ライフサイエンスコーパス: minigenome

1 f viral transcription and replication in the minigenome.

2 s virus transcription and replication in the minigenome.

3 ription and/or replication of a rabies virus minigenome.

4 nscription and replication of a rabies virus minigenome.

5 pression of the reporter gene carried on the minigenome.

6 ailed to direct packaging and passage of the minigenome.

7 individual incorporation into a dicistronic minigenome.

8 , viral RNA, and messenger RNA from the EBOV minigenome.

9 package UUKV and SFTSV S and L segment-based minigenomes.

10 o affected the replication efficiency of the minigenomes.

11 ic, transcription, and replication-competent minigenomes.

12 capable of replicating both the NiV and HeV minigenomes.

13 n by using artificially generated SARS-CoV-2 minigenomes.

14 -CoV-2 variant to support replication of the minigenomes.

15 in support of replication of the respective minigenomes.

16 In a dicistronic SH-HN minigenome, a U4-G combination was functionally equivale

17 mutations at T286 and showed defects in both minigenome activity and viral growth.

18 (L795I) that enhanced both WT-P and P-S156A minigenome activity and was able to partially rescue the

19 t the mutation of eight residues resulted in minigenome activity significantly lower than that of wil

20 The highest minigenome activity was detected with the M segment-base

21 n at K254 to arginine (P-K254R) reduced PIV5 minigenome activity, as well as the sumoylation level of

22 ed NP protein expression and diminished EBOV minigenome activity.

23 esis as MIB2 binding to eVP35 inhibited EBOV minigenome activity.

24 id (T286D), or glutamic acid (T286E) reduced minigenome activity.

25 f heterologous viruses resulted in M segment minigenome activity.

26 tein, via coinfection with an engineered VSV minigenome, also restored polR growth.

27 llular RNA replication of a plasmid-encoded "minigenome" analog of viral genomic RNA was directed by

28 A series of copyback defective interfering minigenome analogs were constructed to contain substitut

29 Intracellular coexpression of the LCMV minigenome and LCMV L and NP proteins supplied from cotr

30 mutations affected the expression of an LCMV minigenome and the infectivity of virus-like particles,

31 This system involves an LCMV minigenome and the minimal viral trans-acting factors (N

32 Mutational analysis of bicistronic minigenomes and recombinant EBOVs showed no direct corre

33 ted due to the short length of monocistronic minigenomes and which is due at least partially to a pre

34 Time-of-addition, minigenome, and viral entry studies demonstrated that th

35 n requirements for packaging and passaging a minigenome are N, P, M, and F, although the efficiency i

36 tions in vitro as well as VP35 function in a minigenome assay and EBOV replication.

37 lowed efficient viral RNA transcription in a minigenome assay and that RNP activity played an essenti

38 TRIM6 enhances EBOV polymerase activity in a minigenome assay and TRIM6 knockout cells have reduced r

39 virus genus, functions poorly in the RSVlacZ minigenome assay despite conservation of the Cys(3)-His(

40 We developed the first minigenome assay for pig cells and compared the activiti

41 protein can be examined by using an RSVlacZ minigenome assay in vitro since the expression of the la

42 ype when coexpressed with wild-type L in the minigenome assay system.

43 ain within L remains unknown, but by using a minigenome assay we showed that it might be involved in

44 In a minigenome assay, nucleotide substitutions within the Le

45 n and avian cells for many years by use of a minigenome assay, similar investigations in pig cells ha

46 Using a luciferase minigenome assay, we quantified the polymerase activity

47 Using a minigenome assay, we show that phosphorylation of VP30 i

48 e results previously mapped with the in vivo minigenome assay.

49 V attachment but reduce RSV replication in a minigenome assay.

50 ins were analyzed for their functions with a minigenome assay.

51 tely abolished the P protein function in the minigenome assay.

52 ted with diminished polymerase activity in a minigenome assay.

53 vity also affect PA polymerase activity in a minigenome assay.

54 (miRNAs) and can be recapitulated in a MARV minigenome assay.

55 teins from the two viruses, as measured in a minigenome assay.

