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1  below 25 PFU/ml (the detection limit of the plaque assay).
2 E); infectious virus was quantified by viral plaque assay.
3  Western blot, and virus infectivity using a plaque assay.
4 analyzed by both quantitative PCR (qPCR) and plaque assay.
5       Viral titers were assessed by standard plaque assay.
6 dardized between the sites with the third, a plaque assay.
7 ning for the nucleocapsid protein and by the plaque assay.
8 l titers in the tear film were determined by plaque assay.
9 uced initial lung viral loads as measured by plaque assay.
10 nd viral replication was ascertained using a plaque assay.
11 enan type IV blocked FHV-1 adsorption in the plaque assay.
12              Virus titers were determined by plaque assay.
13 lation onto confluent cell monolayers in the plaque assay.
14 ription-PCR (RT-PCR) assays or indirectly by plaque assay.
15 ious virions that were readily detectable by plaque assay.
16 sitivities greater than that of the standard plaque assay.
17 drug resistance marker that can be scored by plaque assay.
18 y quantitative reverse transcription-PCR and plaque assay.
19 omide assay, and virus yield was examined by plaque assay.
20 alfa, and viral production was quantified by plaque assay.
21 FN2 increased IHNV infection, as measured by plaque assay.
22  infected tissues was determined by standard plaque assay.
23 racterized in-frame insertion mutants in the plaque assay.
24 t-O139 El Tor biotype V. cholerae strains in plaque assays.
25 magglutinin negative and resistant to 493 in plaque assays.
26 , with minimal infection of neurons based on plaque assays.
27 d females through RT-qPCR as well as through plaque assays.
28 ssed for viral detection through RT-qPCR and plaque assays.
29 n than healthy cells, which was supported by plaque assays.
30 DNA and by the release of phage particles in plaque assays.
31  replication in HCjE cells was determined by plaque assays.
32 ng gene 5-specific short interfering RNAs in plaque assays.
33  replication in HRPE cells were evaluated by plaque assays.
34 on HSV-2 replication in vitro using standard plaque assays.
35 ed droplets and bioaerosols were negative by plaque assay (0 of 58).
36  small amounts of virus could be detected by plaque assay 2 days after infection, and levels slowly d
37                                           In plaque assays, 4-GU-DANA reduced the number (but not the
38                                In a standard plaque assay, 50 microm BIP caused a 50% reduction in pl
39 alpha-lyxose L-isomers were more active in a plaque assay against the AD169 strain of HCMV compared t
40  infection, was determined to be 0.10 in the plaque assay and 0.29 in the gene transfer assay.
41  and infectivity was determined by the viral plaque assay and an enhanced infectivity assay.
42 eukocytes (PBLs), and extraocular tissues by plaque assay and by staining for early antigen (EA) and
43                             Using a standard plaque assay and clinical isolates of herpes simplex vir
44        These experiments are complemented by plaque assay and electron microscopy measurements to det
45 -specific antibody titers were determined by plaque assay and ELISA, respectively.
46 -specific antibody titers were determined by plaque assay and enzyme-linked immunosorbent assay, resp
47 and dengue virus replication was measured by plaque assay and flow cytometry.
48 he virus during infection was explored using plaque assay and fluorescence-based imaging and single p
49  tissues were tested for infectious virus by plaque assay and for the presence of viral DNA and RNA b
50 itory effects of NFV on HSV-1 replication by plaque assay and found that treatment with NFV did not a
51 late acid (MPA), on both BVDV replication by plaque assay and host-cell replication by flow cytometry
52 h adenovirus and wild-type AAV, as judged by plaque assay and infectious center assay, respectively.
53 ith the wild-type phenotype as determined by plaque assay and one-step growth analysis.
54 recombinant baculoviruses were identified by plaque assay and PCR.
55 in a reduced viral load, as measured by both plaque assay and PCR.
56                                              Plaque assay and real-time PCR demonstrated viral replic
57                                In vivo phage plaque assays and in vitro DNA cleavage assays show that
58                                      Reverse plaque assays and quantitative reverse-transcriptase pol
59           Bacteriophage was quantified using plaque assays and reverse transcription quantitative pol
60 f Shigella flexneri, including classic phage plaque assays and time-lapse fluorescence microscopy to
61 t of viral protein synthesis, replication by plaque assay, and cell killing.
