionships of large viruses and should aid in ASFV vaccine development.

91 To examine the function of these genes in ASFV's arthropod host, Ornithodoros porcinus porcinus, a

92 attenuation may be a phenomenon grounded in ASFV-mediated innate immune modulation where the cGAS-ST

93 ASFVsRNA2 led to an up to 1-log reduction in ASFV growth, indicating that ASFV utilizes a virus-encod

94 There was a drastic reduction in ASFV late protein synthesis in MxA-expressing cells, cor

95 design, which could impair genome repair in ASFV and help combat this virus in the future.

96 involvement of the cGAS-STING-IRF3 route in ASFV infection, where IFN-beta production or inhibition

97 In addition, viremia values in ASFV-G-Delta8DR do not differ from those detected in ani

98 t might contribute to genetic variability in ASFV.

99 Initial ASFV replication occurred in phagocytic digestive cells

100 Interestingly, ASFV-G-DeltaI177L confers protection even at low doses (

101 tome study that provides unique insight into ASFV transcription and serves as a resource to aid futur

102 from this study add important insights into ASFV host-pathogen interactions.

103 upport the hypothesis that the intracellular ASFV viral envelope is composed of a single lipid bilaye

104 e highly virulent ASFV Georgia 2007 isolate (ASFV-G) by specifically deleting six genes belonging to

105 ASFV derived from the 2007 Georgia isolate (ASFV-G), a genotype II ASFV.

106 from the genome of ASFV Georgia2010 isolate (ASFV-G-Delta8DR) does not significantly alter the virule

107 erize DNA consensus motifs of early and late ASFV core promoters, as well as a polythymidylate sequen

108 he three-dimensional structure of the mature ASFV particle.

109 (ii) the mechanisms by which the minimalist ASFV DNA repair pathway, consisting of just these three

110 t the construction of a genetically modified ASFV-G strain (ASFV-G-Delta9GLv) harboring a deletion of

111 In the past, genetically modified ASFVs harboring deletions of virulence-associated genes

112 In addition, several natural ASFV isolates showing decreased virulence in swine has b

113 lizing an EGFP reporter system for observing ASFV replication and infectivity can circumvent the time

114 The activities of ASFV APE, when considered alongside those of Pol X and A

115 ttempts to produce vaccines by adaptation of ASFV to cultured cell lines have been made.

116 esource to aid future functional analyses of ASFV genes which are essential to combat this devastatin

117 One interesting aspect of ASFV biology is the molecular mechanism leading to high

118 s in Vero cells, and complete attenuation of ASFV-G was observed at passage 110.

119 To enhance attenuation of ASFV-G, we deleted another gene, UK (DP96R), which was p

120 r knowledge about the fundamental biology of ASFV, including the mechanisms and temporal control of g

121 sed to a higher than normal concentration of ASFV.

122 reveals the multilayer structural details of ASFV at near-atomic resolution, which provides interesti

123 ivity of our system enables the detection of ASFV in femtomolar range.

124 hypothesize that the genetic determinants of ASFV variability are potential hot-spots for recombinati

125 genes acting as independent determinants of ASFV virulence.

126 virulence and to the rational development of ASFV vaccines.

127 ependent on early detection and diagnosis of ASFV.

128 g, and images suggested that the envelope of ASFV consisted of a single lipid membrane.

129 ted that the intracellular viral envelope of ASFV was not significantly different from the outer mito

130 RNA-Seq detected the expression of ASFV genes from the whole blood of the GRG, but not the

131 The data indicate that the TK gene of ASFV is important for growth in swine macrophages in vit

132 ndicate that the highly conserved UK gene of ASFV, while being nonessential for growth in macrophages

133 that deletion of 8DR gene from the genome of ASFV Georgia2010 isolate (ASFV-G-Delta8DR) does not sign

134 lar inoculation of swine with 10(4) HAD50 of ASFV-G-Delta9GL produced a virulent phenotype that, unli

135 A dose of 10(2) HAD50 of ASFV-G-Delta9GLv conferred partial protection when pigs

136 ingly, lower doses (10(2) to 10(3) HAD50) of ASFV-G-Delta9GL did not induce a virulent phenotype in s

137 with 10(4) 50% hemadsorbing doses (HAD50) of ASFV-G-Delta9GL/DeltaUK were protected as early as 14 da

138 ssist in combating the devastating impact of ASFV.

139 Despite the importance of ASFV, little is known about the mechanisms and regulatio

140 romoter resulted in reversible inhibition of ASFV production by >99%.

