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 Polymerase X (AsfvPolX) is the most distinctive

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

5 ASFV is a viral agent with significant economic impact d

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

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

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

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

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

11 ASFV-specific antibodies were first detected from day 10

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

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

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

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

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

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

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

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

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

21 ttempts toward experimental vaccines against ASFV-G.

22 ed by the unavailability of vaccines against ASFV.

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

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

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

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

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

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

29 wo pathogenic ASFV isolates, ASFV Malawi and ASFV Haiti, partially adapted to Vero cells, were used s

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

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

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

33 ted, or genetically modified live attenuated ASFV.

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

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

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

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

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

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

40 nti-inflammatory cytokine, were increased by ASFV infection, suggesting that ASFV-induced inhibition

41 nes whose cellular functions are required by ASFV.

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

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

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

45 n was inhibited by the virus and by a cloned ASFV gene, A238L.

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

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

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

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

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

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

52 ately upstream from the previously described ASFV virulence-associated gene NL-S.

53 this gene is highly conserved among diverse ASFV isolates and that the gene product exists in either

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

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

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

57 form (70 to 72 amino acids in other examined ASFV isolates).

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

59 completely attenuate a highly virulent field ASFV isolate.

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

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

62 or the hemadsorption phenomenon observed for ASFV-infected cells.

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

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

65 This may be of most significance for ASFV infection of its highly adapted natural host, the w

66 asfarvirus family but highly divergent from ASFV.

67 cifically precipitated a 15-kDa protein from ASFV-infected macrophage cell cultures as early as 2 h p

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

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

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

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

72 mechanisms and may provide insights into how ASFV causes a fatal hemorrhagic disease of domestic pigs

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

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

75 t might contribute to genetic variability in ASFV.

76 Initial ASFV replication occurred in phagocytic digestive cells

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

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

79 Two pathogenic ASFV isolates, ASFV Malawi and ASFV Haiti, partially adapted to Vero ce

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

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

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

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

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

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

86 hat this gene may function in some aspect of ASFV virulence and/or host range.

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

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

89 sed to a higher than normal concentration of ASFV.

90 genes acting as independent determinants of ASFV virulence.

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

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

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

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

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

96 icate that the highly conserved NL-S gene of ASFV, while nonessential for growth in swine macrophages

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

120 induces protection in swine against parental ASFV-G.

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

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

123 ion against challenge with virulent parental ASFV-G.

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

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

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

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

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

129 quent challenge with the parental pathogenic ASFV.

130 ertants were constructed from the pathogenic ASFV isolate E70 and an E70 monkey cell culture-adapted

131 Two pathogenic ASFV isolates, ASFV Malawi and ASFV Haiti, partially ada

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

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

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

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

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

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

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

139 ghly virulent and epidemiologically relevant ASFV-G.

140 nd antigenic variability observed among some ASFV isolates.

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

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

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

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

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

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

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

148 This study demonstrates that ASFV effectively inhibited phorbol myristic acid-induced

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

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

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

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

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

154 increased by ASFV infection, suggesting that ASFV-induced inhibition of cytokine synthesis may be lim

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

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

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

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

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

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

161 examined in nymphal ticks infected with the ASFV isolate Chiredzi/83/1.

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

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

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

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

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

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

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

169 bstrates that are expected to be relevant to ASFV.

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

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

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

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

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

175 ine that induces protection against virulent ASFV-G.

176 at induces solid protection against virulent ASFV-G.

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

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

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

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

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

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

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

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

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

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

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

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

189 An African swine fever virus (ASFV) gene with similarity to the T-lymphocyte surface a

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

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

192 e pathogenesis of African swine fever virus (ASFV) infection in Ornithodoros porcinus porcinus was ex

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

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

195 African swine fever virus (ASFV) is a large, double-stranded DNA virus that infects

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

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

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

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

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

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

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

203 of the pathogenic African swine fever virus (ASFV) isolate E70 revealed a novel gene, UK, that is imm

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

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

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

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

208 bed previously an African swine fever virus (ASFV) open reading frame, 23-NL, in the African isolate

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

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

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

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

213 1 (MAL) strain of African swine fever virus (ASFV) was isolated from Ornithodoros sp. ticks, our atte

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

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

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

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

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

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

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

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

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

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

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

225 14 days postinoculation when challenged with ASFV-G.

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

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