62 ochemically, viral titers were determined by plaque assay, and pathology was determined by histologic
63                 We conducted immunostaining, plaque assay, and quantitative reverse transcription-pol
64 ys, quantitative RT-PCR, viral infection and plaque assays, and reporter gene assays, we demonstrate
65 d SPCEs were also validated against standard plaque assays, and very good agreement was found between
66 t each time point was enumerated using viral plaque assays, and viral decay and half-life was estimat
67 nd-site complementation in hemolysin assays, plaquing assays, and cell extract motility assays.
68 -95, and a revertant virus using traditional plaque assays, as well as real-time quantitative PCR-bas
69            Virus tissue titers determined by plaque assay at 5 and 10 days after infection demonstrat
70    The FACS assay is an improvement over the plaque assay because the infection period is reduced fro
71 ation was measured in tracheal secretions by plaque assay before and at 24-h intervals after treatmen
72      Assessment of phage stability relies on plaque assay (bioactivity), which requires powder sample
73 reduction in sensitivity to the inhibitor in plaque assays, but their affinity (1/Kd) to the inhibito
74           Delayed infection was confirmed by plaque assays, by reverse transcription-PCR, and by in s
75 s including site-directed mutagenesis, phage plaque assays, circular dichroism spectroscopy, and in v
76                   Dose-response analyses and plaque assays confirm the antiviral activity (IC(50): 10
77                  Twenty virus clones grew in plaque assays containing zanamivir, indicating possible
78 d P1 and enumeration of infective virions by plaque assays demonstrated control via both removal and
79                                              Plaque assays demonstrated dramatic dose-dependent atten
80 oval/inactivation in water compared with the plaque assay demonstrating that relying solely on RT-qPC
81 he vesicular stomatitis virus, the automated plaque assay detected the first cell-lysing events cause
82 ovided by the authors, but MS2 bacteriophage plaque assays did not support the published results.
83  superior in performance to both the IgM and plaque assays during this time period, suggesting that N
84               Injected eyes were examined by plaque assay, electron microscopy, Western blot analysis
85 ailable for determining virus titers such as plaque assays end-point dilution, quantitative real-time
86 cDNA clone did not yield detectable virus by plaque assay even though intracellular double-stranded R
87                                              Plaque assay experiments demonstrated that Muc5ac-Tg BAL
88 eral times after inoculation and examined by plaque assay for replicating virus, RT-PCR for iNOS RNA,
89 ri, mutants were constructed and tested in a plaque assay for the ability to invade, replicate intrac
90 influenza A as measured by PCR of viral RNA, plaque assay for viable virus, and production of virus n
91                                              Plaque assays for titrating dengue virus (DENV) are time
92 h in a murine macrophage cell line, and in a plaquing assay for cell-to-cell spread.
93                                              Plaque assays further indicated that rRSV replication wa
94 system corroborated classical metrics (qPCR, plaque assay, FVIC, DAPI) and outperformed most of them
95 re the most active, IC50's = 0.2-0.4 microM, plaque assay; IC90's = 0.2-2 microM, yield reduction ass
96 es were less active (IC50's = 60-100 microM, plaque assay; IC90's = 17-100 microM, yield reduction as
97    RSV quantity was measured by quantitative plaque assay in fresh tracheal and nasal aspirates obtai
98 e assays were compared to that of a standard plaque assay in Vero cells.
99      Viral titers in sera were determined by plaque assay in Vero cells.
100 est samples were also determined by a direct plaque assay in Vero cells.
101 or cells was not productive (as shown by the plaque assay), infectious virus could be recovered from
102                         Resistance to 493 in plaque assays is thus not equivalent to resistance to in
103  determination of infectious virus titers by plaque assay, (iv) clonal isolation by plaque purificati
104 l-to-noise ratio in a fluorescent Dulbecco's plaque assay, leading to the construction of a multirepo
105   Corneas were assessed for viral content by plaque assay, leukocyte influx by flow cytometry, and co
106 by real-time RT-PCR, high content screening, plaque assays, luminex analyses, and transepithelial ele
107          Samples positive on RT-qPCR but not plaque assays may indicate that virions at distant sites
108 tial RNA damage following a similar trend as plaque assay measurements of infectious viruses.
109    Infectious SARS-CoV-2 was not detected by plaque assays (minimal level of detection is 67 PFU ml(-
110                                              Plaque assay of homogenized ocular tissue was used to de
111                                              Plaque assay of virus yield from endothelial or Vero cel
112 deaza analogues were essentially inactive in plaque assays of infectivity, a novel 7-deaza-6-methyl-9
113  (transgene transfer and expression) and the plaque assay on 293 cells.
