ライフサイエンスコーパス: helper virus

1 scriptional promoters) were derived from the helper virus.

2 ucks, using woodchuck hepatitis B virus as a helper virus.

3 ith expression plasmids or infection with MV helper virus.

4 enes (p40 and p35) in combination with a HSV helper virus.

5 ty mediated by the replication-competent HSV helper virus.

6 which is completely free of adenovirus (Ad) helper virus.

7 e RNA replication of the guanidine-resistant helper virus.

8 or intensify the symptoms produced by their helper virus.

9 into mice in the presence of a nonpathogenic helper virus.

10 the cells could efficiently encapsidate the helper virus.

11 vaccination by the replication-competent HSV helper virus.

12 To make a gutless virus, we used psi5 as a helper virus.

13 f viruses that can mediate resistance to the helper virus.

14 uently vector stocks were free of detectable helper virus.

15 th a replication-defective (E1 + E3 deleted) helper virus.

16 and replicate only in the presence of wt-HIV helper virus.

17 due to their buoyancy difference relative to helper virus.

18 ce of het DNA in the absence of the parental helper virus.

19 RNA to the negative-strand antigenome of the helper virus.

20 ressed through mitosis in the absence of the helper virus.

21 high levels in the presence of the CYDV-RPV helper virus.

22 n with adenovirus (Ad), AAV's most efficient helper virus.

23 ity to interfere with the replication of the helper virus.

24 was finally obtained, using a nonrevertable helper virus.

25 replicon) but can be amplified by wild-type helper virus.

26 ulfate after infection with adenovirus dl309 helper virus.

27 l passage in the presence of a noncytopathic helper virus.

28 tive cycle after complementation with wt-HIV helper-virus.

29 fected with the corresponding wild-type (wt) helper viruses.

30 usually lack substantial homology with their helper viruses.

31 f species with several different families of helper viruses.

32 ether with functions supplied by coinfecting helper viruses.

33 wn to efficiently inhibit the replication of helper viruses.

34 ar proteins as well as functions supplied by helper viruses.

35 nclude (1) contamination of rAAV with the Ad helper virus, (2) low yields of rAAV and (3) production

36 g either the "non-neurovirulent" amphotropic helper virus, 4070A, or pgag-polgpt (a nonpackaged vecto

37 We demonstrated that DNA methylation of helper virus 5' long terminal repeat occurred in approxi

38 ned with little or no DNA methylation of the helper virus 5' LTR.

39 A of subtype H3 (A/Udorn/72) in a subtype H1 helper virus (A/WSN/33) background.

40 satellite RNAs generally reduce the level of helper virus accumulation and attenuate the disease symp

41 In the absence of helper virus, all four Rep proteins have been shown to r

42 The chimeric helper virus allows the establishment of a mixed populat

43 defective (BM5def) and replication-competent helper viruses among which BM5def is the primary causati

44 sgenic mice through the use of Cre-dependent helper virus and a modified rabies virus.

45 contains Moloney murine leukemia virus as a helper virus and a picornavirus internal ribosome entry

46 Vector supernatants are free of helper virus and are of sufficiently high titer within 2

47 form into HSV-1 capsids in the presence of a helper virus and helper cell line.

48 gene (dvB7Ig) were generated using G207 as a helper virus and tested in the poorly immunogenic murine

49 llite RNAs can have a dramatic effect on the helper virus and the host plant in a manner specific to

50 e possible unwanted interactions between the helper virus and the packaged replicon.

51 To understand the mechanism involved, helper virus and vectors were examined for DNA methylati

52 Since its introduction, new helper viruses and reagents that facilitate complementat

53 of the relationships between subviral RNAs, helper viruses, and hosts.

54 s of recombination with and contamination by helper virus are eliminated.

