ライフサイエンスコーパス: MOI

1 MOI estimates were derived by PCR at the msp-1 and -2 lo

2 MOI inactivates the enzyme to a limit of 14% activity.

3 When transduced with Ad5p53 alone at 1 MOI, the cell lines grew rapidly.

4 lines at a low multiplicity of infection (1 MOI).

5 tly suppressed by high MOI, (i.e., MOI [0.1]/MOI [0.1] > or = 2, P < 0.006).

6 Maximal immunoreactivity was observed at 100 MOI AdMnSOD with both techniques.

7 parental cell levels that also peaked at 100 MOI AdMnSOD.

8 decreased approximately two-thirds with 100 MOI AdMnSOD (P < 0.001).

9 all appeared to show maximal effect with 100 MOI AdMnSOD.

10 as increased 5-fold after infection with 100 MOI of AdCat as compared with control.

11 Five days after infection with 100 MOI of AdCat, cell numbers were reduced as compared with

12 re infected at a moderate (10) or high (100) MOI.

13 uent AEC monolayers (R(t) > 2 kOmega. cm(2); MOI = 10) revealed efficient transduction only when VSV-

14 Adv-caPKCdelta infection (1 to 25 MOI, 4 to 48 hours) increased total PKCdelta levels in a

15 exposure to 100 J/m(2) of UV light and 10(3) MOIs for 8 days.

16 Adv-caPKCdelta (5 MOI) induced a 29-fold increase in phosphorylated p54 JN

17 t, even at very low MOI (>95% infection at a MOI of 6) and did not reduce viability.

18 As expected, increasing the AAV MOI resulted in an increase in the percentage of cells i

19 Additional MOI only marginally effected a further increase in perce

20 empirical power) is approximately 0 for all MOI, there are parameter settings for which the power di

21 After an MOI of 1, GFP expression was high with the human CMV enh

22 provide evidence that in NPCs infected at an MOI as low as 0.001, HSV-1 can establish a latent state,

23 growth occurs in macrophages infected at an MOI of </=1.

24 However, at an MOI of 0.05, viruses lacking CR3 showed replication defe

25 cation defect of MAV-1 in Sur2-/- MEFs at an MOI of 0.05.

26 1A null mutant viruses in Sur2-/- MEFs at an MOI of 0.05.

27 of infection (MOI) of 0.5 and 80-fold at an MOI of 0.1.

28 At an MOI of 1, >3-fold regulation was found for five group 1

29 At an MOI of 10, at which 80% of cells are infected, less than

30 s infected, with 80% of cells infected at an MOI of 10.

31 At an MOI of 100 or greater, however, 35 to 40% of clonal cell

32 ssages) coronary VSMCs were transduced at an MOI of 100 with a recombinant adenovirus encoding human

33 radually from an MOI of 0.02 to a peak at an MOI of 200 (reaching an average of two bacteria internal

34 ss was apparently saturated within 2 h at an MOI of 200, indicating stringent host cell limitations o

35 At an MOI of 30, neutrophils loaded with AZM failed to kill si

36 At an MOI of 5, all genes from group 1 and four of five genes

37 ion (MOI) of 50 to 500 and by 633 only at an MOI of 5,000, while both viruses infected essentially 10

38 were infected with HCMV (strain AD169) at an MOI of 5.

39 infected essentially 100% of BHK cells at an MOI of 5.

40 icity of infection (MOI) of 0.1 to 99% at an MOI of 50 for AEC grown on plastic.

41 At an MOI of 90, neutrophils loaded with AZM killed significan

42 itionally, kinetic studies showed that at an MOI of approximately 400, maximal S. typhi entry is virt

43 ge of BALB/c mice with HSV-IL-2 alone, at an MOI that resulted in only 13% survival when parental vir

44 ampylobacter CFU increased gradually from an MOI of 0.02 to a peak at an MOI of 200 (reaching an aver

45 similarly well at a high MOI, suggesting an MOI-dependent importance of pUL38-TSC2 interaction in su

46 Survival with an MOI of 10 was 39+/-8.7 days.

47 cellular multiplicity of infection (MOI) and MOI model selection, suggested that low levels of cellul

48 At a comparable titer and MOI, transduction of these cells by a similarly pseudoty

49 rse linear relationship with virus titer and MOI.

