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1 thin CNS microglia without the appearance of replication competent virus.
2 rvoir of latently-infected cells that harbor replication competent virus.
3 ded clones of infected CD4+ T cells carrying replication-competent virus.
4 the probability of unintended generation of replication-competent virus.
5 These stocks were free of detectable replication-competent virus.
6 lines with regard to the possible release of replication-competent virus.
7 owth assays in humanized mice did not reveal replication-competent virus.
8 en nsp13-14 and nsp14-15 allowed recovery of replication-competent virus.
9 indicate that these generally do not reflect replication-competent virus.
10 y of latently infected rCD4 cells containing replication-competent virus.
11 uring serial passaging to generate a single, replication-competent virus.
12 izing antibody sensitivity in the context of replication-competent virus.
13 on and viral entry into target cells without replication-competent virus.
14 ble HIV DNA levels, and difficult to isolate replication-competent virus.
15 lenged intravenously with very high doses of replication-competent virus.
16 Gag-Pol to Gag ratio in cells infected with replication-competent virus.
17 omologous to MMTV and revealed features of a replication-competent virus.
18 on, we introduced the PPTSUB mutation into a replication-competent virus.
19 tical model of a tumor that is infected by a replication-competent virus.
20 due to release of an insufficient amount of replication-competent virus.
21 nes that can contribute to the production of replication-competent virus.
22 tool to enhance the antitumor activity of a replication-competent virus.
23 h a retrovirus vector preparation containing replication-competent viruses.
24 in agreement with cell culture studies with replication-competent viruses.
25 typed vesicular stomatitis virus vectors and replication-competent viruses.
26 te engagement of this response is limited to replication-competent viruses.
27 artment was analyzed with assays that detect replication-competent viruses.
28 dditional compensatory mutations to generate replication-competent viruses.
31 mes of temperature, followed by expansion of replication-competent viruses, allowed selection of a te
32 CD4(+) T cells had a median of fourfold more replication-competent virus and a median of sixfold more
34 mor cells are being selectively lysed by the replication-competent virus and the enhanced effect of e
35 mutations, of regions B and C produced a DNA replication-competent virus and typically conferred resi
37 s because of their ability to interfere with replication-competent viruses and induce antiviral immun
38 tive effects through their interference with replication-competent viruses and induction of antiviral
39 n of the interferon pathway does not require replication-competent virus, and envelope glycoprotein B
40 Infection required corneal scarification and replication-competent virus, and the severity of ocular
41 us, inactivated rotavirus, noninfectious but replication-competent virus, and virus-like particles, w
42 s was seen with other CCR5 antagonists, with replication-competent viruses, and did not obviously cor
44 probability of reactivation, suggesting that replication-competent viruses are less likely to be foun
45 but reducing the generation of contaminating replication-competent virus below the limit of detection
46 ion of peripheral blood mononuclear cells by replication-competent virus but did not bind to cardioli
47 se and found that despite the elimination of replication-competent virus by day 10, we were able to r
48 ed to minimize the possibility of generating replication-competent virus by recombination or nucleoti
50 full-length HIV proviruses and to construct replication-competent viruses by adding a patient-specif
51 uted in various tissues including the brain; replication-competent virus can be rescued ex vivo from
52 below detectable levels for up to 30 months, replication-competent virus can routinely be recovered f
53 ighly active antiretroviral therapy (HAART), replication-competent virus can still be isolated from p
55 f the latent reservoir capable of generating replication competent virus cannot be induced in the lab
56 of E1-/E4- vectors and 293-ORF6 cell lines, replication-competent virus cannot be generated by homol
57 nical dye system in situ, we characterized a replication-competent virus capable of being tracked pre
58 at reflect the full phylogenetic spectrum of replication-competent virus circulating in donor plasma.
59 nts of cell-associated SIV DNA, SIV RNA, and replication-competent virus comparable to those in PB.
60 e-based, single-round infection assays using replication-competent virus confirmed the relative sensi
62 y of viruses with insertions in the M gene a replication-competent virus containing a fluorescent M a
66 ermine, partly because there is no efficient replication-competent virus expressing an easily traceab
69 T-cell activation, it is possible to isolate replication-competent virus from resting CD4(+) T lympho
70 tected in primate fecal samples, recovery of replication-competent virus from such samples has not be
72 anning mutagenesis was used to isolate fully replication-competent viruses harbouring a potent foreig
78 n CD4(+) T cell numbers, then elimination of replication-competent virus in 58% of infected mice.
