ライフサイエンスコーパス: defective virus

1 segment of viral DNA, leading to replication-defective virus.

2 ique host factors rather than infection with defective virus.

3 d immunization with the parental replication-defective virus.

4 CMs infected (vaccinated) with a replication-defective virus.

5 osis that rescue cells infected with the p35 defective virus.

6 als previously vaccinated with a replication-defective virus.

7 ary human macrophages infected with cleavage defective viruses.

8 ral DNA, most of which is known to represent defective viruses.

9 ontrolled by the wild-type virus than by the defective viruses.

10 r proteins, exogenous agents, or replication-defective viruses.

11 enged with wild-type, Nef-defective, and Vpr-defective viruses.

12 pressed in mammalian cells with HSV amplicon-defective viruses.

13 tive-site residues resulted in amplification-defective viruses.

14 alization in cells infected with replication-defective viruses.

15 n, the influenza virus generates genetically defective viruses.

16 Most defective viruses (15 of 17) displayed reverse transcrip

17 As defective viruses account for the majority of integrated

18 These defective viruses achieved high titers in a cell line co

19 body induced by vaccination with replication-defective virus aids in reducing establishment of latent

20 a-producing CD4 T cells than did replication-defective virus alone.

21 challenge than immunization with replication-defective virus alone.

22 immunization with B7-expressing, replication-defective virus also effectively suppressed infection of

23 In addition, exonuclease-defective viruses also induced different spectra of supF

24 se of intravitreal injections of replication-defective viruses and molecular probes allows the geneti

25 (i) helper free amplicons, (ii) replication defective viruses, and (iii) genetically engineered repl

26 In the current study, controlled levels of defective viruses are coinfected with viable viruses tha

27 Some versions of these defective viruses are thought to have protective effects

28 In order to develop a replication-defective virus as a vaccine candidate, we constructed R

29 to decreased viral genome replication (CR3), defective virus assembly (MNV-1), or altered cellular eg

30 This highlights one way in which nef-defective virus-bearing immature DCs that mature while m

31 Coinfections of viable and defective viruses behave in unpredictable ways, but they

32 rine leukemia viruses including an etiologic defective virus (BM5def) causes an immunodeficiency synd

33 Mice infected with the replication-defective virus (BM5def) in the LP-BM5 murine leukemia v

34 terminally differentiated macrophages by vpr-defective virus but not wild-type virus.

35 demonstrated that some ES are infected with defective viruses, but it remains unclear whether others

36 y has strong biological consequences because defective viruses can carry genetic diversity that can b

37 ious integrase-LexA proteins to an integrase-defective virus containing an integrase mutation at aspa

38 Replication-defective viruses containing subtle mutations in the hel

39 All reassortant-defective viruses could be amplified and propagated to h

40 to growing and producing a vaccine from two defective viruses could be generally applicable to vacci

41 Most interestingly, we found that these two defective viruses could be grown together and passaged i

42 ZIKV in the absence of DOX (as a replication-defective virus) developed robust levels of E-peptide-sp

43 Superinfection by an exogenous Vif-defective virus did not rescue packaging of endogenous V

44 d both in vitro and in vivo with replication-defective virus (DL312) and no treatment as controls.

45 h replication-defective HSV-2 or replication-defective virus encoding B7-2 and compared their capacit

46 Replication-defective virus encoding B7-2 induced more IFN-gamma-pro

47 Additionally, an RNA packaging-defective virus exhibited significantly reduced packagin

48 was unable to rescue the infectivity of vif-defective viruses generated from H9 T-cells, suggesting

49 is the addition of its natural or engineered defective virus genomes (DVGs) (have no pathogenicity) t

50 on of parainfluenza virus 5 (PIV5), copyback defective virus genomes (DVGs) are erroneously produced

51 for their amplification.IMPORTANCE Copyback defective virus genomes (DVGs) are powerful inducers of

52 Early-passage LCLs derived from the lytic-defective viruses had substantially decreased expression

53 fied from mice infected with the replication-defective virus harbored viral genome at a frequency tha

54 Thus, these defective viruses have the potential to be used for the

55 t appear in numerous viral isolates yields a defective virus; however, simultaneous introduction of b