50 linkage, and (3) adequacy of the approximate MOI for the true MOI.

51 /2) genes is a standard method for assessing MOI, despite the apparent problem of underestimation.

52 ion for linkage analysis is that the assumed MOI at the disease locus being tested is approximately c

53 At MOI 50, the protein levels of pro-MMP-1, -3, and -9 also

54 ciency of internalization was the highest at MOI of 0.02 and decreased steadily at higher MOIs, presu

55 IMP-1 and PAI-1 protein levels, increased at MOI 25.

56 ase in cytolysis within 24 h was observed at MOI > or = 25.

57 not impaired following exposure to AdGFP at MOIs of 1 to 1,000.

58 nd was not observed with epithelial cells at MOIs of as high as 2000.

59 ict physical limitation on S. typhi entry at MOIs of >/=40.

60 t only limited rotavirus replication even at MOIs of 100 or 500, but delivery of rotavirus particles

61 , we found very low levels of integration at MOIs of less than 10.

62 ls were infected after 2 h with C. jejuni at MOIs of 200 to 2,000.

63 Application of these four phages at MOIs of 5-15 significantly reduced Gordonia host levels

64 resulting antiviral effect was only seen at MOIs greater than 10 PFU/cell.

65 cell lines including U87, U118, and U251 at MOIs 0.1, 1, and 10 resulted in significant cytopathic e

66 The k for inactivation by MOI is decreased 20-fold by S-hexylglutathione but only

67 changes in chromatin condensation induced by MOIs of 10:1 and 1:1 required more time and had a reduce

68 w multiplicity of infection (MOI) challenge (MOI = 0.1) results in substantial production of IL-8 and

69 Positive control challenges (MOI = 10) induced levels of IL-8 that were comparable to

70 rossing risk including the number of clones (MOI), their relative proportions and genetic divergence.

71 re tracked longitudinally by Amp-Seq despite MOI > 1, thus providing an additional parameter for inve

72 type profiles in cells infected at different MOIs are correlated with differences in interferon-stimu

73 4.7 murine macrophage cell line at different MOIs.

74 ion efficiency was dependent on the UV dose, MOI, and time.

75 significantly suppressed by high MOI, (i.e., MOI [0.1]/MOI [0.1] > or = 2, P < 0.006).

76 rrier injury to repair following endotoxemic MOI.

77 chain reaction-based approaches to estimate MOI can lack sensitivity.

78 Here, we present a method to estimate MOI, which considers unique combinations of polymorphism

79 re not independently associated with fasting MOI, although they were independently inversely associat

80 skin, lungs, and colon, demonstrating fatal MOI induced by CD103-independent mechanism.

81 , accelerating barrier restoration following MOI.

82 HP-1 cells were infected with P. gingivalis (MOI = 20:1) and a panel of cytokines were measured.

83 contrast to its effect on the pi class GST, MOI inactivates much less rapidly and extensively alpha

84 Incorporation of [(3)H]MOI up to approximately 1 mol/mol of enzyme dimer concom

85 tionation of the proteolytic digest of [(3)H]MOI-modified GST pi yielded Trp38 as the only labeled am

86 that osteosarcoma (OS) tumors with IGF2/H19 MOI exhibit allele-specific differential methylation of

87 Even though at a high MOI (10 PFU/cell), the murine CMV enhancer was as effici

88 or with 2009 pandemic H1N1 viruses at a high MOI (10 PFU/cell).

89 (MOI), but it grew similarly well at a high MOI, suggesting an MOI-dependent importance of pUL38-TSC

90 Apoptosis at high MOI differs markedly from low MOI apoptosis: it is poten

91 approach reduces the starting cells at high MOI significantly with greatly improved efficiency and a

92 these working parts are dispensable at high MOI, partly because of compensatory stimulation of MIE p

93 At high MOI, stochastic influences appear to dictate the virus's

94 At high MOI, the macrophage growth defect was not apparent.

95 At high MOI, viral infection suppressed the interferon (IFN)-med

96 s regulatory function is unnecessary at high MOI.

