ライフサイエンスコーパス: virus titer

1 of protection (>1,500-fold reduction in lung virus titer).

2 the 627K mutant, but it did enhance the lung virus titer.

3 xpression of IFIT3 resulted in a decrease of virus titer.

4 There was no effect of carrageenan on virus titer.

5 rrespond to the 1- to 2-log-unit decrease in virus titer.

6 onsible for an early rapid decrease in HSV-2 virus titer.

7 ndent upon the duration of APC infection and virus titer.

8 n nasal-lavage specimens, or on quantitative-virus titer.

9 iter against egg-grown influenza A/Hong Kong virus titer.

10 n the G tract had little or no effect on the virus titer.

11 d of the PPT and determined their effects on virus titer.

12 re complex mutations had stronger effects on virus titer.

13 V-activated CD4(+) T-cell blasts reduced the virus titer.

14 ent resulting in > or =100-fold reduction in virus titer.

15 (10- to 50-fold) in viral RNA packaging and virus titer.

16 gnal mutants has defects in RNA packaging or virus titer.

17 tion of vRNPs and the reduction of influenza virus titers.

18 ologic changes, reflecting reduced levels of virus titers.

19 sed impaired vRNP export and reduced progeny virus titers.

20 t a 12-fold increase in encephalomyocarditis virus titers.

21 related to preexisting antibody or to higher virus titers.

22 ectedly, anti-IL-22-treated mice had reduced virus titers.

23 lung tissue correlated with the reduction of virus titers.

24 , including a drastic reduction in challenge virus titers.

25 ut do not ultimately control cell-associated virus titers.

26 g both no phenotype and a >1-log decrease in virus titers.

27 n-deficient mice contained similar influenza virus titers.

28 ncreased cell-cell fusion and produced lower virus titers.

29 hods, from clinical specimens containing low virus titers.

30 ducing a 10- to 1,000-fold reduction in peak virus titers.

31 matic increase in viral RNA accumulation and virus titers.

32 .0 +/- 0.3 days; p < 0.02) despite increased virus titers.

33 and were positively correlated with tracheal virus titers.

34 eter and a 51-fold decrease in extracellular virus titers.

35 ated with severe illness and higher vaccinia virus titers.

36 ection domain generally had small effects on virus titers.

37 the R-peptide yet does not adversely affect virus titers.

38 nes, while anti-F antibody treatment reduced virus titers.

39 rus production onset, and (iii) reduced peak virus titers.

40 s virus (WHV) induces a transient decline in virus titers.

41 g but altered neither antibody responses nor virus titers.

42 alpha-globin mRNA per copy) without reducing virus titers.

43 rotein levels in viral pellets or infectious virus titers.

44 A549 cells consistent with higher infectious virus titers.

45 nt reduction of viral protein expression and virus titers.

46 ttC or dptB showed a significant increase in virus titers.

47 lded at least a 1 log decrease in infectious virus titers.

48 Lesion expression did not correlate with virus titers.

49 howed relatively little suppression of DEN-2 virus titer (0.1 and 0.9 log10, respectively).

50 I1 and HI8), (ii) particles with a decreased virus titer (1 log) but normal infectivity (HI4), and (i

51 was delivered to >80% of cells and inhibited virus titers 10- to 100-fold in a sequence-specific and

52 Treatment on day 0 reduced peak pulmonary virus titers 10- to 100-fold, reduced the severity of vi

53 In contrast, the peak virus titers (10(3.6) to 10(4.3) TCID(50)/ml) for Mal08

54 n (>10 h postinfection [p.i.]) after maximal virus titers (150 to 200 PFU/cell) have been reached, wi

55 RNA displayed widespread eGFP expression and virus titers 16-fold higher than dsbetagal controls afte

56 e vaginal mucosa; 2) had significantly lower virus titers; 3) had decreased overt signs of genital he

57 nes, the hemolytic complement gene, affected virus titer 7 days after infection.