56 Results of minigenome assays and an EBOV reverse genetic system res

57 g L-mCherry fusion protein was functional in minigenome assays and incorporated into virus-like parti

58 (RT-PCR) measurements of RNAs synthesized in minigenome assays established that each of these NP amin

59 e present study describes the development of minigenome assays for the tick-borne viruses Uukuniemi p

60 We used these minigenome assays in conjunction with the existing minig

61 e viral polymerase (L protein), and by using minigenome assays we showed that the mutant polymerases

62 ription and genome replication in cell-based minigenome assays, indicating that it inhibits a step co

63 Here we use minigenome assays, virus infections, and viral promoter

64 However, minigenome assays, which assess viral RNA polymerase com

65 ctional T7 polymerase-based M- and S-segment minigenome assays, which revealed errors in the publishe

66 All blocked RSV polymerase activity in minigenome assays.

67 Here we have used minigenome-based approaches to evaluate expression level

68 revent the encapsidation of plasmid supplied minigenome, but it affected both transcription and RNA r

69 the replication capacity of the NiV and HeV minigenomes by exchanging the helper plasmids coding for

70 ciferase reporter gene expression from HPIV3 minigenomes by viral proteins in a recombinant vaccinia

71 A minigenome carrying the 5' proximal 634 nucleotides repl

72 The minigenomes consist of the 5'-proximal region, an open r

73 To this end, we constructed an LCMV S minigenome consisting of a negative-sense copy of the ch

74 es (VLPs), which contain an Ebola virus-like minigenome consisting of a negative-sense copy of the gr

75 The monocistronic RSV-CAT minigenome consists of the chloramphenicol acetyltransfe

76 Intracellular minigenome contained only the mutant assignment, indicat

77 Unexpectedly, each recovered minigenome contained the complement of this nonviral ext

78 n complex was supplied from cDNA plasmids, a minigenome containing either the APV leader or trailer w

79 A dicistronic minigenome containing the M-F gene junction was used to

80 In a minigenome containing the NS1 and NS2 genes in their aut

81 nd avian pneumovirus (APV) was studied using minigenomes containing a reporter gene.

82 A panel of minigenomes containing additional sequence at the 3' end

83 Minigenomes containing heterologous extensions of 6 nucl

84 s studies indicated that a 719-nt subgenomic minigenome (DENV-MINI) is an efficient template for tran

85 Deletion of the cre(2C) RNA sequences from minigenomes eliminates their ability to serve as templat

86 (L), nucleocapsid protein (N) and a reporter minigenome expressed in human HuH-7 cells resulted in fo

87 ely 10-fold lower inhibitory activity on ARM minigenome expression.

88 ection of the Z cDNA strongly inhibited LCMV minigenome expression.

89 roteins not related to Z did not affect LCMV minigenome expression.

90 ion of overlapping genes in EBOV bicistronic minigenomes followed the stop-start mechanism, similar t

91 due to reduced availability of encapsidated minigenomes for packaging.

92 ic, transcription, and replication-competent minigenomes for the Nipah, Hendra, and Cedar viruses, wh

93 tly driving replication and transcription of minigenomes from all tested henipaviruses.

94 y (NJ) serotype of VSV was inserted into the minigenome gene junction.

95 anscripts produced from di- and tricistronic minigenomes indicated that a significant proportion of a

96 immunoprecipitation analysis of the mutated minigenomes indicated that the first three nucleotides o

97 nations together with a plasmid containing a minigenome into cells infected with a vaccinia virus rec

98 The dicistronic RSV-CAT-LUC minigenome is a derivative of RSV-CAT into which the ORF

99 We therefore adapted a reverse-genetics minigenome (MG) rescue system based on Junin virus, the

100 studied the role of the LCMV IGR by using a minigenome (MG) rescue system based on RNA analogues of

101 pothesis, we established a helper-virus-free minigenome (MG) system where intracellular synthesis of

102 ning the 3'-terminal 20-nt region of an LCMV minigenome (MG) was generated, and the mutant MGs were a

103 ransfected with a plasmid containing an LCMV minigenome (MG).

104 protein with N and L proteins also enhanced minigenome mRNA transcription in the cells expressing vi

105 ranscribe, and replicate the M segment-based minigenome of a heterologous virus.