55 Mo-MuLVDelta28 served as a helper virus as efficiently as the wt virus; in contrast

56 In this study, we employed a helper virus-based reverse genetics system to identify N

57 be replicated, transcribed, and packaged by helper virus, both rinderpest virus and the related meas

58 s were partially purified from the wild-type helper virus by CsCl equilibrium density-gradient centri

59 Mutualism between satRNA and helper virus can be seen for the satRNA of Groundnut ros

60 cted BHK cells with VSV DIPs and recombinant helper virus carrying a gene encoding a red fluorescent

61 In the absence of helper virus coinfection AAV can integrate its genome si

62 e (ORF2) of both the defective and ecotropic helper virus components of LP-BM5.

63 her's RNA was investigated by cotransfecting helper virus constructs with vectors derived from both v

64 to that observed following transduction with helper virus-containing HSV (HC HSVlac) and helper virus

65 ported short-term, inducible expression from helper virus-containing HSV-1 vector systems.

66 Defective interfering (DI) RNAs, helper virus-dependent deletion mutant RNAs derived from

67 vector system is based on nonpathogenic and helper-virus-dependent parvoviruses.

68 tein v-Rel is a chimeric protein that has 11 helper virus-derived Envelope (Env) amino acids (aa) at

69 own that three mutant residues in the eleven helper virus-derived Envelope (Env) amino acids (aa) at

70 al vector in the presence of a nonpathogenic helper virus developed long-latency erythroblastosis, an

71 ethylation inhibitor, partially reversed the helper virus DNA methylation and restored a portion of v

72 AAV2 replication requires coinfection with a helper virus (e.g., adenovirus or herpesvirus) or treatm

73 rus type 2 (AAV) requires coinfection with a helper virus, e.g., adenovirus or herpesviruses.

74 the nucleus and requires coinfection with a helper virus, either adenovirus (Ad) or herpesvirus, for

75 AAV) replication requires coinfection with a helper virus, either adenovirus or herpesvirus.

76 esidues to the residues present in the Rev-A helper virus Env protein abolish this transactivation ab

77 three aa substitutions compared to the Rev-A helper virus Env.

78 NAs usurp the replication machinery of their helper viruses, even though they bear little or no seque

79 These dRNAs were not supported by helper viruses expressing both replicase-associated prot

80 ed with nonpathogenic Friend murine leukemia helper virus (F-MuLV), which replicates poorly in adult

81 Capsid proteins provided in trans by helper virus failed to rescue the nonreplicating delta P

82 pidly convert to the wild-type leader of the helper virus following DI RNA transfection into helper v

83 rus that requires adenovirus (Ad) or another helper virus for a fully permissive infection.

84 d by the presence of adenovirus, the primary helper virus for a productive AAV infection.

85 nique characteristics of a dependence upon a helper virus for a productive infection and the ability

86 The identification of HBoV1 as a helper virus for AAV2 replication has implications for t

87 Here, we report that HBoV1 is a novel helper virus for AAV2 replication.

88 Adeno-associated viruses (AAVs) depend on a helper virus for efficient replication.

89 packaging Ad7 DNA, it may be a more suitable helper virus for the growth of Ad7 gutted vectors for ge

90 s could facilitate the creation of efficient helper viruses for influenza virus reverse genetics expe

91 us which usually requires the presence of a "helper" virus for strong DNA replication.

92 productive phase requires coinfection with a helper virus, for instance adenovirus, while the latent

93 constructed, and murine immune responses to helper virus-free amplicon preparations derived from thi

94 Gene transfer used a helper virus-free Herpes Simplex Virus (HSV-1) vector sy

95 Helper virus-free Herpes Simplex Virus (HSV-1) vectors h

96 Long-term expression from helper virus-free Herpes Simplex Virus (HSV-1) vectors i

97 g-term expression in forebrain neurons, from helper virus-free Herpes Simplex Virus (HSV-1) vectors.

