ライフサイエンスコーパス: defective virus

1 ique host factors rather than infection with defective virus.

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

3 d immunization with the parental replication-defective virus.

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

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

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

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

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

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

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

11 alization in cells infected with replication-defective viruses.

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

13 As defective viruses account for the majority of integrated

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

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

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

17 challenge than immunization with replication-defective virus alone.

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

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

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

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

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

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

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

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

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

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

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

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

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

31 Replication-defective viruses containing subtle mutations in the hel

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 Defective viruses often have pivotal roles in virus-indu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

84 Defective viruses were typed as class I mutants (specifi

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

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