58 ment of IRF-3(-/-) BMDCs resulted in reduced virus titers, a far greater reduction was seen after IFN

59 l result in a drastic decrease in infectious virus titers, a reduction in the amount of packaged vira

60 uced EHV-1 production by 23-fold compared to virus titers achieved in cells transfected with the empt

61 ions at Y501 have been shown to decrease the virus titer and affect the specificity of RNase H cleava

62 In vivo, PLD2 inhibition reduced virus titer and correlated with significant increases in

63 g the most appropriate systems for assessing virus titer and fitness, which has implications for vacc

64 s were evaluated, namely level of infection, virus titer and genome copy number.

65 Consequently, increased lung virus titer and higher mortality were observed.

66 dministration of rshDPP4 led to reduced lung virus titer and histopathology.

67 gs, rather than with traditional measures of virus titer and host responses.

68 ed mice exhibited a significant reduction in virus titer and improvement in survival that is associat

69 revealed an inverse linear relationship with virus titer and MOI.

70 RSHZ19 reduced virus titer and protected against illness when used in p

71 th a approximately 10-fold reduction in lung virus titer and protection against weight loss when comp

72 sed vector and determined the effects on the virus titer and RNase H cleavage specificity.

73 n using 2-bromopalmitate (2-BP) affected the virus titer and the interaction of UL20 and gK but did n

74 virus replication, as judged both by maximum virus titer and time of viral clearance.

75 ve CD8 T cells failed to clear the pulmonary virus titer and to promote host survival.

76 s could be a major factor in determining the virus titer and, by extension, viral fitness, which coul

77 ulted in a 6-fold reduction of extracellular virus titers and a 13% reduction of plaque diameters, wh

78 selected until after the initial decrease in virus titers and after the development of immune respons

79 e severe pulmonary inflammation, higher lung virus titers and greater weight loss compared with mice

80 assessed by the quantification of infectious virus titers and HCMV genome copies and the detection of

81 l NSV-induced encephalomyelitis, we compared virus titers and immune responses in adult B6 and Bc mic

82 ed with higher virus load because equivalent virus titers and immunohistochemical staining were obser

83 and blockade of PD-L1 in vivo led to reduced virus titers and increased CD8(+) T cell numbers in high

84 able Mcl-1-knockdown cells led to restricted virus titers and increased physical to infectious partic

85 accination decreased postchallenge tear film virus titers and ocular disease incidence and severity w

86 virus, resulted in significant reductions in virus titers and pathological lesions in the liver compa

87 d systemic infection in the ducks, with high virus titers and pathology in multiple organs, particula

88 d virus increased the reproducibility of the virus titers and PRN titers.

89 llowing RSV inoculation despite similar lung virus titers and rates of virus clearance.

90 at this stimulatory effect is independent of virus titers and RSV-induced inflammation; that it is as

91 ted in asymptomatic infection with lower CNS virus titers and undetectable CNS apoptosis.

92 High virus titers and viral replication in many tissues were

93 creased survival, lowered the peak of ocular virus titer, and cleared the ocular disease.

94 sms, including direct cytotoxicity, elevated virus titer, and reduced tumor neovascularization.

95 lted in a significant reduction in pulmonary virus titers, and largely reduced virus-induced lung pat

96 lence in vivo as measured by disease scores, virus titers, and mortality.

97 C-CX3CR1 binding and chemotaxis, reduce lung virus titers, and prevent body weight loss and pulmonary

98 influenza-associated morbidity and influenza virus titers, and that these changes in disease severity

99 V-1 can replicate without UL21, although the virus titers are greatly reduced.

100 to no discernible cytopathic effect, and low virus titers are produced.

101 strategies for retroviral transduction, the virus titers are relatively high and stable and can be f

102 s difference in inflammatory damage, cardiac virus titers are similar between C57BL/6 and Bl.Tg.Ealph

103 corneal infection were found to have ocular virus titers as much as 10(5)-fold higher than that seen

104 Infectious virus titers at day 8 postinfection in liver, spleen, an

105 However, within 6 to 12 months, virus titers begin to increase towards pretreatment leve

106 o a glycine resulted in a modest decrease in virus titer but a substantial decrease (1 log order) in

107 tible tomato Moneymaker (MM) revealed higher virus titers but lower amounts of siRNAs.

