ライフサイエンスコーパス: plaque assay

1 below 25 PFU/ml (the detection limit of the plaque assay).

2 alfa, and viral production was quantified by plaque assay.

3 E); infectious virus was quantified by viral plaque assay.

4 l titers in the tear film were determined by plaque assay.

5 uced initial lung viral loads as measured by plaque assay.

6 nd viral replication was ascertained using a plaque assay.

7 enan type IV blocked FHV-1 adsorption in the plaque assay.

8 Virus titers were determined by plaque assay.

9 lation onto confluent cell monolayers in the plaque assay.

10 ription-PCR (RT-PCR) assays or indirectly by plaque assay.

11 ious virions that were readily detectable by plaque assay.

12 l titers in the tear film were determined by plaque assay.

13 sitivities greater than that of the standard plaque assay.

14 drug resistance marker that can be scored by plaque assay.

15 y quantitative reverse transcription-PCR and plaque assay.

16 omide assay, and virus yield was examined by plaque assay.

17 FN2 increased IHNV infection, as measured by plaque assay.

18 infected tissues was determined by standard plaque assay.

19 racterized in-frame insertion mutants in the plaque assay.

20 magglutinin negative and resistant to 493 in plaque assays.

21 DNA and by the release of phage particles in plaque assays.

22 replication in HCjE cells was determined by plaque assays.

23 ng gene 5-specific short interfering RNAs in plaque assays.

24 replication in HRPE cells were evaluated by plaque assays.

25 on HSV-2 replication in vitro using standard plaque assays.

26 t-O139 El Tor biotype V. cholerae strains in plaque assays.

27 small amounts of virus could be detected by plaque assay 2 days after infection, and levels slowly d

28 In plaque assays, 4-GU-DANA reduced the number (but not the

29 In a standard plaque assay, 50 microm BIP caused a 50% reduction in pl

30 alpha-lyxose L-isomers were more active in a plaque assay against the AD169 strain of HCMV compared t

31 infection, was determined to be 0.10 in the plaque assay and 0.29 in the gene transfer assay.

32 and infectivity was determined by the viral plaque assay and an enhanced infectivity assay.

33 eukocytes (PBLs), and extraocular tissues by plaque assay and by staining for early antigen (EA) and

34 Using a standard plaque assay and clinical isolates of herpes simplex vir

35 These experiments are complemented by plaque assay and electron microscopy measurements to det

36 -specific antibody titers were determined by plaque assay and ELISA, respectively.

37 -specific antibody titers were determined by plaque assay and enzyme-linked immunosorbent assay, resp

38 and dengue virus replication was measured by plaque assay and flow cytometry.

39 tissues were tested for infectious virus by plaque assay and for the presence of viral DNA and RNA b

40 itory effects of NFV on HSV-1 replication by plaque assay and found that treatment with NFV did not a

41 late acid (MPA), on both BVDV replication by plaque assay and host-cell replication by flow cytometry

42 h adenovirus and wild-type AAV, as judged by plaque assay and infectious center assay, respectively.

43 ith the wild-type phenotype as determined by plaque assay and one-step growth analysis.

44 recombinant baculoviruses were identified by plaque assay and PCR.

45 in a reduced viral load, as measured by both plaque assay and PCR.

46 Plaque assay and real-time PCR demonstrated viral replic

47 Reverse plaque assays and quantitative reverse-transcriptase pol

48 f Shigella flexneri, including classic phage plaque assays and time-lapse fluorescence microscopy to

49 t of viral protein synthesis, replication by plaque assay, and cell killing.

50 ochemically, viral titers were determined by plaque assay, and pathology was determined by histologic

51 We conducted immunostaining, plaque assay, and quantitative reverse transcription-pol

52 nd-site complementation in hemolysin assays, plaquing assays, and cell extract motility assays.

53 -95, and a revertant virus using traditional plaque assays, as well as real-time quantitative PCR-bas

54 Virus tissue titers determined by plaque assay at 5 and 10 days after infection demonstrat

55 The FACS assay is an improvement over the plaque assay because the infection period is reduced fro

56 ation was measured in tracheal secretions by plaque assay before and at 24-h intervals after treatmen

57 reduction in sensitivity to the inhibitor in plaque assays, but their affinity (1/Kd) to the inhibito

58 Delayed infection was confirmed by plaque assays, by reverse transcription-PCR, and by in s

59 s including site-directed mutagenesis, phage plaque assays, circular dichroism spectroscopy, and in v

60 Twenty virus clones grew in plaque assays containing zanamivir, indicating possible

61 Plaque assays demonstrated dramatic dose-dependent atten

62 superior in performance to both the IgM and plaque assays during this time period, suggesting that N

63 Injected eyes were examined by plaque assay, electron microscopy, Western blot analysis

64 ailable for determining virus titers such as plaque assays end-point dilution, quantitative real-time

65 cDNA clone did not yield detectable virus by plaque assay even though intracellular double-stranded R

66 Plaque assay experiments demonstrated that Muc5ac-Tg BAL

67 eral times after inoculation and examined by plaque assay for replicating virus, RT-PCR for iNOS RNA,

68 ri, mutants were constructed and tested in a plaque assay for the ability to invade, replicate intrac

69 Plaque assays for titrating dengue virus (DENV) are time

70 h in a murine macrophage cell line, and in a plaquing assay for cell-to-cell spread.