141 Strikingly, the inhibition of ASFV replication was linked to the recruitment of MxA pr

142 ion of macrophages with virulent isolates of ASFV increased the expression of MHC class I genes, but

143 d by using two highly pathogenic isolates of ASFV through homologous recombination with an ASFV p72 p

144 Our findings are discussed in light of ASFV biology and the mutagenic DNA repair hypothesis des

145 These results are discussed in light of ASFV biology and the mutagenic DNA repair hypothesis des

146 on and a phenotypic screen for limitation of ASFV replication in cultured human cells, we identified

147 uting to uncover the molecular mechanisms of ASFV virulence and to the rational development of ASFV v

148 oining reaction during DNA repair process of ASFV and plays important roles in mutagenesis of the vir

149 known about the mechanisms and regulation of ASFV transcription.

150 Subsequent infection and replication of ASFV in undifferentiated midgut cells was observed at 15

151 Replication of ASFV-G in Vero cells increased with successive passages,

152 Results suggest that the mean risk of ASFV introduction into the US via this route has increas

153 The risk of ASFV release was shown to be high, and improving farmers

154 present here the development of a strain of ASFV that has been shown to retain its ability to cause

155 t outbreaks caused by circulating strains of ASFV derived from the 2007 Georgia isolate (ASFV-G), a g

156 Infection with attenuated strains of ASFV leads to the upregulation of genes controlled by IF

157 Previous ultrastructural studies of ASFV using chemical fixation and cryosectioning for elec

158 e mismatch specificity of Pol X with that of ASFV DNA ligase suggests that the latter may have evolve

159 Transfection of ASFV-infected Vero cells with a plasmid encoding epitope

160 Successful tick-to-pig transmission of ASFV at 48 days p.i. correlated with high viral titers i

161 can be used to further the understanding of ASFV gene function, virus attenuation, and protection ag

162 Studies on ASFV virulence lead to the production of genetically mod

163 Deletion of 9GL, unlike with other ASFV isolates, did not attenuate completely ASFV-G.

164 rophages are infected with attenuated NH/P68 ASFV.

165 induces protection in swine against parental ASFV-G.

166 uced a lethal disease in swine like parental ASFV-G.

167 d by the same doses of the virulent parental ASFV Georgia2010 isolate.

168 equently exposed to highly virulent parental ASFV-G, no signs of the disease were observed, although

169 ion against challenge with virulent parental ASFV-G.

170 responses following infection with parental ASFV (Pr4) and an MGF360/530 deletion mutant (Pr4 Delta

171 eletion mutants of two additional pathogenic ASFV isolates, Malawi Lil-20/1 and Pr4, remained highly

172 Genomic cosmid clones from pathogenic ASFV isolate E70 were used in marker rescue experiments

173 n of this same region from highly pathogenic ASFV isolate Pr4 significantly reduced viral growth in m

174 genes in pigs infected with a low pathogenic ASFV isolate, OUR T88/3 (OURT), or the highly pathogenic

175 quent challenge with the parental pathogenic ASFV.

176 ysis of the UK genes from several pathogenic ASFVs from Europe, the Caribbean, and Africa demonstrate

177 In this study we prepared ASFV-infected cells for EM using chemical fixation, cryo

178 alawi g5R) that encodes a decapping protein (ASFV-DP) that has a Nudix hydrolase motif and decapping

179 the extracted nucleic acid facilitated rapid ASFV sequence identification, with reads specific to ASF

180 Here we produced a recombinant ASFV lacking virulence-associated gene 9GL in an attempt

181 e we have produced an attenuated recombinant ASFV derived from highly virulent ASFV strain Georgia (A

182 n delivered once at low dosages, recombinant ASFV-G-Delta9GL induces protection in swine against pare

183 Antisense transcription of BAT3 reduced ASFV production without affecting abundance of the virus

184 ing pigs from the epidemiologically relevant ASFV Georgia isolate.

185 ghly virulent and epidemiologically relevant ASFV-G.

186 ned fluorometer, enabling compact and simple ASFV detection, intended for low resource settings.

187 nd antigenic variability observed among some ASFV isolates.

188 challenged with the virulent parental strain ASFV-G.

189 ion of a genetically modified ASFV-G strain (ASFV-G-Delta9GLv) harboring a deletion of the 9GL (B119L

190 Simulation modeling was used to study ASFV transmission in backyard and small-scale farms as w

191 ral replication in the midgut for successful ASFV infection of the arthropod host.

