ライフサイエンスコーパス: viral production

1 d a complex effect on cell proliferation and viral production.

2 the HIV-infected cells and caused decreased viral production.

3 and either had no effect or caused increased viral production.

4 ce is expected if IFN-alpha partially blocks viral production.

5 endogenous IL-1 was involved in LPS-mediated viral production.

6 mponent of the Torsin system with respect to viral production.

7 ral entry and thereby blocks early stages of viral production.

8 both at the level of cellular infection and viral production.

9 al response that drives HIV-1 expression and viral production.

10 marked decrease in S phase arrest as well as viral production.

11 ay and extreme heterogeneity of duration and viral production.

12 omplex results in a significant reduction in viral production.

13 glucose uptake in infected cells as well as viral production.

14 hether these interactions may play a role in viral production.

15 of target cells available for infection and viral production.

16 pecific ERK inhibitor, significantly reduced viral production.

17 thelial gene expression in order to optimize viral production.

18 and protein expression and severely impaired viral production.

19 modest, approximately threefold, decrease in viral production.

20 xploiting the dynamics of CAR expression and viral production.

21 n of whether viral or cellular factors limit viral production.

22 se against cellular mechanisms that decrease viral production.

23 bly and leading to the overall inhibition of viral production.

24 n part due to an impaired ability to inhibit viral production.

25 n may be associated with different stages of viral production.

26 ication and ORF 45 is required for efficient viral production.

27 d DN cells, like CD4(+) cells, contribute to viral production and are sensitive to highly active anti

28 nfection, dynamic equilibrium exists between viral production and clearance.

29 and the apparently concomitant high rate of viral production and death are consistent with a large a

30 mer R12-2 (0.5 microg/mL) markedly inhibited viral production and exhibited a dose response of inhibi

31 e during ART by enhancing residual levels of viral production and inducing proliferation of latently

32 The efficiency of viral production and infectivity of generated virus is s

33 We measured viral production and infectivity using conventional tran

34 Inhibiting miR-29a enhanced HIV-1 viral production and infectivity, whereas expressing a m

35 d that disrupting P body structures enhances viral production and infectivity.

36 ritical insights into the dynamic process of viral production and its interplay with the infected hos

37 hibit HIV-1 release, resulting in diminished viral production and replication.

38 ase that is incorporated into virions during viral production and subsequently triggers massive deami

39 required for Tax transactivation and HTLV-1 viral production and that the PBAF complex appears to be

40 , which reflect fluctuations in the rates of viral production and/or clearance that may be caused by

41 y system at the stages of surface targeting, viral production, and gene expression.

42 terogeneity in shedding episode duration and viral production, and predicted rapid early viral expans

43 in host systemic and CNS monocyte/macrophage viral production are associated with the development of

44 t that inherent differences in host monocyte viral production are related to development of encephali

45 g down DDX5 reduced HIV RNA and consequently viral production as measured by CA-p24 (capsid p24) and

46 d to determine the efficacy of inhibition of viral production, as well as kinetic constants for the c

47 ected subjects is lacking, and viral load or viral production assays invariably focus on CD4(+) T cel

48 hagosome accumulation increase extracellular viral production but do not affect viral protein synthes

49 ional signals have the capacity to influence viral production, but the magnitude of these effects wil

50 HIV clone, at the same weight ratio, reduced viral production by 88%.

51 Enhanced viral production by dendritic cells and macrophages in i

52 BMCs from HIV-infected individuals inhibited viral production by greater than 90% without affecting l

53 ivation expedites viral proliferation due to viral production by nTreg itself and not to reduced Natu

54 mechanisms by which RA cells were reduced in viral production capacity, RA and RO cells were exposed

55 If all the parameters, such as the rate of viral production, cell life-span and the neutralizing ca

56 Both ATP and viral production could be rescued in glutamine-starved c

57 at least two cell compartments, one in which viral production decays over time and a second in which

58 host biomass production, leaf N and leaf P, viral production depended most strongly on host biomass,

59 est a role for CD8(+) T cells in controlling viral production during ART, thus providing a rationale

60 tation of oncolytic effect caused by progeny viral production followed by replication.

61 old, but there was only a modest increase in viral production from CEM cells (<14-fold) and a decreas

62 with HIV demonstrated 95-99.5% inhibition of viral production from host cells.

63 ot influence viral dynamics when the rate of viral production from infected cells is independent of t

64 the viral replicase, resulting in decreased viral production from infected ribozyme-expressing cells

65 que class of anti-HIV drugs that may inhibit viral production from stable reservoirs and reduce resid

66 assuming that the effectiveness in blocking viral production gradually increased over time to reach

67 ciate with a PAK kinase, leading to enhanced viral production; however, the exact identity of the kin

68 and Delta133p53alpha acting as regulators of viral production in a p53-dependent manner.