98 Helper virus-free Herpes Simplex Virus vector-mediated g

99 We microinjected helper virus-free herpes simplex virus vectors that expr

100 t transduction of mesencephalic cells with a helper virus-free HSV amplicon (HF HSV-TH9lac) that harb

101 therapy of hematologic malignancies and that helper virus-free HSV amplicon preparations are better s

102 helper virus-containing HSV (HC HSVlac) and helper virus-free HSV amplicons (HF HSVlac) expressing l

103 obtain long-term, inducible expression from helper virus-free HSV-1 vectors.

104 r virus (HSVlac, HSVB7.1, and HSVCD40L) or a helper virus-free method (hf-HSVlac, hf-HSVB7.1, and hf-

105 To develop a helper virus-free packaging system for these vectors, th

106 Thus, highly purified, helper virus-free rAAV vectors can achieve high-frequenc

107 Helper virus-free vector stocks were delivered into post

108 Using helper virus-free vector stocks, we showed that this vec

109 cloned into HSV amplicons and packaged into helper virus-free vectors.

110 ansduced ex vivo with replication-defective, helper virus-free, herpes simplex virus type 1 (HSV-1) a

111 s demonstrated the feasibility of generating helper-virus-free inducible AAV producer cell lines.

112 To test this hypothesis, we established a helper-virus-free minigenome (MG) system where intracell

113 suggest that in pneumovirus-infected cells, helper virus functions can discriminate between genomes

114 V (rAAV) vectors and may even substitute for helper virus functions.

115 titer production was tightly associated with helper virus gene expression and varied between 0 and 2.

116 ted in trans with the helper virus sequence, helper virus gene expression could be inactivated by hos

117 ot analysis demonstrated that suppression of helper virus gene expression decreased Env-receptor inte

118 and correlated closely with inactivation of helper virus gene expression.

119 the DI RNA rapidly conformed to that in the helper virus genome through a previously described templ

120 he brain, but several problems caused by the helper virus have compromised their utility.

121 to liver cirrhosis upon coinfection with its helper virus, HBV.

122 eracts with envelope proteins of the natural helper virus, hepatitis B virus.

123 the interaction between AAV2 and one of its helper viruses, herpes simplex virus 1 (HSV-1).

124 L) and were packaged using either a standard helper virus (HSVlac, HSVB7.1, and HSVCD40L) or a helper

125 ly modified an adenovirus (Ad) to generate a helper virus (HV) that was detargeted for native adenovi

126 perative interaction between STMV CP and the helper virus (HV) Tobacco mosaic virus (TMV) replicase.

127 Virus is dependent on replicase proteins of helper virus (HV).

128 thought to be completely dependent on their helper virus (HV).

129 RNAs), parasites of viruses, depend on their helper viruses (HVs) for replication, encapsidation, and

130 issive DNA replication in the absence of the helper virus in cells that have been treated with genoto

131 The assay indicated the presence of helper virus in medium exposed to hematopoietic cells fr

132 ermitted selection for intact and functional helper virus in transfected cells without subcloning.

133 in the long terminal repeat (LTR) region of helper virus in vector producer cells (VPC) in up to 2%

134 ed stable ts phenotypes, they were tested as helper viruses in reverse genetics experiments.

135 rvovirus that replicates efficiently without helper viruses in Walter Reed/3873D (WRD) canine cells.

136 he successful development of efficient CCHFV helper virus-independent S, M, and L segment minigenome

137 dues were replicated after transfection into helper virus-infected cells.

138 per virus following DI RNA transfection into helper virus-infected cells.

139 ng constructs were tested for replication in helper virus-infected cells.

140 However, in the absence of helper virus infection, AAV2 establishes latency by inte

141 his efficient system, which does not require helper virus infection, should be useful in viral mutage

142 lines that require neither transfection nor helper virus infection.