97 s that survived infection with HSV-1 at high MOI.

98 obustly and significantly suppressed by high MOI, (i.e., MOI [0.1]/MOI [0.1] > or = 2, P < 0.006).

99 Caspase inhibitors failed to prevent high MOI apoptosis, and macrophages deficient in caspase-3, M

100 apies must remain effective against the high MOI observed during cell-to-cell transmission to inhibit

101 ) markedly inhibited apoptosis, whereas high MOI (> or =75) potentiated apoptosis.

102 + population expanded 10- to 15-fold at high MOIs (500 to 1,000), indicating multiple copies of the t

103 Infections performed at high MOIs resulted in increased viral gene expression per cel

104 Stop infection of murine fibroblasts at high MOIs was substantially more cytotoxic than infection wit

105 t competition between genomes occurs at high MOIs.

106 While high MOIs caused cytotoxicity and irreversible host cell deat

107 onsensus sequences of the viruses after high-MOI passages, and mutation rates increased under low-MOI

108 ry settings, viral propagation includes high-MOI conditions.

109 ever, infection of BALB/c BMDC with a higher MOI of 50 PFU/cell resulted in a productive infection wi

110 iversity to local cases but exhibited higher MOI (2.4 vs 2.0; P = .004) and lower mean FWS (0.82 vs 0

111 e subtypes than cells infected at the higher MOI.

112 MOI of 0.02 and decreased steadily at higher MOIs, presumably due to reported C. jejuni autoagglutina

113 the macrophage-Candida interaction at higher MOIs, we introduced a luciferase reporter gene into wild

114 per epithelial cell) and decreased at higher MOIs.

115 However, MOI greater than 100 resulted in a significant inhibitio

116 (22.1%; OR, 4.4; P < .0001), and high-impact MOIs (16.5%; OR, 3.1; P < .0001) were independent predic

117 nisms involved in maintenance of imprinting (MOI) and loss of imprinting (LOI) are unresolved.

118 1.5h for each order of magnitude decrease in MOI.

119 ctions between the IGF2 promoter and ICR1 in MOI cells, while the model of LOI lung cancer cells is f

120 s infection of RDC increased with increasing MOIs.

121 Transfer of Sf CD4(+) T cells induced MOI more rapidly than CD103(-)CD4(+) T cells, indicating

122 ere, the multiplicity of cellular infection (MOI) and population bottlenecks were quantified during p

123 f vector at a low multiplicity of infection (MOI = 5).

124 mycobacteria at multiplicities of infection (MOI) < or = 10 triggers TNF-alpha-mediated apoptosis whi

125 After a low multiplicity of infection (MOI) (0.01 PFU/cell), recombinant human CMV with the mur

126 infections, mean multiplicity of infection (MOI) 2.2, and mean within-host infection fixation index

127 cubated with RSV (multiplicity of infection (MOI) = 10) induced IL-8, macrophage inflammatory protein

128 , or zero (0.0) multiplicities of infection (MOI) and harvested at different times after infection (1

129 at low or high multiplicities of infection (MOI) and measured viral genomic replication and infectio

130 s of the cellular multiplicity of infection (MOI) and MOI model selection, suggested that low levels

131 normally at high multiplicity of infection (MOI) but replicate poorly at low MOI in comparison to wi

132 Multiplicity of infection (MOI) by Amp-Seq was 2.32 versus 1.73 for msp2.

133 own how the viral multiplicity of infection (MOI) can affect IFN induction.

134 Multiplicity of infection (MOI) can be an indicator of immune status and transmissi

135 dicate that a low multiplicity of infection (MOI) challenge (MOI = 0.1) results in substantial produc

136 , and that higher multiplicity of infection (MOI) correlates with detachment of longer F-pili.

137 d in terms of the multiplicity of infection (MOI) derived by PCR-based genotyping.

138 passaged at high multiplicity of infection (MOI) in cells permitting high titer growth.