108 wn of IFITMs by RNA interference reduced the virus titer by about 100-fold on day 8 postinfection, ac

109 ed a smaller plaque diameter and reduced the virus titer by approximately 1 log.

110 he adjacent region caused a reduction in the virus titer by blocking virus release, and some affected

111 yping contributed to the elevated polytropic virus titer by increasing the efficiency of packaging an

112 diately, evidenced by a 30-fold reduction in virus titer by week 2, declining to a nonquantifiable le

113 The most potent oligonucleotides lowered virus titer by ~90%.

114 inhibitors that block HSP70 function reduces virus titers by up to 1,000-fold, suggesting that this i

115 verexpression of the top ten ISGs attenuates virus titers by up to 1000-fold.

116 at 14 days postinfection, a period when the virus titer comes primarily from reactivated latent geno

117 on shutoff (100-fold or greater reduction in virus titer compared to that at 37 degrees C) at 39 degr

118 tantial (5-12 log(10)) reduction in vaccinia virus titer compared with mock-immunized controls.

119 mice showed a complete reduction in vaccinia virus titers compared to HCV DNA prime/boost- and mock-i

120 otent antiretroviral therapy and that plasma virus titers correlate, albeit in a nonlinear fashion, w

121 T cells and remained unmethylated even when virus titers decreased.

122 These mutations increased infectious virus titers, demonstrated a strong positive impact on v

123 guinea pigs by both viruses, as measured by virus titer determination and seroconversion.

124 h we have demonstrated clearly that absolute virus titer does not predict clinical outcome.

125 Normalized virus titers dramatically increased after adult emergenc

126 lt does not exclude infection due to the low virus titer during infection depending on the timing of

127 in a significant decrease in the normalized virus titer during larval and pupal development.

128 ced morbidity but had no effect on pulmonary virus titers during primary H1N1 infection compared to p

129 RDR, and it had no significant influence on virus titers during systemic infection.

130 and not Tc2 effectors reduced the pulmonary virus titer early during infection.

131 ice to SARS-CoV was associated with elevated virus titers, enhanced vascular leakage, and alveolar ed

132 ons caused an initial increase of infectious virus titer followed by a decrease with a longer duratio

133 crease in sarcolemmal disruption and cardiac virus titer following CV infection.

134 51g rescued virus (51gR) but yielded reduced virus titers following infection of permissive bovine ce

135 modalities were able to significantly reduce virus titer for all viruses investigated, with the excep

136 Virus titers from nasal swabs peaked on day 2, and low t

137 In contrast, virus titers from the PBMC of morphine-naive SIVmac239-i

138 ic relief in addition to reducing infectious virus titers, FST-100 should be a valuable addition to t

139 els in HuH-7 cells significantly affects HCV virus titers, further demonstrating the requirement for

140 Virus titers, genome copies, and lesion size were decrea

141 SERCA virus titers >5 to 6 plaque-forming units per cell produ

142 No difference in virus titers, HRV species, and inflammatory or allergic

143 The peak virus titer in cotton rat lungs occurred on day 4 postin

144 tigen, the virus genome copy number, and the virus titer in IHH culture fluid.

145 verse transcriptase PCR (RT-PCR) analysis of virus titer in L1 thrips revealed a significant increase

146 that eosinophil deficiency had no impact on virus titer in PVM Ag-vaccinated mice, nor on weight los

147 t there is a significant correlation between virus titer in the bloodstream of infected individuals a

148 packaging by studying the RNA packaging and virus titer in the context of proviruses.

149 e is no absolute correlation between primary virus titer in the eye and TG and the level of viral DNA

150 with CX4C had a 0.7 to 1.2 log10-fold lower virus titer in the lung at 5 days postinfection (p.i.) a

151 b titers translated to a 6- to 40-fold lower virus titer in the lungs of the RSV-challenged offspring

152 Average virus titer in the patient specimens was 1.05 e4 copies/

153 tion mutant in terms of disease severity and virus titer in vaginal swabs and central nervous system

154 vitro and that cyclopamine is able to reduce virus titers in a mouse model of hRSV infection.

