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1 ught animals that could serve as a potential helper virus.
2 scriptional promoters) were derived from the helper virus.
3 ucks, using woodchuck hepatitis B virus as a helper virus.
4 ith expression plasmids or infection with MV helper virus.
5 enes (p40 and p35) in combination with a HSV helper virus.
6 ty mediated by the replication-competent HSV helper virus.
7  which is completely free of adenovirus (Ad) helper virus.
8 e RNA replication of the guanidine-resistant helper virus.
9  or intensify the symptoms produced by their helper virus.
10 into mice in the presence of a nonpathogenic helper virus.
11  the cells could efficiently encapsidate the helper virus.
12 vaccination by the replication-competent HSV helper virus.
13   To make a gutless virus, we used psi5 as a helper virus.
14 f viruses that can mediate resistance to the helper virus.
15 uently vector stocks were free of detectable helper virus.
16 th a replication-defective (E1 + E3 deleted) helper virus.
17 and replicate only in the presence of wt-HIV helper virus.
18 due to their buoyancy difference relative to helper virus.
19 g their very dynamical interactions with the helper virus.
20  in plants in the absence of any discernible helper virus.
21 iruses that have a life cycle dependent on a helper virus.
22 ce of het DNA in the absence of the parental helper virus.
23 RNA to the negative-strand antigenome of the helper virus.
24  high levels in the presence of the CYDV-RPV helper virus.
25 n with adenovirus (Ad), AAV's most efficient helper virus.
26 ressed through mitosis in the absence of the helper virus.
27 ity to interfere with the replication of the helper virus.
28  was finally obtained, using a nonrevertable helper virus.
29  replicon) but can be amplified by wild-type helper virus.
30 ulfate after infection with adenovirus dl309 helper virus.
31 l passage in the presence of a noncytopathic helper virus.
32 tive cycle after complementation with wt-HIV helper-virus.
33 wn to efficiently inhibit the replication of helper viruses.
34 fected with the corresponding wild-type (wt) helper viruses.
35 co-infections involving AAV2 and one or more helper viruses.
36 usually lack substantial homology with their helper viruses.
37 f species with several different families of helper viruses.
38 ether with functions supplied by coinfecting helper viruses.
39 ar proteins as well as functions supplied by helper viruses.
40 nclude (1) contamination of rAAV with the Ad helper virus, (2) low yields of rAAV and (3) production
41 g either the "non-neurovirulent" amphotropic helper virus, 4070A, or pgag-polgpt (a nonpackaged vecto
42      We demonstrated that DNA methylation of helper virus 5' long terminal repeat occurred in approxi
43 ned with little or no DNA methylation of the helper virus 5' LTR.
44 A of subtype H3 (A/Udorn/72) in a subtype H1 helper virus (A/WSN/33) background.
45 satellite RNAs generally reduce the level of helper virus accumulation and attenuate the disease symp
46                            In the absence of helper virus, all four Rep proteins have been shown to r
47                                 The chimeric helper virus allows the establishment of a mixed populat
48 defective (BM5def) and replication-competent helper viruses among which BM5def is the primary causati
49 sgenic mice through the use of Cre-dependent helper virus and a modified rabies virus.
50  contains Moloney murine leukemia virus as a helper virus and a picornavirus internal ribosome entry
51              Vector supernatants are free of helper virus and are of sufficiently high titer within 2
52 form into HSV-1 capsids in the presence of a helper virus and helper cell line.
53 gene (dvB7Ig) were generated using G207 as a helper virus and tested in the poorly immunogenic murine
54 llite RNAs can have a dramatic effect on the helper virus and the host plant in a manner specific to
55 e possible unwanted interactions between the helper virus and the packaged replicon.
56        To understand the mechanism involved, helper virus and vectors were examined for DNA methylati
57                  Since its introduction, new helper viruses and reagents that facilitate complementat
58  of the relationships between subviral RNAs, helper viruses, and hosts.
59 s of recombination with and contamination by helper virus are eliminated.
60                   Mo-MuLVDelta28 served as a helper virus as efficiently as the wt virus; in contrast
61                 In this study, we employed a helper virus-based reverse genetics system to identify N
62            Furthermore, we developed a novel helper virus-based system for the rescue of FV3 from pur
63  be replicated, transcribed, and packaged by helper virus, both rinderpest virus and the related meas
64 s were partially purified from the wild-type helper virus by CsCl equilibrium density-gradient centri
65                 Mutualism between satRNA and helper virus can be seen for the satRNA of Groundnut ros
66 cted BHK cells with VSV DIPs and recombinant helper virus carrying a gene encoding a red fluorescent
67                            In the absence of helper virus coinfection AAV can integrate its genome si
68  in the liver, and possibly does not require helper virus coinfection.
