ライフサイエンスコーパス: replication-competent virus

1 rvoir of latently-infected cells that harbor replication competent virus.

2 thin CNS microglia without the appearance of replication competent virus.

3 y of latently infected rCD4 cells containing 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 on and viral entry into target cells without replication-competent virus.

8 ble HIV DNA levels, and difficult to isolate replication-competent virus.

9 lenged intravenously with very high doses of replication-competent virus.

10 Gag-Pol to Gag ratio in cells infected with replication-competent virus.

11 omologous to MMTV and revealed features of a replication-competent virus.

12 on, we introduced the PPTSUB mutation into a replication-competent virus.

13 tical model of a tumor that is infected by a replication-competent virus.

14 nes that can contribute to the production of replication-competent virus.

15 izing antibody sensitivity in the context of replication-competent virus.

16 tool to enhance the antitumor activity of a replication-competent virus.

17 te engagement of this response is limited to replication-competent viruses.

18 artment was analyzed with assays that detect replication-competent viruses.

19 dditional compensatory mutations to generate replication-competent viruses.

20 h a retrovirus vector preparation containing replication-competent viruses.

21 mes of temperature, followed by expansion of replication-competent viruses, allowed selection of a te

22 CD4(+) T cells had a median of fourfold more replication-competent virus and a median of sixfold more

23 mor cells are being selectively lysed by the replication-competent virus and the enhanced effect of e

24 mutations, of regions B and C produced a DNA replication-competent virus and typically conferred resi

25 n of the interferon pathway does not require replication-competent virus, and envelope glycoprotein B

26 Infection required corneal scarification and replication-competent virus, and the severity of ocular

27 us, inactivated rotavirus, noninfectious but replication-competent virus, and virus-like particles, w

28 s was seen with other CCR5 antagonists, with replication-competent viruses, and did not obviously cor

29 Replication-competent viruses are currently being evalua

30 probability of reactivation, suggesting that replication-competent viruses are less likely to be foun

31 but reducing the generation of contaminating replication-competent virus below the limit of detection

32 ion of peripheral blood mononuclear cells by replication-competent virus but did not bind to cardioli

33 se and found that despite the elimination of replication-competent virus by day 10, we were able to r

34 ed to minimize the possibility of generating replication-competent virus by recombination or nucleoti

35 full-length HIV proviruses and to construct replication-competent viruses by adding a patient-specif

36 uted in various tissues including the brain; replication-competent virus can be rescued ex vivo from

37 below detectable levels for up to 30 months, replication-competent virus can routinely be recovered f

38 ighly active antiretroviral therapy (HAART), replication-competent virus can still be isolated from p

39 However, replication-competent virus can still be recovered from

40 of E1-/E4- vectors and 293-ORF6 cell lines, replication-competent virus cannot be generated by homol

41 nical dye system in situ, we characterized a replication-competent virus capable of being tracked pre

42 e-based, single-round infection assays using replication-competent virus confirmed the relative sensi

43 Using a panel of full-length replication-competent virus constructs that reflect natu

44 y of viruses with insertions in the M gene a replication-competent virus containing a fluorescent M a

45 We found that primary infection with a replication-competent virus did not protect against acqu

46 and decreased CD4(+) T cell levels harboring replication-competent virus during ART.

47 ermine, partly because there is no efficient replication-competent virus expressing an easily traceab

48 ive coculture assay in an attempt to isolate replication-competent virus from a cohort of 10 ES.

49 This is the first report of detecting a replication-competent virus from a source animal after x

50 T-cell activation, it is possible to isolate replication-competent virus from resting CD4(+) T lympho

51 tected in primate fecal samples, recovery of replication-competent virus from such samples has not be

52 We also let ducks select replication-competent viruses from a replication-incompe

53 anning mutagenesis was used to isolate fully replication-competent viruses harbouring a potent foreig

54 Also, genetically engineered attenuated replication-competent viruses have been investigated in

55 However, replication-competent viruses have not resulted heretofo

56 rom the risk of formation and propagation of replication competent virus in vivo.

57 By analyzing the replication-competent virus in both cell subsets, we sho

58 Here, we demonstrate the persistence of replication-competent virus in CD4+ T cells in a cohort

59 The percentage of patients with replication-competent virus in peripheral blood mononucl

60 estimated that the half-life of the latent, replication-competent virus in resting CD4 lymphocytes w

61 quencies of resting CD4(+) T cells harboring replication-competent virus in the pooled head lymph nod

62 ssible, several models use primary cells and replication-competent viruses in combination with antire

63 and, as might be expected, the sequences of replication-competent viruses in the active reservoir sh

64 ts potential to serve as a lasting source of replication-competent viruses, including the infecting w

65 table virus in the peripheral plasma harbors replication-competent virus is not known.