192 expressing human MxA protein did not support ASFV plaque formation, and virus replication in these ce

193 Surprisingly, ASFV pol X binds the dsDNA with significant positive coo

194 A virulent fluorescently tagged ASFV is a suitable tool to conduct pathogenesis studies

195 early and late stages of infection and that ASFV RNA polymerase (RNAP) undergoes promoter-proximal t

196 Our results demonstrate that ASFV utilizes alternative transcription start sites betw

197 Here, we demonstrate that ASFV-DP is a novel RNA-binding protein implicated in the

198 We discovered that ASFV infection had only a modest effect on host miRNAs,

199 respectively, thus reinforcing the idea that ASFV virulence versus attenuation may be a phenomenon gr

200 Our results indicate that ASFV DNA ligase is the lowest-fidelity DNA ligase ever r

201 These findings indicate that ASFV MGF360 and MGF530 genes perform an essential macrop

202 These data indicate that ASFV MGF360 genes are significant tick host range determ

203 og reduction in ASFV growth, indicating that ASFV utilizes a virus-encoded small RNA to disrupt its o

204 n of vesicular stomatitis virus to show that ASFV significantly reduces the rate at which the protein

205 capping activity in vitro Here, we show that ASFV-DP was expressed from early times and accumulated t

206 The ASFV infection rate in ticks was 100% in these experimen

207 to be able to induce protection against the ASFV Georgia isolate, and it is the first vaccine capabl

208 osed of the mature products derived from the ASFV polyproteins pp220 and pp62.

209 y shown to be involved in attenuation of the ASFV E70 isolate.

210 tructural and functional similarities of the ASFV gene product to CD2, a cellular protein involved in

211 The large size of the ASFV genome (~180 kb) has historically hindered efforts

212 egion within the left variable region of the ASFV genome containing the MGF 360 and 530 genes represe

213 th a noticeable decrease in virulence of the ASFV Georgia isolate.

214 eaction during the DNA repair process of the ASFV virus genome; it is highly error prone and plays an

215 amined the nick ligation capabilities of the ASFV-encoded DNA ligase and here report the first comple

216 Our results show that the ASFV virion, with a radial diameter of ~2,080 angstrom,

217 m macrophage cell cultures infected with the ASFV isolate Malawi Lil-20/1 (MAL).

218 en similar deletions were created within the ASFV Georgia 2007 (ASFV-G) genome, attenuation was achie

219 Therefore, ASFV-G-DeltaI177L is a novel efficacious experimental AS

220 Thus, ASFV 9GL gene deletion mutants may prove useful as live-

221 ailed, suggesting a growth deficiency of TK- ASFV on macrophages.

222 Swine surviving TK- ASFV infection remained free of clinical signs of Africa

223 This high-level organization confers to ASFV a unique architecture among the NCLDVs that likely

224 e response of macrophages and lymphocytes to ASFV infection, as well as reveal unique gene pathways u

225 This study points to ASFV-DP as a viral decapping enzyme involved in both the

226 bstrates that are expected to be relevant to ASFV.

227 uence identification, with reads specific to ASFV detected within 6 min after the initiation of seque

228 surface marker phenotype, susceptibility to ASFV infection and virus production.

229 tandem with the exceptionally error-tolerant ASFV DNA ligase to effect viral mutagenesis.

230 Studies focusing on understanding ASFV virulence led to the production of genetically modi

231 Upon ASFV DNA binding, the Cas12a/crRNA/ASFV DNA complex beco

232 to host sncRNA abundances were observed upon ASFV infection, we discovered and characterized a novel

233 ring the process of adaptation of a virulent ASFV field isolate from the Republic of Georgia (ASFV-G)

234 ttempt to produce a vaccine against virulent ASFV-G, a highly virulent virus isolate detected in the

235 ine that induces protection against virulent ASFV-G.

236 at induces solid protection against virulent ASFV-G.

237 G-DeltaMGF) derived from the highly virulent ASFV Georgia 2007 isolate (ASFV-G) by specifically delet

238 ne that protects against the highly virulent ASFV Georgia 2007 isolate as early as 2 weeks postvaccin

239 the 9GL (B119L) gene in the highly virulent ASFV isolates Malawi Lil-20/1 (Mal) and Pretoriuskop/96/

240 eading frame [ORF] B119L) in highly virulent ASFV Malawi-Lil-20/1 produced an attenuated phenotype ev

241 ecombinant ASFV derived from highly virulent ASFV strain Georgia (ASFV-G) lacking only six of the mul

242 erized gene, I177L, from the highly virulent ASFV-G produces complete virus attenuation in swine.

243 ion of viral transcripts.IMPORTANCE Virulent ASFV strains cause a highly infectious and lethal diseas

244 l challenge model with a moderately virulent ASFV.

245 nd after infection by attenuated or virulent ASFV strains, respectively, thus reinforcing the idea th

246 The virulent ASFV Armenia/07, E70 or the naturally attenuated NHV/P68

247 Recombinant virus ASFV-G-DeltaMGF effectively confers protection in pigs a

248 enzyme NP868R of African swine fever virus (ASFV) and the T7 RNA polymerase were expressed.