56 Passive transfer of replication-defective virus-immune serum at physiologic concentratio

57 SIVnef+ replicates more rapidly than nef-defective viruses in both human and rhesus peripheral bl

58 To investigate the role of defective viruses in KSHV-induced pathogenesis, we isola

59 These results point to a potential role for defective viruses in the regulation of KSHV infection an

60 Furthermore, vhs-defective viruses induce increased and physiologically a

61 guishable between wild-type and reactivation-defective virus infection, indicating that, in contrast

62 ivo, we inoculated wild-type and replication-defective viruses into the posterior chamber of mouse ey

63 f an RT-expressing cell with a high titer RT-defective virus, intracellular reverse transcription can

64 lable against hepatitis delta virus (HDV), a defective virus leading to the most severe form of chron

65 Instead, viruses are often accompanied by defective virus-like particles that carry large deletion

66 and spread in the host, however, replication-defective virus may have relatively limited capacity to

67 e studies have suggested that infection with defective viruses may be the cause of the lack of high l

68 bility that genetically tailored replication-defective viruses may make effective and safe therapeuti

69 yocardium may be related to the selection of defective virus mutants.

70 We also observed that in cells producing Vpu-defective virus, NF-kappaB activity was significantly in

71 Adeno-associated virus (AAV) is a defective virus of the parvovirus family that has a numb

72 Defective viruses often have pivotal roles in virus-indu

73 does not discriminate between infectious and defective viruses, or by viral outgrowth assays, which r

74 We have previously shown that replication-defective virus particles are able to induce a strong IF

75 terfere with the viraemia, but the generated defective virus particles are not adequate to reduce hig

76 translation termination factor eRF1 produces defective virus particles containing 20 times more gRNA.

77 responses were markedly reduced if envelope-defective virus particles or reverse transcriptase inhib

78 e interference and spontaneous generation of defective virus particles, but have not examined both th

79 h two fewer amino acids produced replication-defective virus particles, despite containing apparently

80 of the mutant, most likely corresponding to defective virus particles.

81 to heterodimerization in both wild-type and defective virus particles.

82 be a possible alternative explanation for a defective virus phenotype resulting from changes in prot

83 Wild-type HFV Env partially complemented the defective virus phenotype.

84 ng infection with UV-irradiated, replication-defective viruses possessing transcriptionally active in

85 assay vectors based on two distinct movement-defective viruses, Potato virus X and Turnip crinkle vir

86 exhibit greater infectivity than matched nef-defective viruses (R7SIV delta nef).

87 Expression of the defective virus responsible for MAIDS was enhanced in sp

88 he unique Gag polyprotein of the replication-defective virus responsible for murine AIDS (MAIDS) indu

89 In addition to many defective viruses, resting hematopoietic cells harbor tr

90 ation of sink leaves with a movement protein-defective virus showed that virally expressed GFP, but n

91 the nef position of a full-length, integrase-defective virus strain yielded efficient replication in

92 we used a reverse genetics system to rescue defective virus strains with large deletions in an essen

93 t observed after infection with an integrase-defective virus, suggesting that abortive integration is

94 IMPORTANCE The use of defective viruses that interfere with the replication of

95 ivering an antigen and GM-CSF in replication-defective viruses to enhance antigen-specific immunity;

96 ch has implications for studies that use Nef-defective viruses to study ADCC responses.

97 open reading frames (ORFs), suggesting that defective virus transcription does not account for the l

98 We have previously described a replication-defective virus vaccine based on strain AD169 (D.

99 We previously described a replication-defective virus vaccine that has been demonstrated safe

100 ponse reduced the uptake of this replication-defective virus vaccine.

101 this signal may be limiting for replication-defective virus vaccines.

102 l genomes and how replication-competent and -defective virus variants can provide means for adaptatio

103 This mixture of complementing defective viruses was also highly effective at generatin

104 Replication of V- or C-protein-defective viruses was short-lived and reached lower leve

105 gap and overcome limitations of replication-defective viruses, we generated a recombinant murine gam

106 Defective viruses were typed as class I mutants (specifi

107 that following vaccination of a replication-defective virus with the restored pentameric complex, rh

108 phalomyocarditis virus IRES, translationally defective viruses with small-plaque phenotypes were gene