139 at a high or low multiplicity of infection (MOI) in human foreskin fibroblast (HFF)- or NTera2-deriv

140 nfection at a low multiplicity of infection (MOI) in the presence of acyclovir results in a quiescent

141 ging from 4% at a multiplicity of infection (MOI) of 0.1 to 99% at an MOI of 50 for AEC grown on plas

142 h as 50-fold at a multiplicity of infection (MOI) of 0.5 and 80-fold at an MOI of 0.1.

143 At a multiplicity of infection (MOI) of 1 at 24 h postinfection (p.i.), the expression o

144 At a multiplicity of infection (MOI) of 1, viruses containing CR3 replicated better in S

145 ion with SV5 at a multiplicity of infection (MOI) of 10 PFU/cell compared to BALB/c BMDC, as determin

146 ntly greater at multiplicities of infection (MOI) of 10 PFU/cell or greater, and the resulting antivi

147 s and primed at a multiplicity of infection (MOI) of 10(2) with different A. actinomycetemcomitans or

148 the corresponding multiplicity of infection (MOI) of 10.

149 s infected with a multiplicity of infection (MOI) of 100 of AdGFP show that 78% of megakaryocytic (CD

150 s infected with a multiplicity of infection (MOI) of 25:1 developed chromatin condensation and DNA fr

151 n inoculated at a multiplicity of infection (MOI) of 3 PFU/cell.

152 us 1 (HSV-1) at a multiplicity of infection (MOI) of 3 with the majority of cells surviving.

153 fected by TE at a multiplicity of infection (MOI) of 50 to 500 and by 633 only at an MOI of 5,000, wh

154 AV-CIP vectors at multiplicity of infection (MOI) of 5000, in the absence or presence of a recombinan

155 nfection with 100 multiplicity of infection (MOI) of AdCat, cellular catalase activity was increased

156 nd because a high multiplicity of infection (MOI) of H. pylori is needed to induce apoptosis in vitro

157 dependent on the multiplicity of infection (MOI) of rAAV.

158 hages infected at multiplicity of infection (MOI) of ~1.0.

159 the effect of the multiplicity of infection (MOI) on costimulatory ligand upregulation and inflammato

160 itted at a higher multiplicity of infection (MOI) that, in vitro, results in a higher number of provi

161 depending on the multiplicity of infection (MOI) used for transduction, and 0.13 to 0.19 for the ret

162 ne tested and the multiplicity of infection (MOI) used.

163 V at increasing multiplicities of infection (MOI) without or with IFN-beta or IFN-lambda.

164 es were infected (multiplicity of infection (MOI), 100; 24 h) with replication-defective adenoviruses

165 nments with low multiplicities of infection (MOI), a phenomenon that may have impacted past host rang

166 rrelates with the multiplicity of infection (MOI), and optimal chlamydial growth occurs in macrophage

167 ects the observed multiplicity of infection (MOI), as well as the relationship between the MOI and th

168 pe virus at a low multiplicity of infection (MOI), but it grew similarly well at a high MOI, suggesti

169 cription at a low multiplicity of infection (MOI), but this increase is not mediated by the CREs; (ii

170 y used measure of multiplicity of infection (MOI), computed as the ratio of the number of phage to th

171 mutants at a low multiplicity of infection (MOI), so that individual plaques were formed, reactivate

172 nt virus at a low multiplicity of infection (MOI), there is a marked delay in the production of infec

173 ls, even at a low multiplicity of infection (MOI), though a reduction in titer was observed.

174 cularly for low multiplicities of infection (MOI), where few virus particles initiate the infection.

175 1 (HSV-1) at high multiplicity of infection (MOI).

176 a relatively high multiplicity of infection (MOI).

177 e by using a high multiplicity of infection (MOI).

178 pe virus at a low multiplicity of infection (MOI).

179 pe virus at a low multiplicity of infection (MOI).

180 lication at low multiplicities of infection (MOI).

181 e with increasing multiplicity of infection (MOI).

182 ially with a high multiplicity of infection (MOI).

183 viruses at a high multiplicity of infection (MOI).