69 e (ORF2) of both the defective and ecotropic helper virus components of LP-BM5.
70 her's RNA was investigated by cotransfecting helper virus constructs with vectors derived from both v
71 to that observed following transduction with helper virus-containing HSV (HC HSVlac) and helper virus
72 ported short-term, inducible expression from helper virus-containing HSV-1 vector systems.
73             Defective interfering (DI) RNAs, helper virus-dependent deletion mutant RNAs derived from
74  vector system is based on nonpathogenic and helper-virus-dependent parvoviruses.
75 tein v-Rel is a chimeric protein that has 11 helper virus-derived Envelope (Env) amino acids (aa) at
76 own that three mutant residues in the eleven helper virus-derived Envelope (Env) amino acids (aa) at
77 al vector in the presence of a nonpathogenic helper virus developed long-latency erythroblastosis, an
78 ethylation inhibitor, partially reversed the helper virus DNA methylation and restored a portion of v
79 AAV2 replication requires coinfection with a helper virus (e.g., adenovirus or herpesvirus) or treatm
80 rus type 2 (AAV) requires coinfection with a helper virus, e.g., adenovirus or herpesviruses.
81  the nucleus and requires coinfection with a helper virus, either adenovirus (Ad) or herpesvirus, for
82 AAV) replication requires coinfection with a helper virus, either adenovirus or herpesvirus.
83 esidues to the residues present in the Rev-A helper virus Env protein abolish this transactivation ab
84 three aa substitutions compared to the Rev-A helper virus Env.
85 es it difficult to distinguish them from the helper virus, especially using high-throughput RNA seque
86 NAs usurp the replication machinery of their helper viruses, even though they bear little or no seque
87            These dRNAs were not supported by helper viruses expressing both replicase-associated prot
88 ed with nonpathogenic Friend murine leukemia helper virus (F-MuLV), which replicates poorly in adult
89         Capsid proteins provided in trans by helper virus failed to rescue the nonreplicating delta P
90 pidly convert to the wild-type leader of the helper virus following DI RNA transfection into helper v
91 rus that requires adenovirus (Ad) or another helper virus for a fully permissive infection.
92 d by the presence of adenovirus, the primary helper virus for a productive AAV infection.
93 nique characteristics of a dependence upon a helper virus for a productive infection and the ability
94             The identification of HBoV1 as a helper virus for AAV2 replication has implications for t
95        Here, we report that HBoV1 is a novel helper virus for AAV2 replication.
96  Adeno-associated viruses (AAVs) depend on a helper virus for efficient replication.
97 packaging Ad7 DNA, it may be a more suitable helper virus for the growth of Ad7 gutted vectors for ge
98 nd long-distance MPs and by not relying on a helper virus for trans-encapsidation and plant-to-plant
99 s could facilitate the creation of efficient helper viruses for influenza virus reverse genetics expe
100 us which usually requires the presence of a "helper" virus for strong DNA replication.
101 productive phase requires coinfection with a helper virus, for instance adenovirus, while the latent
102  constructed, and murine immune responses to helper virus-free amplicon preparations derived from thi
103                         Gene transfer used a helper virus-free Herpes Simplex Virus (HSV-1) vector sy
104                                              Helper virus-free Herpes Simplex Virus (HSV-1) vectors h
105                    Long-term expression from helper virus-free Herpes Simplex Virus (HSV-1) vectors i
106 g-term expression in forebrain neurons, from helper virus-free Herpes Simplex Virus (HSV-1) vectors.
107                                              Helper virus-free Herpes Simplex Virus vector-mediated g
108                             We microinjected helper virus-free herpes simplex virus vectors that expr
109 t transduction of mesencephalic cells with a helper virus-free HSV amplicon (HF HSV-TH9lac) that harb
110 therapy of hematologic malignancies and that helper virus-free HSV amplicon preparations are better s
111  helper virus-containing HSV (HC HSVlac) and helper virus-free HSV amplicons (HF HSVlac) expressing l
112  obtain long-term, inducible expression from helper virus-free HSV-1 vectors.