66 ey finding is that the independently derived replication-competent viruses lacked the virion host shu

67 By using these replication-competent viruses, latently infected T-cell

68 ng minigenome systems and transcription- and replication-competent virus-like particle (trVLP) system

69 In contrast, replication-competent viruses may be used for cancer the

70 ents of both total and integrated HIV-1 DNA, replication-competent virus measurement by large cell in

71 ells in peripheral lymphoid tissues, neither replication-competent virus nor integrated SIV DNA was d

72 Proviral DNA and replication-competent virus obtained from peripheral-blo

73 voirs of infected cells capable of producing replication-competent virus persist even after years of

74 integrated latent HIV-1 genomes that encode replication-competent virus persist in resting CD4(+) T

75 Phylogenetic analysis of replication-competent viruses persisting in resting CD4(

76 ating viral load in those infected with HIV, replication-competent virus persists.

77 The provirus displays typical features of a replication competent virus, plus the open reading frame

78 nce of transmissible retroviral elements and replication-competent viruses possessing altered tropic

79 Cultures infected with replication-competent virus produced progressively incre

80 HIV-1 RNA and DNA in human cells, as well as replication-competent-virus-producing cells, were measur

81 s indicated by the quantity of HIV-1 DNA and replication-competent-virus-producing cells.

82 Sequencing of independent clonal isolates of replication-competent virus revealed that 57% had env se

83 to attenuate or restrict cellular tropism of replication-competent viruses, such as oncolytic adenovi

84 Replication-competent viruses, such as Vaccinia virus (V

85 infection of PCLs, again without generating replication-competent virus, suggesting utility for prod

86 ity was seen with i.v. administration of the replication-competent viruses than with Ad.TK and in imm

87 replication incompetence, and elimination of replication-competent virus that can be produced during

88 truction of one of these (94UG114.1) yielded replication-competent virus that grew to high titers in

89 lasts expressing the RCAS constructs release replication-competent viruses that are able to elicit th

90 uses, such as Delta-24-RGD (Delta24RGD), are replication-competent viruses that are genetically engin

91 Oncolytic viruses are genetically altered replication-competent viruses that infect, and reproduce

92 great deal of progress in the development of replication-competent viruses that kill cancer cells (on

93 This replication-competent virus, the glioma-adapted vesicula

94 s safety concerns, such as the generation of replication-competent viruses through recombination with

95 ONYX-015 is the first genetically engineered replication-competent virus to demonstrate selective int

96 is an emerging treatment modality that uses replication-competent viruses to destroy cancers.

97 ic for the treatment of cancer that exploits replication-competent viruses to selectively infect and

98 dvances are being made in the engineering of replication-competent viruses to treat cancer.

99 Replication-competent virus vector vaccines might have a

100 ion CD4(+) T cells) in these 4 children, but replication competent virus was detected by quantitative

101 Replication-competent virus was detected in spleen cells

102 The frequency of cells carrying replication-competent virus was less than 1 per 10(6) ci

103 ng titers as high as 7 x 10(3) CFU/ml, while replication-competent virus was not detectable at any ti

104 Replication-competent virus was recovered after activati

105 Replication-competent virus was recovered from all LT yo

106 Replication-competent virus was recovered from pooled re

107 circulating resting CD4(+) T cells harboring replication-competent virus was reduced to a low steady-

108 ls at 7 weeks after ART interruption, and no replication-competent virus was rescued from the tissue

109 ully treated with HAART for up to 30 months, replication-competent virus was routinely recovered from

110 Replication-competent virus was undetectable after treat

111 ents the first gene therapy trial in which a replication-competent virus was used to deliver a therap

112 ystem (CNS), with the potential to emerge as replication-competent virus, we tracked the longitudinal

113 ese mutations were isolated by selection for replication-competent viruses, we conclude that retrovir

114 ecotropic retroviral producer cells free of replication competent virus were generated and used to t

115 onses, and the persistence of cells carrying replication-competent virus were quantified during long-

116 ttempts to delete the G5R gene and isolate a replication-competent virus were unsuccessful, suggestin

117 Replication-competent viruses were evaluated by cell-coc

118 Replication-competent viruses were recovered from periph

119 ection but has the increased safety of a non-replication-competent virus, which makes this approach a

120 ssing viral genes for their replication, the replication competent viruses will replicate on approved

121 ve viruses, and (iii) genetically engineered replication competent viruses with restricted host range

122 the first example of a naturally occurring, replication-competent virus with sequences closely relat

123 suggest that approximately 30 to 40% of the replication-competent viruses with 7- to 10-kb genomes u

124 nd packaging vectors, which may give rise to replication-competent viruses with pathogenic potential.

125 rom both the cell-associated HIV RNA and the replication-competent virus within the detectable pool o

126 netic elements involved in the generation of replication-competent virus without impairing vector pro