184 function of viral multiplicity of infection (MOI); efficiency of site-specific integration; and disru

185 viruses at a low multiplicity of infection (MOI; 0.0001 PFU/cell) or with 2009 pandemic H1N1 viruses

186 nge of starting multiplicities of infection (MOI; from 0.02 to 20,000 bacteria/epithelial cell).

187 fected (100 multiplicity of viral infection (MOI); 24 h) with a replication-deficient adenovirus expr

188 (1 to 25 multiplicities of viral infection (MOI); 4 to 48 hours) increased total PKCepsilon levels i

189 segments using multiplicities of infection (MOIs) 25 or 50.

190 culture at low multiplicities of infection (MOIs) and found that 73.Stop growth was impaired in muri

191 ns at different multiplicities of infection (MOIs) and initial ratios of the wild type to the mutant

192 at high and low multiplicities of infection (MOIs) for 11 generations and the genome sequences, growt

193 ls at different multiplicities of infection (MOIs) have revealed a strict physical limitation on S. t

194 antibiotic) at multiplicities of infection (MOIs) of 30 and 90 bacteria per neutrophil.

195 macrophages at multiplicities of infection (MOIs) of as low as 20 and was not observed with epitheli

196 th AdCTLA4Ig at multiplicities of infection (MOIs) ranging from 0.1 to 10 were transplanted into stre

197 equiring higher multiplicities of infection (MOIs) to yield similar levels of infection.

198 cted at various multiplicities of infection (MOIs) with rAAV containing the enhanced green fluorescen

199 ication at high multiplicities of infection (MOIs), analyses of plaque morphology and intra- and extr

200 albicans at low multiplicities of infection (MOIs).

201 s, even at high multiplicities of infection (MOIs); (ii) limited HSV-1 replication and gene expressio

202 titers of virus (multiplicity of infection [MOI] of 100).

203 infecting a cell (multiplicity of infection [MOI]) influences the magnitude of virus antagonism of th

204 ve C. pneumoniae (multiplicity of infection [MOI], 5), UVCP (MOI, 5), or cHSP60 for 24 h, and the exp

205 ae cultures (at multiplicities of infection [MOIs] of 0.01, 0.1, and 1.0) were incubated with mouse b

206 s and develop fatal multiorgan inflammation (MOI) mediated by CD4(+) T cells.

207 g concentrations of markers of inflammation (MOI) than do lean children.

208 inding linkage when the mode of inheritance (MOI) is known.

209 ominant and a recessive mode of inheritance (MOI), (b) ASP methods, and (c) nonparametric linkage (NP

210 to be a consequence of either a low initial MOI or a high superinfecting MOI.

211 cords were reviewed for mechanism of injury (MOI).

212 tion is a hallmark of multiple organ injury (MOI).

213 t on top of the microfluidic open interface (MOI) for desorption in the isolated droplet.

214 Low MOI also induced cellular proliferation.

215 Low MOI reduced mitochondrial membrane depolarization, caspa

216 In the superficial chondrocytes, a low MOI and 200 J/m(2) of UV light increased the transductio

217 ontext of MHV if cells are infected at a low MOI and accelerates disease in mice transgenic for the h

218 rs also replicated less efficiently at a low MOI and expressed lower levels of GFP from the UL127 pro

219 the human CMV enhancer and promoter at a low MOI are discussed.

220 d increase in viral DNA replication at a low MOI but only when basal levels of MIE promoter activity

221 herefore, we propose a mechanism where a low MOI gonococcal challenge results in diminished AP-1 acti

222 RNA levels in a CRE-specific manner at a low MOI in both HFF- and NTera2-derived neuronal cells; and

223 ad a direct effect on HIV-1 virions at a low MOI in the absence of serum.

224 At a low MOI, IL-1beta secretion was minimal in CFT073-infected m

225 However, at a low MOI, only one of the genomes is delivered into the cells

226 M-G52, were tested for the ability, at a low MOI, to progressively infect the culture over time, caus

227 ring infection with the VRS mutants at a low MOI.

228 the transduction efficiency 2-fold at a low MOI.