249 African swine fever virus (ASFV) can cause highly lethal disease in pigs and is bec

250 African swine fever virus (ASFV) causes a contagious and often lethal disease of fe

251 African swine fever virus (ASFV) causes a lethal hemorrhagic disease of domestic pi

252 African swine fever virus (ASFV) causes a lethal, haemorrhagic disease in domestic

253 African swine fever virus (ASFV) causes hemorrhagic fever in domestic pigs, present

254 isease.IMPORTANCE African swine fever virus (ASFV) causes incurable and often lethal hemorrhagic feve

255 African swine fever virus (ASFV) disrupts the trans-Golgi network (TGN) by altering

256 The African swine fever virus (ASFV) g5R gene encodes a protein containing a Nudix hydr

257 The CD2-like African swine fever virus (ASFV) gene 8DR, (also known as EP402R) encodes for a str

258 The African swine fever virus (ASFV) genome contains a gene, 9GL, with similarity to ye

259 ns encoded by the African swine fever virus (ASFV) genome do not have significant similarity to known

260 ination events in African swine fever virus (ASFV) genomes have been poorly annotated.

261 African swine fever virus (ASFV) infection is characterized by a progressive decrea

262 African swine fever virus (ASFV) is a complex nucleocytoplasmic large DNA virus (NC

263 African swine fever virus (ASFV) is a complex, cytoplasmic double-stranded DNA (dsD

264 African swine fever virus (ASFV) is a highly pathogenic, double-stranded DNA virus

265 African swine fever virus (ASFV) is a macrophage-tropic virus responsible for ASF,

266 African swine fever virus (ASFV) is a member of a family of large nucleocytoplasmic

267 African swine fever virus (ASFV) is among the most complex DNA viruses known.

268 em encoded by the African swine fever virus (ASFV) is both extremely error-prone during the single-nu

269 African swine fever virus (ASFV) is contagious and can cause highly lethal disease

270 X, encoded by the African swine fever virus (ASFV) is one of the most error-prone polymerases known,

271 African swine fever virus (ASFV) is the causative agent of a severe and highly cont

272 African swine fever virus (ASFV) is the causative pathogen of the recent African sw

273 African swine fever virus (ASFV) is the etiological agent of a contagious and often

274 African swine fever virus (ASFV) is the etiological agent of a contagious and often

275 African swine fever virus (ASFV) is the etiological agent of an often lethal diseas

276 urally attenuated African swine fever virus (ASFV) isolate OURT88/3 and deletion mutant BeninDeltaMGF

277 Pathogenic African swine fever virus (ASFV) isolates primarily target cells of the mononuclear

278 we reported that African swine fever virus (ASFV) multigene family (MGF) 360 and 530 genes are signi

279 African swine fever virus (ASFV) multigene family 360 and 530 (MGF360/530) genes af

280 ve shown that the African swine fever virus (ASFV) NL gene deletion mutant E70DeltaNL is attenuated i

281 African swine fever virus (ASFV) produces a fatal acute hemorrhagic fever in domest

282 The risk of African swine fever virus (ASFV) release via this emergency sale was investigated.

283 African swine fever virus (ASFV) replicates in the cytoplasm of infected cells and

284 an) PCR assay for African swine fever virus (ASFV) was developed and evaluated in experimentally infe

285 1 (MAL) strain of African swine fever virus (ASFV) was isolated from Ornithodoros sp. ticks, our atte

286 tiological agent, African swine fever virus (ASFV), is a highly structurally complex double stranded

287 se encoded by the African swine fever virus (ASFV), is extremely error prone during single-nucleotide

288 virus (FMDV) and African swine fever virus (ASFV).

289 ection system for African Swine Fever Virus (ASFV).

290 le virus species, African swine fever virus (ASFV).

291 and virulence of African swine fever virus (ASFV).

292 ort the construction of a recombinant virus (ASFV-G-DeltaMGF) derived from the highly virulent ASFV G

293 of a double-gene-deletion recombinant virus, ASFV-G-Delta9GL/DeltaUK.

294 epublic of Georgia, a highly virulent virus, ASFV Georgia 2007 (ASFV-G), has caused an epizootic that

295 In vivo, ASFV-G-DeltaMGF is completely attenuated in swine, since

296 t components may provide a mechanism whereby ASFV can disrupt the correct secretion and/or cell surfa

297 rs protection in pigs against challenge with ASFV-G when delivered once via the intramuscular (i.m.)

298 14 days postinoculation when challenged with ASFV-G.

299 ral identities that have been connected with ASFV host range specificity, blocking of the host innate

300 African swine fever virus DNA polymerase X (ASFV Pol X) with one-nucleotide gapped DNA.