113 r virus (HSVlac, HSVB7.1, and HSVCD40L) or a helper virus-free method (hf-HSVlac, hf-HSVB7.1, and hf-
114                                 To develop a helper virus-free packaging system for these vectors, th
115                       Thus, highly purified, helper virus-free rAAV vectors can achieve high-frequenc
116                                              Helper virus-free vector stocks were delivered into post
117                                        Using helper virus-free vector stocks, we showed that this vec
118  cloned into HSV amplicons and packaged into helper virus-free vectors.
119 ansduced ex vivo with replication-defective, helper virus-free, herpes simplex virus type 1 (HSV-1) a
120 s demonstrated the feasibility of generating helper-virus-free inducible AAV producer cell lines.
121    To test this hypothesis, we established a helper-virus-free minigenome (MG) system where intracell
122  suggest that in pneumovirus-infected cells, helper virus functions can discriminate between genomes
123 V (rAAV) vectors and may even substitute for helper virus functions.
124 titer production was tightly associated with helper virus gene expression and varied between 0 and 2.
125 ted in trans with the helper virus sequence, helper virus gene expression could be inactivated by hos
126 ot analysis demonstrated that suppression of helper virus gene expression decreased Env-receptor inte
127  and correlated closely with inactivation of helper virus gene expression.
128  the DI RNA rapidly conformed to that in the helper virus genome through a previously described templ
129 he brain, but several problems caused by the helper virus have compromised their utility.
130 to liver cirrhosis upon coinfection with its helper virus, HBV.
131 eracts with envelope proteins of the natural helper virus, hepatitis B virus.
132  the interaction between AAV2 and one of its helper viruses, herpes simplex virus 1 (HSV-1).
133 L) and were packaged using either a standard helper virus (HSVlac, HSVB7.1, and HSVCD40L) or a helper
134 ly modified an adenovirus (Ad) to generate a helper virus (HV) that was detargeted for native adenovi
135 perative interaction between STMV CP and the helper virus (HV) Tobacco mosaic virus (TMV) replicase.
136  Virus is dependent on replicase proteins of helper virus (HV).
137  thought to be completely dependent on their helper virus (HV).
138 RNAs), parasites of viruses, depend on their helper viruses (HVs) for replication, encapsidation, and
139 issive DNA replication in the absence of the helper virus in cells that have been treated with genoto
140          The assay indicated the presence of helper virus in medium exposed to hematopoietic cells fr
141 ermitted selection for intact and functional helper virus in transfected cells without subcloning.
142  in the long terminal repeat (LTR) region of helper virus in vector producer cells (VPC) in up to 2%
143        This explains the lack of discernable helper viruses in many ULV-infected plants and evokes co
144 ed stable ts phenotypes, they were tested as helper viruses in reverse genetics experiments.
145 rvovirus that replicates efficiently without helper viruses in Walter Reed/3873D (WRD) canine cells.
146 he successful development of efficient CCHFV helper virus-independent S, M, and L segment minigenome
147 dues were replicated after transfection into helper virus-infected cells.
148 per virus following DI RNA transfection into helper virus-infected cells.
149 ng constructs were tested for replication in helper virus-infected cells.
150                   However, in the absence of helper virus infection, AAV2 establishes latency by inte
151 his efficient system, which does not require helper virus infection, should be useful in viral mutage
152  lines that require neither transfection nor helper virus infection.
153 on the state of the cell (Rep expression and helper virus influences), the p5IEE operates as a transc
154 n which free leader supplied in trans by the helper virus interacts by way of its flanking 5'UCUAAAC3
155                               Thus, although helper virus is not required for maximal transduction, i
156                                   Because no helper virus is required to propagate these vectors, the
157 regulation by Rep, it undergoes induction by helper virus, it is a target substrate for Rep-mediated
158 ransgene in trans during superinfection by a helper virus, leading to "mobilization" of the vector ge
159  New models for DI RNA-mediated reduction in helper virus levels and symptom attenuation include DI R
160                          In the absence of a helper virus, little expression of the AAV Rep proteins
161            D satellite RNA (satRNA) with its helper virus, namely, cucumber mosaic virus, causes syst
162  or intensify disease symptoms caused by the helper virus, only recently have clues concerning the me
163 ession, we constructed a chimeric retroviral helper virus, pAM3-IRES-Zeo, that contains Moloney murin
164 e panicum mosaic virus (SPMV) depends on its helper virus, panicum mosaic virus (PMV), to provide tra
165 l packaging cell lines were established by a helper virus plasmid cotransfected with a separate plasm
166  between the capsid proteins of SPMV and its helper virus (PMV).