106 d a transcription- and replication-competent minigenome of VSV to generate a series of deletions span

107 tivity was detected with the M segment-based minigenomes of cognate viruses.

108 Progeny minigenomes of six different mutants were recovered post

109 Genome analogs ("minigenomes") of Sendai and measles viruses replicate ef

110 were analyzed with cDNA-encoded RNA analogs (minigenomes) of nonsegmented negative-sense RSV genomic

111 )-tagged L, and viral minigenome resulted in minigenome replication and transcription, a finding that

112 acid residue changes (Vcpi-) still inhibits minigenome replication as does the wild-type V protein.

113 In conclusion, we successfully developed a minigenome replication assay and a robust reverse-geneti

114 In addition, we developed an IDV minigenome replication assay and identified the E697K mu

115 Finally, by using the minigenome replication assay, we demonstrated that a sin

116 deleted P with wild-type P had no effect on minigenome replication in vivo, notwithstanding the form

117 This study details the construction of a minigenome replication system that can be used in a bios

118 Here, we describe a minigenome replication system to study BDBV transcriptio

119 nd in vivo chloramphenicol acetyltransferase minigenome replication were studied under conditions tha

120 The in vivo system takes advantage of minigenome replication, which measures luciferase report

121 uses equally affected mRNA transcription and minigenome replication.

122 the NSP1 coding region are required for the minigenome replication.

123 n the partial NSP1 coding sequence abrogated minigenome replication.

124 icts dsRNA accumulation during infection and minigenome replication.

125 that this interaction is essential for EBOV minigenome replication.

126 relevant doses of ribavirin inhibited CCHFV minigenome replication.

127 ' proximal 634 nucleotides are important for minigenome replication.IMPORTANCESARS-CoV-2, the causati

128 the replication and transcription of an RSV minigenome replicon at 37 and 39 degrees C.

129 When tested in an RSV minigenome replicon system using beta-galactosidase as a

130 ncreased translation of nonreplicating viral minigenome reporter RNAs during infection and also delay

131 y, replication and transcription of the RVFV minigenome required expression of viral N and L proteins

132 n and gene expression were exchangeable in a minigenome rescue assay.

133 oriomeningitis virus (LCMV), in vivo using a minigenome rescue assay.

134 of N, hemagglutinin (HA)-tagged L, and viral minigenome resulted in minigenome replication and transc

135 Consistent with the minigenome results, cells transiently expressing Z exhib

136 hable from previously studied negative-sense minigenome RNA in its ability to participate in transcri

137 ed for the efficient packaging of SARS-CoV-2 minigenome RNA into SARS-CoV-2 particles.

138 were sufficient for packaging an Ebola virus minigenome RNA into VLPs.

139 Since the minigenome RNA needs to be encapsidated before transcrip

140 Minigenome RNA replication was not affected by changes i

141 indicating that the effect of NSs protein on minigenome RNA replication was unrelated to a putative N

142 ins resulted in a significant enhancement of minigenome RNA replication.

143 Enhancement of minigenome RNA synthesis by NSs protein occurred in cell

144 Our finding that RVFV NSs protein augmented minigenome RNA synthesis was in sharp contrast to report

145 genus Bunyavirus) NSs protein inhibits viral minigenome RNA synthesis, suggesting that RVFV NSs prote

146 on of RNA transcripts for viral proteins and minigenome RNA transcripts carrying a reporter gene betw

147 cription in the cells expressing viral-sense minigenome RNA transcripts.

148 in LCMV-infected cells transfected with the minigenome RNA.

149 Introduction of synonymous mutations in the minigenome RNAs also affected the replication efficiency

150 Minigenome RNAs carrying a specific amino acid substitut

151 a series of replication-competent SARS-CoV-2 minigenome RNAs to identify the specific viral RNA regio

152 ength mRNA and, in the case of a dicistronic minigenome, sequential transcription.

153 A previous study, using an RSV minigenome, suggested that the leader (Le) promoter regi

154 within these domains were identified using a minigenome system able to recapitulate CCHFV-specific RN

155 Here we describe a Junin virus functional minigenome system and a reverse genetics system for prod

156 robust decrease in EBOV replication using a minigenome system and infectious virus.