79 proviral HIV before transplantation, but no replication-competent virus in blood or intestinal tissu
80 1 remission for 30 months with no detectable replication-competent virus in blood, CSF, intestinal ti
84 estimated that the half-life of the latent, replication-competent virus in resting CD4 lymphocytes w
86 quencies of resting CD4(+) T cells harboring replication-competent virus in the pooled head lymph nod
87 ssible, several models use primary cells and replication-competent viruses in combination with antire
88 and, as might be expected, the sequences of replication-competent viruses in the active reservoir sh
89 ts potential to serve as a lasting source of replication-competent viruses, including the infecting w
90 RNA+ reservoir, which is highly enriched in replication-competent virus, increases in women after me
93 assay used to measure reservoirs containing replication-competent virus is the quantitative viral ou
94 tently infected cells harbouring integrated, replication-competent virus (known as the virus reservoi
95 ey finding is that the independently derived replication-competent viruses lacked the virion host shu
97 ng minigenome systems and transcription- and replication-competent virus-like particle (trVLP) system
98 es/10(6) CD4(+) T-cells) without evidence of replication-competent viruses (<0.025 IUPM), consistent
100 ents of both total and integrated HIV-1 DNA, replication-competent virus measurement by large cell in
101 ells in peripheral lymphoid tissues, neither replication-competent virus nor integrated SIV DNA was d
103 he Delta variant, the infectivity (amount of replication competent virus per viral genome copy) may b
104 voirs of infected cells capable of producing replication-competent virus persist even after years of
105 integrated latent HIV-1 genomes that encode replication-competent virus persist in resting CD4(+) T
108 The provirus displays typical features of a replication competent virus, plus the open reading frame
109 nce of transmissible retroviral elements and replication-competent viruses possessing altered tropic
111 HIV-1 RNA and DNA in human cells, as well as replication-competent-virus-producing cells, were measur
113 Sequencing of independent clonal isolates of replication-competent virus revealed that 57% had env se
114 to attenuate or restrict cellular tropism of replication-competent viruses, such as oncolytic adenovi
116 infection of PCLs, again without generating replication-competent virus, suggesting utility for prod
117 ity was seen with i.v. administration of the replication-competent viruses than with Ad.TK and in imm
118 ears are transcriptionally silent but harbor replication-competent virus that can be induced upon TLR
119 replication incompetence, and elimination of replication-competent virus that can be produced during
120 argely transcriptionally silent, but contain replication-competent virus that drives resurgence of th
121 truction of one of these (94UG114.1) yielded replication-competent virus that grew to high titers in
122 lasts expressing the RCAS constructs release replication-competent viruses that are able to elicit th
123 uses, such as Delta-24-RGD (Delta24RGD), are replication-competent viruses that are genetically engin
124 Oncolytic viruses are genetically altered replication-competent viruses that infect, and reproduce
125 great deal of progress in the development of replication-competent viruses that kill cancer cells (on
128 e proviruses are unable to encode intact and replication-competent viruses, they have long been thoug
129 s safety concerns, such as the generation of replication-competent viruses through recombination with
131 ast some elite controllers are infected with replication-competent virus, thus they may serve as a mo
132 ONYX-015 is the first genetically engineered replication-competent virus to demonstrate selective int
134 ic for the treatment of cancer that exploits replication-competent viruses to selectively infect and
136 ay provide an accessible marker of inducible replication-competent virus, total numbers of infected c
138 ion CD4(+) T cells) in these 4 children, but replication competent virus was detected by quantitative
145 ng titers as high as 7 x 10(3) CFU/ml, while replication-competent virus was not detectable at any ti
150 circulating resting CD4(+) T cells harboring replication-competent virus was reduced to a low steady-
151 ls at 7 weeks after ART interruption, and no replication-competent virus was rescued from the tissue
152 ully treated with HAART for up to 30 months, replication-competent virus was routinely recovered from
154 ents the first gene therapy trial in which a replication-competent virus was used to deliver a therap
155 ystem (CNS), with the potential to emerge as replication-competent virus, we tracked the longitudinal
156 ese mutations were isolated by selection for replication-competent viruses, we conclude that retrovir
157 ecotropic retroviral producer cells free of replication competent virus were generated and used to t
158 onses, and the persistence of cells carrying replication-competent virus were quantified during long-
159 ttempts to delete the G5R gene and isolate a replication-competent virus were unsuccessful, suggestin
162 ection but has the increased safety of a non-replication-competent virus, which makes this approach a
163 elucidate which anatomic compartments harbor replication-competent virus, which upon ART interruption
164 ssing viral genes for their replication, the replication competent viruses will replicate on approved
165 ve viruses, and (iii) genetically engineered replication competent viruses with restricted host range
166 the first example of a naturally occurring, replication-competent virus with sequences closely relat
167 suggest that approximately 30 to 40% of the replication-competent viruses with 7- to 10-kb genomes u
168 nd packaging vectors, which may give rise to replication-competent viruses with pathogenic potential.
169 rom both the cell-associated HIV RNA and the replication-competent virus within the detectable pool o
170 netic elements involved in the generation of replication-competent virus without impairing vector pro