155 Virus titers in all four woodchucks were only transientl

156 It may be reasonable to obtain West Nile Virus titers in any patient presenting with the above fi

157 Virus titers in cell culture supernatants and lung homog

158 ignificant reduction of dengue and West Nile virus titers in cell-based assays of virus replication,

159 that overlapped with transient increases in virus titers in CXCR3-deficient mice.

160 Virus titers in heart and spleen were dramatically lower

161 No significant differences in virus titers in heart or pancreas were observed between

162 y of these siRNAs significantly reduced lung virus titers in infected mice and protected animals from

163 the CNS of infected mice, it does not affect virus titers in infected mice thymi, spleens or infected

164 na, and this delay correlated with decreased virus titers in infected tissues, compared with mice inf

165 In contrast, mean virus titers in liver, spleen, and lung tissues from pla

166 ic reductions in weight loss, mortality, and virus titers in lung and bronchoalveolar lavage fluid af

167 o doses of MVA prevented illness and reduced virus titers in mice who were challenged with either vSC

168 ociated with a broad tissue tropism and high virus titers in multiple organs, including the brain.

169 cation kinetics were assessed by determining virus titers in nasal swabs and respiratory tissues, whi

170 In contrast, although virus titers in neural tissues of p55-/- N13 mice were e

171 of 1 and 10 mg/kg/day significantly reduced virus titers in organs and provided 60% and 80% survival

172 characterized by high levels of viremia and virus titers in peripheral organs.

173 against lethal challenge and displayed high virus titers in respiratory tissues.

174 Virus titers in serum, peripheral organs, and the brain

175 absence of NK cells has a profound effect on virus titers in spleen and liver.

176 at 5 days postinfection (peak of infectious virus titers in the central nervous system) compared to

177 peripheral organs, which resulted in higher virus titers in the central nervous system.

178 Although minocycline reduces virus titers in the CNS of infected mice, it does not af

179 delayed until 2 and 4 days after infection, virus titers in the eye were analogous to those in the c

180 even after corneal scarification, had lower virus titers in the eye, had less latency in the TG, and

181 avirulent (KOS and RE) strains of HSV-1, and virus titers in the eyes and TG during primary infection

182 s, (ii) virus antigen shedding or infectious virus titers in the feces or intestinal contents measure

183 the liver, there was no correlation between virus titers in the gut and detection of virus in the li

184 / SA11-Cl4 reassortants and determination of virus titers in the gut and liver revealed that the extr

185 CVB3 resulted in approximately 50-fold-lower virus titers in the heart and approximately 6-fold-lower

186 Virus titers in the heart were equivalent at days 3 and

187 TSWV titers in the vector were unrelated to virus titers in the leaf tissue from which they acquired

188 tion with RSV showed substantially decreased virus titers in the lung and decreased inflammation and

189 nza virus resulted in dramatically increased virus titers in the lung and intranasal cavity of mutant

190 or BALB/c mice enhanced survival and reduced virus titers in the lung.

191 favipiravir significantly reduced infectious virus titers in the lungs and markedly improved lung his

192 ein gene and PEI87 resulted in a 94% drop of virus titers in the lungs of influenza-infected animals.

193 Virus titers in the lungs of KyA-immunized mice were 1,0

194 Virus titers in the lungs of mice unable to respond to I

195 d lower at 2 days post-RacL11 challenge than virus titers in the lungs of nonimmunized mice, indicati

196 A comparison of virus titers in the mouse respiratory tract versus MDCK

197 gher virus excretion via the nose and higher virus titers in the nasal turbinates than intratracheal

198 in the heart and approximately 6-fold-lower virus titers in the pancreas.

199 ociated with lethality, significantly higher virus titers in the respiratory tract, virus disseminati

200 but can reduce disease severity, deaths, and virus titers in the respiratory tract.