69 uclear import, and integration, and enhances viral production in a spreading-infection assay.

70 at is acceptable worldwide without impacting viral production in cell culture.

71 ation, but it causes a strong attenuation of viral production in culture when deleted.

72 nd metabolic blocks contribute to preventing viral production in latently infected cells.

73 subjects, we demonstrate that IL-7 enhances viral production in productively infected cells but does

74 that multiple independent mechanisms control viral production in the livers of infected individuals.

75 blotting, indicating that the restriction of viral production in these cells is principally due to th

76 es viral assembly, leading to an increase in viral production in transfected or infected cells.

77 ind to heparan sulfate allows more efficient viral production in vivo, which may in turn lead to incr

78 V efficiently replicated in CEM-SS cells and viral production increased by >4,000-fold, but there was

79 f HSV-1 replication centers is retarded, and viral production is compromised.

80 asmids into a mammalian packaging cell line, viral production is conveniently followed with the aid o

81 e cells are infected, a regime expected when viral production is limited by cellular rather than vira

82 reproductive number R0 is 10.7, the rate of viral production is rapid (>25,000 virions d(-1)), and t

83 or ZIKV, the time between cell infection and viral production, is most likely short ( approximately 4

84 behaved similarly to wild-type (wt) BAC36 in viral production, latency gene transcription, and viral

85 This MTB-mediated viral production likely occurs through Ag-specific activ

86 nfection and interleukin-2 (IL-2) induction, viral production measured on day 13 was 19-fold greater

87 ckage ultra-efficiently while downregulating viral production moderately.

88 IL-2 plus IL-4 increased the viral production of all pediatric isolates, but IL-4 and

89 utilizes NV1066-guided cancer cell-specific viral production of GFP to enable real-time intraoperati

90 ion, depleting endogenous tetherin increased viral production of influenza virions, both in cells con

91 We show that viral production of Japanese fulminant hepatitis type 1

92 ression of the eclipse phase and the rate of viral production of the resistant strain, and explore ho

93 th played less of a role in the differential viral production of these strains, as the cell viability

94 Vp2 capsid proteins, does not interfere with viral production or trafficking of intact AAV capsids to

95 Finally, to assess infectious viral production, other primary human cells (human umbil

96 .993 +/- 0.008, indicating that only 0.7% of viral production persisted during therapy.

97 during reactivation changes our view of the viral production process from one that is facilitated an

98 The ranges chosen for beta and the viral production rate (p) resulted in bHCV-RNA levels th

99 nder lamivudine selection pressure, the high viral production rate and the low fidelity viral polymer

100 the optimal progression rate and the optimal viral production rate, which maximize the fitness of a d

101 ction decays over time and a second in which viral production remains stable for at least 7 years.

102 It is a site associated with viral production, storage of viral particles in immune c

103 anti-Fas antibodies markedly inhibited HSV-2 viral production, suggesting that the capacity of the vi

104 e-dependent, final effectiveness in blocking viral production that rapidly dropped upon treatment ces

105 ilence viral replication, and can reactivate viral production upon specific treatments.

106 that BONCAT can be used to directly quantify viral production (via epifluorescence microscopy) with m

107 Viral abundance (VA) and viral production (VP) were monitored in the Chesapeake B

108 induced comparable levels of cytopathicity, viral production was considerably higher in the R5-infec

109 ith proviral DNA distribution, we found that viral production was favored in CD69(+) cells.

110 Replicating Moloney murine leukemia virus viral production was greater in XPB or XPD mutant cells

111 troduced in an infectious clone of HIV-1, no viral production was measured in the absence of TNF-alph

112 ting cells (APC), at least a 10-fold drop in viral production was observed.

113 The differential viral production was partially due to the severe cytopat

114 in the presence of RBV and/or IFN alfa, and viral production was quantified by plaque assay.

115 Viral production was suppressed with an efficacy of 0.99

116 f Jun N-terminal kinase, and the increase of viral production were blocked by an inhibitory peptide t

117 by the R5 strain, and yet similar levels of viral production were detected in both infected cultures

118 strain JR-CSF and yet that higher levels of viral production were detected in the R5-infected cultur

119 were successfully rescued, and the yields of viral production were similar to that of unmodified Ad5.

120 ally restricts the first measurable burst of viral production, which occurs at approximately 32 h.

121 The hope is that the increase in viral production will lead to killing of the infected ce

122 anoprevir significantly blocks intracellular viral production (with mean effectiveness 99.2%), enhanc

123 Integration is mandatory for viral production, yet HIV infection of CD4 T cells in vi