157 To address this question, we used a minigenome system and recombinant viruses to study the e

158 Interpretation of the data from the minigenome system and the full-length infectious virus i

159 hese results demonstrated the utility of the minigenome system for use in BSL-2 laboratory settings t

160 established an RVFV T7 RNA polymerase-driven minigenome system in which T7 RNA polymerase from an exp

161 nome assays in conjunction with the existing minigenome system of severe fever with thrombocytopenia

162 Studies with the minigenome system showed that the 530 and 1009 mutations

163 In this work, we established a novel minigenome system that allows the domains of P to be com

164 Using mutational analysis and a minigenome system, we identified regions in the N and C

165 Using an RSV minigenome system, we individually mutated each of the l

166 of a set of PB1 mutants in a model reporter minigenome system.

167 the 1009 mutation also was observed with the minigenome system.

168 ome transcription and replication by using a minigenome system.

169 NA synthesis using mutational analysis and a minigenome system.

170 (T101A) significantly enhanced activity in a minigenome system.

171 ed effects on virus polymerase activity in a minigenome system.

172 reduced M2-2 activity as measured by the RSV minigenome system.

173 Life cycle modeling systems, including minigenome systems and transcription- and replication-co

174 helper virus-independent S, M, and L segment minigenome systems for analysis of virus RNA and protein

175 Here, we developed robust minigenome systems for the Nipah virus (NiV) and Hendra

176 itial studies of some of these viruses using minigenome systems have yielded insights into their mech

177 hinery of these viruses, we developed robust minigenome systems that can be safely used in BSL-2 cond

178 and thus essential support components of the minigenome systems.

179 ccumulation and impaired LASV replication in minigenome systems.

180 region with nonviral sequences resulted in a minigenome template (Rep 22) that was defective in termi

181 tion, it had no effect on replication of any minigenome tested, suggesting that it is not an active p

182 eight times more reporter protein from an MV minigenome than the three wild-type L proteins.

183 nfectious trVLPs containing a tetracistronic minigenome that encodes a reporter and the viral protein

184 Use of a minigenome that incorporated two nucleotide changes foun

185 expression increased the RNA replication of minigenomes that originated from S and L RNA segments.

186 e previously shown, using an SV5 dicistronic minigenome, that replacement of the 22-base M-F intergen

187 dicistronic vesicular stomatitis virus (VSV) minigenome to investigate the effects of either single o

188 dicistronic vesicular stomatitis virus (VSV) minigenomes to dissect the functional importance of the

189 Minigenome transcription also yielded a CAT-LUC readthro

190 t Z has a strong inhibitory activity on LCMV minigenome transcription and RNA replication.

191 With an in vivo VSV minigenome transcription system, we further show that a

192 owever, the same mutant protein complemented minigenome transcription when expressed together with a

193 the N(0)-P complex was unable to support VSV minigenome transcription, although it efficiently suppor

194 P E619K mutation moderately reduced the EBOV minigenome transcription, which was restored by the trea

195 In two different dicistronic minigenomes, transcription of each gene was equally sens

196 Four of the minigenome variants containing naturally occurring inter

197 ency of encapsidation of the plasmid-derived minigenome was not altered by coexpression of NS1, indic

198 The RSV-CAT-LUC minigenome was synthesized in vitro and transfected into

199 Each minigenome was synthesized in vitro and transfected into

200 Using single-round replicating EBOV minigenomes, we investigated the effect of the 3' termin

201 cription and replication of the rabies virus minigenome were significantly lower with the unphosphory

202 The termini of the recovered minigenomes were examined for five mutants by RNA circul

203 The minigenomes were generated entirely from cDNA and contai

204 Two minigenomes were used.

205 activities on the expression of the LCMV ARM minigenome, whereas the Z protein of the genetically mor

206 uential transcription were investigated with minigenomes which contained one to five genes which were

207 ively initiate the replication of both viral minigenomes, which suggests that the interaction regions

208 However, the activity of a minigenome with a 56-nucleotide extension could be resto

209 A series of minigenomes with mutant Le sequences was generated, and