201 Virus titers in the serum of vaccinated mice were signif

202 Topical drug treatment markedly reduced virus titers in the skin and snout, whereas parenteral t

203 ric TSWV isolate-T. tabaci isoline pairings, virus titers in the thrips vector were significantly low

204 Immunized ferrets had significantly lower virus titers in the upper respiratory tract and less-sev

205 This study characterizes differences in virus titers in the vector among TSWV isolate-T. tabaci

206 Virus titers in these tissues reached 10(9) pfu/g.

207 d NA-T342A, N2 numbering) that increased the virus titers in three mammalian cell lines (i.e., Madin-

208 Pr4Delta3-C2 virus titers in ticks were significantly reduced 100- to

209 yet retained growth dynamics, stability, and virus titers in vitro that were similar to those of the

210 irus initially replicated to low titers, but virus titer increased significantly after mutations appe

211 Furthermore, virus titer increased with apoptosis progression, sugges

212 l of intravenous JEV infection, we show that virus titers increased exponentially in the brain from 2

213 However, DC480 mutant virus titers increased nearly 20-fold when the virus was

214 ion of mouse cells with 16/L leads to higher virus titers, increased production of RNA, and total cyt

215 s among healthy, full-term infants; however, virus titers, inflammation, and Th2 bias are proposed ex

216 In contrast to the 30-fold increase in virus titers, intracellular levels of viral RNA were inc

217 ce were euthanized 5 days postinfection, and virus titers, levels of neutralizing antibodies, and num

218 e non-1 (75% vs. 56%) and in patients with a virus titer < 2 x 10(6) copies/mL (93% vs. 43%).

219 and had no significant reductions in tissue virus titers observed on day 5 post-H5N1 virus challenge

220 erefore, based on the analysis of CIT50, the virus titer of a given sample can be determined from the

221 e (ORF), had little effect on the infectious virus titer of PR8 or PR8 7:1 reassortants with T/E segm

222 were similar for Ncal99 and Sw30, with peak virus titers of 10(5.1) 50% tissue culture infectious do

223 Virus titers on chicken embryo cells were reduced by app

224 eutralizing-antibody titers and reduced lung virus titers on day 3 postchallenge.

225 8 U/ml) of cells reduced 40% E2-G pseudotype virus titer only.

226 in apoptosis at 10 h p.i., with no effect on virus titers (only SB203580 tested).

227 here were no differences among the groups in virus titers or the route and timing of virus spread in

228 progression, hematology, serum biochemistry, virus titers, or lethality in nonhuman primates infected

229 IFN-I remains detectable until after virus titers peak, but early IFN-I administration amelio

230 Laryngeal virus titers peaked at 10(5.0)-10(6.0) plaque-forming un

231 In all guinea pigs, virus titers peaked in nasal secretions at day 2 after i

232 Virus titers peaked in the CNS between postnatal days 10

233 revealed that cycling cells generated higher virus titers per cell.

234 l cell shedding accelerated the reduction of virus titers, presumably by clearing virus-infected cell

235 ssembly is largely responsible for increased virus titers produced during S-phase.

236 A linear relationship was found in the virus titer range of 2(-10)-2(2)HAU.

237 ical serum specimens (genotypes 1 to 6, with virus titers ranging from 15.1 to 2.1 x 10(7) IU/ml) sho

238 Despite the high virus titers, rCVB3 infection of naive mice failed to in

239 Virus titers reached 10(8) TCID50/ml in the blood and be

240 Whereas there was no difference in the virus titer recovered from the cornea comparing vaccinat

241 e observed a log-linear relationship between virus titer reduction and the number of rPMP molecules i

242 eases in morbidity, mortality, and pulmonary virus titers relative to controls.

243 Because virus titers resulting from sampling downstream of the U

244 In no case was the peak virus titer substantially reduced following infection of

245 different methods available for determining virus titers such as plaque assays end-point dilution, q

246 although this mutation significantly reduced virus titer, suggesting that removing three nucleotides

247 Loss of P58(IPK) leads to reduced virus titer, suggesting that wild-type P58(IPK) protein

248 cided with a 100- to 1,000-fold reduction in virus titer, supporting the hypothesis that the HPIV1 C

249 fectious progeny for weeks, producing higher virus titers than late-gestation cells that varied by do

250 tro and the SSTT mutation resulted in higher virus titers than were observed for the parental rOka st

251 negligible T-cell-mediated injury, and high virus titers that persist.