143 on the state of the cell (Rep expression and helper virus influences), the p5IEE operates as a transc

144 n which free leader supplied in trans by the helper virus interacts by way of its flanking 5'UCUAAAC3

145 Thus, although helper virus is not required for maximal transduction, i

146 Because no helper virus is required to propagate these vectors, the

147 regulation by Rep, it undergoes induction by helper virus, it is a target substrate for Rep-mediated

148 ransgene in trans during superinfection by a helper virus, leading to "mobilization" of the vector ge

149 New models for DI RNA-mediated reduction in helper virus levels and symptom attenuation include DI R

150 In the absence of a helper virus, little expression of the AAV Rep proteins

151 D satellite RNA (satRNA) with its helper virus, namely, cucumber mosaic virus, causes syst

152 or intensify disease symptoms caused by the helper virus, only recently have clues concerning the me

153 ession, we constructed a chimeric retroviral helper virus, pAM3-IRES-Zeo, that contains Moloney murin

154 e panicum mosaic virus (SPMV) depends on its helper virus, panicum mosaic virus (PMV), to provide tra

155 l packaging cell lines were established by a helper virus plasmid cotransfected with a separate plasm

156 between the capsid proteins of SPMV and its helper virus (PMV).

157 by AAV2 may be responsible for inhibition of helper virus replication.

158 When infectious HRSV or APV was used as helper virus, replication could occur only if both the l

159 Here we determine helper virus requirements and the effects of mutations a

160 limit its own replication by diminishing the helper virus reservoir.

161 at the nonpermissive temperature for the ts helper virus resulted in replication and transcription o

162 bear little or no sequence similarity to the helper virus RNA.

163 of both DI RNAs but not in synthesis of the helper virus RNAs.

164 Thus, the helper virus's polymerase is the sole determinant of the

165 selection marker coexisted in trans with the helper virus sequence, helper virus gene expression coul

166 combination of retroviruses with genomic and helper virus sequences and that these novel viruses then

167 The preference for methylation of helper virus sequences over vector sequences may have im

168 a human parvovirus that normally requires a helper virus such as adenovirus (Ad) for replication.

169 only a host cell for replication but also a helper virus such as an adenovirus or a herpesvirus.

170 2) depends on the simultaneous presence of a helper virus such as herpes simplex virus 1 (HSV-1) for

171 ether with functions supplied by coinfecting helper viruses such as adenovirus (Ad).

172 on mechanism and requires coinfection with a helper virus, such as adenovirus, to achieve a productiv

173 nhibited by MRN and dependent on coinfecting helper virus, such as adenovirus, to remove this factor.

174 licate in cells that have been infected with helper viruses, such as adenovirus or herpesvirus.

175 ration vectors or by using the Cre/lox-based helper virus system.

176 ttenuate the disease symptoms induced by the helper virus that they depend upon for replication and p

177 aic virus (TMV) were examined in planta with helper viruses that expressed one (183 kDa) or both (126

178 We generated helper viruses that target gene expression to Cre-expres

179 Upon subsequent infection with a helper virus, the AAV genome is released from chromosome

180 multaneously or subsequently infected with a helper virus, the AAV genome is released from the plasmi

181 In coinfections with helper virus, the diversion of viral proteins to the rep

182 In the absence of helper virus, the vectors efficiently infected rat neura

183 P) subunit, relying on the polymerase of its helper virus TNV for replication.

184 We passaged a satellite RNA of CMV with its helper virus to determine whether a satellite RNA that a

185 oductive infection but relies on coinfecting helper virus to do so.

186 Designing a helper virus to overcome cellular DNA methylation may th

187 we used a sensitive marker rescue assay for helper virus to screen vector-transduced cells prior to

188 of an RNA- temperature-sensitive (ts) mutant helper virus, two coronavirus mouse hepatitis virus (MHV

189 The HIV-2 helper virus was unable to package the HIV-1 vector RNA,

190 mpts to plaque it as a virus with a standard helper virus were unsuccessful.

191 All of the helper viruses were in a single interference group.

192 tivate production of an apparently identical helper virus, which we have named M. dunni endogenous vi

193 the system in two ways: We constructed a new helper virus with a modified packaging signal and enhanc