71 Plaque assays further indicated that rRSV replication wa

72 system corroborated classical metrics (qPCR, plaque assay, FVIC, DAPI) and outperformed most of them

73 re the most active, IC50's = 0.2-0.4 microM, plaque assay; IC90's = 0.2-2 microM, yield reduction ass

74 es were less active (IC50's = 60-100 microM, plaque assay; IC90's = 17-100 microM, yield reduction as

75 RSV quantity was measured by quantitative plaque assay in fresh tracheal and nasal aspirates obtai

76 e assays were compared to that of a standard plaque assay in Vero cells.

77 Viral titers in sera were determined by plaque assay in Vero cells.

78 est samples were also determined by a direct plaque assay in Vero cells.

79 or cells was not productive (as shown by the plaque assay), infectious virus could be recovered from

80 Resistance to 493 in plaque assays is thus not equivalent to resistance to in

81 Corneas were assessed for viral content by plaque assay, leukocyte influx by flow cytometry, and co

82 tial RNA damage following a similar trend as plaque assay measurements of infectious viruses.

83 Plaque assay of homogenized ocular tissue was used to de

84 Plaque assay of virus yield from endothelial or Vero cel

85 deaza analogues were essentially inactive in plaque assays of infectivity, a novel 7-deaza-6-methyl-9

86 (transgene transfer and expression) and the plaque assay on 293 cells.

87 ately 200-fold lower than that determined by plaque assay on BmN cells.

88 dition, the titer of eh2-AcNPV determined by plaque assay on Sf-9 cells was approximately 200-fold lo

89 s corneal titers were determined by standard plaque assay on Vero cells.

90 s in media or cell extracts were measured by plaque assay or radioimmunoassay.

91 tor, gp130, on HSV-1 replication in vitro by plaque assay or reactivation ex vivo by explant cocultiv

92 e infection in mouse tissues was analyzed by plaque assay, PCR, and explantation cocultivation in bot

93 Results were compared with those of RSV plaque assays performed on fresh aliquots from the same

94 As judged by reverse hemolytic plaque assays, phorbol-12-myristate-13-acetate (PMA) sti

95 Plaque assay quantified HSV-1 in the tear film of infect

96 r viral replication and immune response with plaque assay, quantitative polymerase chain reaction, We

97 Viral load by RTrtPCR correlated with plaque assay results (r2 = 0.158; P < 0.0001).

98 By plaque assay, serum samples were negative for infectious

99 Titration and plaque assays showed no virus spread in ac92-knockout ba

100 Virus titers measured by plaque assays showed that 8 of 10 normally resistant non

101 ickettsia rickettsii were determined using a plaque assay system for enumeration and isolation of mut

102 Previous studies have used the plaque assay technique.

103 ric assay that measures viral antigen, and a plaque assay that analyzes virion production.

104 results of tissue-culture cell invasion and plaque assays, the Sereny test, and serum-sensitivity as

105 In plaque assays, these viruses showed approximately 1,000-

106 Here we have used the reverse hemolytic plaque assay to assess, at the single-cell level, basal

107 Here we have used the reverse hemolytic plaque assay to determine the ontogeny of basal and regu

108 ced from 6 days using the conventional viral plaque assay to several minutes using the proposed metho

109 To estimate this diversity, we used lysis plaque assays to detect viruses that infect the widespre

110 Furthermore, we have employed NMR and viral plaque assays to probe the interaction between the C-USP

111 VZV replication was analyzed by plaque assay, transmission electron microscopy, and hist

112 ing techniques for counting viruses, namely, plaque assays, transmission electron microscopy (TEM), e

113 tivity of SQ-PCR was comparable to that of a plaque assay using centrifugation for inoculation.

114 Based on these observations of lysis, a plaque assay was developed for STIV.

115 By reverse hemolytic plaque assay, we showed that glucose-stimulated insulin

116 quantify virus in Vero E6 cells by standard plaque assay were often unsuccessful.

117 Plaque assays were performed to determine adenovirus tit

118 e antiviral activity was confirmed through a plaque assay where viral titer reduction was observed in

119 h experiment detected no phage production by plaque assay, whereas phageFISH and geneELISA revealed p

120 1 h latent period and a burst size of 871 by plaque assay, whereas phageFISH identified cell lysis st