ライフサイエンスコーパス: viral production

1 hat specifically recognizes m(5)C, regulates viral production.

2 te energetic and biosynthetic bottlenecks to viral production.

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

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

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

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

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

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

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

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

11 ductions in the levels of ZIKV infection and viral production.

12 directly to suppress SG assembly and promote viral production.

13 athic effects of CD8(+) T cells occur before viral production.

14 y, while its insertion into HIV-1 suppresses viral production.

15 direct, non-cytolytic effect by suppressing viral production.

16 tion frequency and 1 that directly inhibited viral production.

17 of cross-species components interferes with viral production.

18 ing global KSHV lytic mRNA transcription and viral production.

19 , but approximately the same total amount of viral production.

20 on triggers the toxSAS activity to shut down viral production.

21 thelial gene expression in order to optimize viral production.

22 dify the codons for mouse gene targeting and viral production.

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

24 of other ND10 components, leading to delayed viral production.

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

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

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

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

29 ay and extreme heterogeneity of duration and viral production.

30 omplex results in a significant reduction in viral production.

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

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

33 of target cells available for infection and viral production.

34 pecific ERK inhibitor, significantly reduced viral production.

35 maintained BKPyV-mediated S phase to enhance viral production.

36 and protein expression and severely impaired viral production.

37 modest, approximately threefold, decrease in viral production.

38 xploiting the dynamics of CAR expression and viral production.

39 s prevents DNA damage and leads to increased viral production.

40 ecreased HIV-1 infectivity without affecting viral production.

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

42 se against cellular mechanisms that decrease viral production.

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

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

45 e susceptible to CHIKV infection, exhibiting viral production and bioluminescence activity.

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

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

48 ts a temperature-dependent threshold between viral production and degradation.

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

50 the lungs of COVID-19 patients and enhances viral production and hyperinflammatory responses.

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

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

53 We measured viral production and infectivity using conventional tran

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

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

56 s, respectively), capable to sustain ongoing viral production and initial liver damage.

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

58 zation of oAd into hMSC, leading to superior viral production and release from hMSCs, along with high

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

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

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

62 a long-term culture system also suitable for viral production and the study of HBV transcription.

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

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

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

66 infection, establish essential pathways for viral production, and recommend targeted mechanisms to b

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

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

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

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

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

72 we show that the engagement of PD-1 inhibits viral production at the transcriptional level and abroga

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

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

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

76 A treatment able to reduce viral production by 90% upon hospital admission would sh

77 evere host and viral DNA damage that impairs viral production by an unknown mechanism.

78 Enhanced viral production by dendritic cells and macrophages in i

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

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

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

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

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

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

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

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

87 d deep mixing alter community physiology and viral production, effectively shaping accumulation rates

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

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

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

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

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

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

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

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

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

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

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

99 interact with other vPIC factors and restore viral production in cells harboring the ORF34-deficient

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

101 isk of infection more than drugs that reduce viral production in infected cells.

102 iral infection is achieved by drugs reducing viral production in infected cells.

103 Increasing HIV transcription and viral production in latently infected cells could facili

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

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

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

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

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

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

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

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

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

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

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

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

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

117 ver, the OrNV-Palau1 isolate exhibited lower viral production levels and longer larval survival times

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

119 ntegrants can maintain the capacity for full viral production, making it sometimes difficult to disce

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

121 ckage ultra-efficiently while downregulating viral production moderately.

122 including CD8(+) cell-mediated reduction of viral production (non-cytolytic) were found to best expl

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

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

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

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

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

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

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

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

131 .993 +/- 0.008, indicating that only 0.7% of viral production persisted during therapy.

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

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

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

135 After the eclipse phase, the viral production rate increased over time, starting with

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

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

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

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

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

141 eplication-competent HIV-1, which reactivate viral production upon autocrine/paracrine S100A8-mediate

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

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

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

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

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

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

148 Light was required for EhV adsorption, and viral production was highest when host cultures were mai

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

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

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

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

153 Viral production was suppressed with an efficacy of 0.99

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

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

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

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

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

159 1, PEX7, ABCD3, PEX3, and PEX5L, during peak viral production, which was accompanied by reduced expre

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

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

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