167 eby providing an explanation for the lack of helper viruses present in many ULV-infected plants.
168 by AAV2 may be responsible for inhibition of helper virus replication.
169      When infectious HRSV or APV was used as helper virus, replication could occur only if both the l
170                            Here we determine helper virus requirements and the effects of mutations a
171 limit its own replication by diminishing the helper virus reservoir.
172  at the nonpermissive temperature for the ts helper virus resulted in replication and transcription o
173 bear little or no sequence similarity to the helper virus RNA.
174  of both DI RNAs but not in synthesis of the helper virus RNAs.
175                                    Thus, the helper virus's polymerase is the sole determinant of the
176 selection marker coexisted in trans with the helper virus sequence, helper virus gene expression coul
177 combination of retroviruses with genomic and helper virus sequences and that these novel viruses then
178            The preference for methylation of helper virus sequences over vector sequences may have im
179  a human parvovirus that normally requires a helper virus such as adenovirus (Ad) for replication.
180  only a host cell for replication but also a helper virus such as an adenovirus or a herpesvirus.
181 2) depends on the simultaneous presence of a helper virus such as herpes simplex virus 1 (HSV-1) for
182 ether with functions supplied by coinfecting helper viruses such as adenovirus (Ad).
183 actors, which can be provided by coinfecting helper viruses such as adenoviruses and herpesviruses.
184 lication machinery as well as coinfection by helper viruses such as adenoviruses or herpesviruses, or
185 on mechanism and requires coinfection with a helper virus, such as adenovirus, to achieve a productiv
186 nhibited by MRN and dependent on coinfecting helper virus, such as adenovirus, to remove this factor.
187   AAV replication requires co-infection of a helper virus, such as adenovirus.
188 licate in cells that have been infected with helper viruses, such as adenovirus or herpesvirus.
189 ration vectors or by using the Cre/lox-based helper virus system.
190 ttenuate the disease symptoms induced by the helper virus that they depend upon for replication and p
191 aic virus (TMV) were examined in planta with helper viruses that expressed one (183 kDa) or both (126
192                                 We generated helper viruses that target gene expression to Cre-expres
193             Upon subsequent infection with a helper virus, the AAV genome is released from chromosome
194 multaneously or subsequently infected with a helper virus, the AAV genome is released from the plasmi
195                         In coinfections with helper virus, the diversion of viral proteins to the rep
196                            In the absence of helper virus, the vectors efficiently infected rat neura
197 P) subunit, relying on the polymerase of its helper virus TNV for replication.
198 uppressors, would require association with a helper virus to complete an infection cycle.
199  We passaged a satellite RNA of CMV with its helper virus to determine whether a satellite RNA that a
200 oductive infection but relies on coinfecting helper virus to do so.
201 ated virus (AAV), which require a coinfected helper virus to inactivate the local host DDR.
202                                  Designing a helper virus to overcome cellular DNA methylation may th
203  for ASFV using a CRISPR-Cas9-inhibited self-helper virus to reconstitute live recombinant ASFV from
204 atives of the parental genome that require a helper virus to replicate.
205  we used a sensitive marker rescue assay for helper virus to screen vector-transduced cells prior to
206       Adeno-associated viruses (AAV) rely on helper viruses to transition from latency to lytic infec
207 an adenovirus that is usually required as a 'helper virus' to support AAV2 replication) and disease s
208 of an RNA- temperature-sensitive (ts) mutant helper virus, two coronavirus mouse hepatitis virus (MHV
209                                    The HIV-2 helper virus was unable to package the HIV-1 vector RNA,
210 mbination of rabies virus and retrograde AAV helper virus, we mapped the impact of NMU across three d
211 mbination of rabies virus and retrograde AAV helper virus, we mapped the impact of NMU across three d
212 mpts to plaque it as a virus with a standard helper virus were unsuccessful.
213                                   All of the helper viruses were in a single interference group.
214 tivate production of an apparently identical helper virus, which we have named M. dunni endogenous vi
215 the system in two ways: We constructed a new helper virus with a modified packaging signal and enhanc
216                                        Using helper viruses with cell type specific promoters to targ

 
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