252 replicate in primary fibroblasts, attaining virus titers that were 2 to 3 orders of magnitude lower

253 ated in all animals with a 2-log decrease in virus titer, the timing occurred approximately 2 weeks l

254 ere characterized by a continual decrease in virus titer, the titers in the persistent infections rea

255 000-fold and also caused the cell-associated virus titer to increase.

256 virulent HSV-2 strain resulted in a rise in virus titers to levels comparable to those of nonimmune

257 erienced less morbidity but had similar lung virus titers to placebo-treated females.

258 iameter change data were used to compute the virus titer using a statistical method called the method

259 mosquito pools could be detected when the WN virus titer was 10(2.1) to 10(3.7) PFU/0.1 ml.

260 The reduction in B virus titer was attributed to the complete growth of typ

261 Virus titer was maximal 96 hpi in CaCo-2 cells, and viru

262 Input virus titer was not correlated with SMV recovery.

263 was competent for virion formation, but the virus titer was reduced 4.5-fold relative to that of the

264 on and binding to the receptor; however, the virus titer was reduced 5- to 45-fold, indicating a post

265 amples and challenged with HSV-2(G), and the virus titer was then determined.

266 However, at high influenza virus titers, we were able to reconstruct >99% complete

267 Serum antibodies, lung virus titers, weight loss, and pulmonary pathology were

268 mal cell damage in rat myocytes if the SERCA virus titer were maintained within 1 to 4 plaque-forming

269 Lower virus titers were also detected in other tissues, includ

270 Further, 22/n199 virus titers were below the level of detection in trigem

271 f resistant lines carrying Ty-1 or Ty-3, low virus titers were detected concomitant with the producti

272 High virus titers were detected in the lungs and brains of tr

273 ected monkeys secreted virus, while marginal virus titers were detected in tracheal lavage fluid cell

274 Virus titers were determined by plaque assay.

275 cells, whereas lymphocytic choriomeningitis virus titers were dramatically increased.

276 Virus titers were elevated in the trigeminal ganglia and

277 The resulting virus titers were greatly reduced from those of JFH1, an

278 At all times and in all organs analyzed, virus titers were higher in CAST than in BALB/c mice.

279 the heart; in the absence of such signaling, virus titers were markedly elevated by day 3 postinfecti

280 In the absence of an intact ISG15 system, virus titers were markedly elevated by postinfection day

281 Surprisingly, virus titers were not elevated in MAVS-deficient mice, d

282 Higher egg-grown influenza A/Hong Kong virus titers were not significantly associated with infe

283 with the parental virus (pH1N1/NS1-wt), yet virus titers were not significantly increased in cell cu

284 Increased virus titers were observed among 1:7 viruses containing

285 However, lower virus titers were observed in all corresponding tissues

286 High virus titers were present in lung and brain tissues 2 an

287 Infectious virus titers were present in the blood and most tissues

288 us were treated with the 5'End or 3'CSI PMO, virus titers were reduced by approximately 5 to 6 logs a

289 Consistent with antibody responses, lung virus titers were significantly higher in obese mice tha

290 erforin and Fas or neither perforin nor Fas, virus titers were significantly lower than in control mi

291 Nasal wash virus titers were similar for Ncal99 and Sw30, with peak

292 an Ifit2(-/-) mice, although their pulmonary virus titers were similarly high.

293 ry steps of the virus life cycle because the virus titers were similarly inhibited from infected cell

294 induces apoptosis in cells containing dsRNA, virus titers were strongly reduced.

295 gs of dual-infected mice, although influenza virus titers were unaffected.

296 ions in lung pathology without reductions in virus titer when treated with two intranasal doses of RT

297 geny production (a reduction of 95 to 99% in virus titer), which correlated with the phosphorylation

298 s were not exhausted by the presence of high virus titers, which persisted in the SMG despite the str

299 Addition of monocytes restored the virus titer, while addition of resting T cells or EBV-ac

300 egulation decreases extracellular infectious virus titers with little effect on intracellular RNA con