114 ately 200-fold lower than that determined by plaque assay on BmN cells.
115 dition, the titer of eh2-AcNPV determined by plaque assay on Sf-9 cells was approximately 200-fold lo
116 s corneal titers were determined by standard plaque assay on Vero cells.
117 s in media or cell extracts were measured by plaque assay or radioimmunoassay.
118 tor, gp130, on HSV-1 replication in vitro by plaque assay or reactivation ex vivo by explant cocultiv
119 ted by researchers, and tested by using PCR, plaque assay, or lateral flow antigen test.
120  assays for viability, such as plate counts, plaque assays, or animal infectivity.
121 on (qRT-PCR) and infectious viral titers via plaque assay over time in a variety of temperature condi
122 e infection in mouse tissues was analyzed by plaque assay, PCR, and explantation cocultivation in bot
123      Results were compared with those of RSV plaque assays performed on fresh aliquots from the same
124                         When compared to the plaque assay (performed once at site 3), there was less
125               As judged by reverse hemolytic plaque assays, phorbol-12-myristate-13-acetate (PMA) sti
126                                              Plaque assay quantified HSV-1 in the tear film of infect
127 r viral replication and immune response with plaque assay, quantitative polymerase chain reaction, We
128        Viral load by RTrtPCR correlated with plaque assay results (r2 = 0.158; P < 0.0001).
129                                Additionally, plaque assay results demonstrated the ability of phages
130 mics of bacterial antagonists of diatoms via plaque assay sampling in the Western English Channel (WE
131                                           By plaque assay, serum samples were negative for infectious
132 e phages were confirmed to be stable, as the plaque assay showed negligible titer reduction after spr
133                                Titration and plaque assays showed no virus spread in ac92-knockout ba
134            Immunofluorescence microscopy and plaque assays showed presence of viable IAV particles in
135                     Virus titers measured by plaque assays showed that 8 of 10 normally resistant non
136 ickettsia rickettsii were determined using a plaque assay system for enumeration and isolation of mut
137               Previous studies have used the plaque assay technique.
138  agreement between results of the liquid and plaque assays than between the two sites performing the
139 ric assay that measures viral antigen, and a plaque assay that analyzes virion production.
140  results of tissue-culture cell invasion and plaque assays, the Sereny test, and serum-sensitivity as
141                                            A plaque assay-the gold-standard method for measuring the
142                                           In plaque assays, these viruses showed approximately 1,000-
143      Here we have used the reverse hemolytic plaque assay to assess, at the single-cell level, basal
144      Here we have used the reverse hemolytic plaque assay to determine the ontogeny of basal and regu
145 ced from 6 days using the conventional viral plaque assay to several minutes using the proposed metho
146    To estimate this diversity, we used lysis plaque assays to detect viruses that infect the widespre
147                                      We used plaque assays to model the localized spread of SARS-CoV-
148  Furthermore, we have employed NMR and viral plaque assays to probe the interaction between the C-USP
149 systems overcomes limitations of traditional plaque assays to quantify viral replication dynamics.
150              VZV replication was analyzed by plaque assay, transmission electron microscopy, and hist
151 ing techniques for counting viruses, namely, plaque assays, transmission electron microscopy (TEM), e
152 tivity of SQ-PCR was comparable to that of a plaque assay using centrifugation for inoculation.
153 ent of infected cells late in infection, and plaque assays using sparse cell monolayers indicated tha
154      Based on these observations of lysis, a plaque assay was developed for STIV.
155                                            A plaque assay was used to determine the viable virus airb
156         Consistent with these results, using plaque assays we observed that, in contrast to the preva
157 ughput single-cell sorting, and miniaturized plaque assay, we have quantified the progeny released fr
158                         By reverse hemolytic plaque assay, we showed that glucose-stimulated insulin
159  quantify virus in Vero E6 cells by standard plaque assay were often unsuccessful.
160                                              Plaque assays were performed to determine adenovirus tit
161                                              Plaque assays were performed to investigate fitness diff
162 e antiviral activity was confirmed through a plaque assay where viral titer reduction was observed in
163 h experiment detected no phage production by plaque assay, whereas phageFISH and geneELISA revealed p
164 1 h latent period and a burst size of 871 by plaque assay, whereas phageFISH identified cell lysis st
165                           Disc diffusion and plaque assays with MAgNPs demonstrated strong antifungal

 
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