229 d with the canonical CRISPR screens at a low MOI.

230 hancer, the impairment in replication at low MOI corresponds to a deficiency in production of MIE RNA

231 infection (MOI) but replicate poorly at low MOI in comparison to wild-type virus (WT) or HCMVs that

232 ene expression and genome replication at low MOI, but this regulatory function is unnecessary at high

233 At low MOI, stochastic influences appear as kinetic effects whi

234 At low MOI, these working parts likely function in cis to direc

235 poptosis and undergoing proliferation at low MOI, whereas CD3+ T cells did not exhibit this pattern.

236 xamined were protected from apoptosis at low MOI.

237 mediated host antiviral response seen at low MOI.

238 ion of viral US3 RNA was also evident at low MOI.

239 ion of viral components was observed for low MOI stochastic simulations.

240 ptosis at high MOI differs markedly from low MOI apoptosis: it is potently induced by virulent M. tub

241 Induction of IL-8 expression in low MOI challenges was not mediated by an autocrine response

242 virus is required to complete infection (low MOI), the 3'CS is retained due to the need for NSP1 to b

243 The protective effect of low MOI on apoptosis persisted even when B cells were isolat

244 els of HCMV DNA replication at a high or low MOI in HFF.

245 Analysis of various MAPKs indicated that low MOI challenges were able to efficiently activate both th

246 vels of IL-8 that were comparable to the low MOI challenges, but now induced significant levels of TN

247 fection was very efficient, even at very low MOI (>95% infection at a MOI of 6) and did not reduce vi

248 biphasic response to H. pylori, in which low MOI (1-10) markedly inhibited apoptosis, whereas high MO

249 limits the efficiency of reactivation at low MOIs and that competition between genomes occurs at high

250 oductively infected these macrophages at low MOIs but yielded few viable elementary bodies (EBs) when

251 n viral spread during HSV-1 infection at low MOIs.

252 ger antagonist effect than infections at low MOIs.

253 observed in 3 macaques using relatively low MOIs (5-10) in a 48-hour ex vivo transduction protocol.

254 rgeting that we achieved with relatively low MOIs suggest that combining rAAV vectors with DSBs is a

255 longed survival was even found with very low MOIs of 0.1 and 0.5, with survivals of 24+/-4.2 and 25+/

256 lation required populations generated in low-MOI environments.

257 ages, and mutation rates increased under low-MOI-passage conditions.

258 Cells infected at the lower MOI induced more subtypes than cells infected at the hig

259 in human foreskin fibroblast cells, at lower MOIs, the murine CMV enhancer was less efficient.

260 in infected RAW264.7 and THP-1 macrophages (MOI of ~ 0.1).

261 ines in which IGF2 imprinting is maintained (MOI), essentially all of the 3C interactions seen in nor

262 ts place, we propose an alternative measure, MOI(actual), that takes into account the cell concentrat

263 The compound 3-methyleneoxindole (MOI), a photooxidation product of the plant auxin indole

264 ll death, macrophages infected at a moderate MOI did not show signs of cytotoxicity until late in the

265 idarum in macrophages infected at a moderate MOI, implying that chlamydial growth was blocked by acti

266 ent following infection at low multiplicity (MOI = 0.1 PFU/cell) inhibited HCMV in a dose-dependent m

267 Addition of MOI and FWS to multivariate analyses did not increase di

268 In addition, the concept of MOI(actual) allows us to write simple formulas for compu

269 etection of minority clones and estimates of MOI.

270 MDP did not induce IFN-beta, irrespective of MOI.

271 that explain the demonstrated usefulness of MOI at high cell densities, as well as some unexpected c

272 te the relations of fasting and postprandial MOI with total and regional adiposity and insulin sensit

273 ssociated with both fasting and postprandial MOI.

274 hether adiposity influences the postprandial MOI response is unknown.

275 The postprandial MOI response may be influenced by central adiposity in c

276 ed by infection and normalized by the PreS1*-MOI, which is the multiplicity of infection that reflect

277 nfected hepatocytes normalized by the PreS1*-MOI.

278 At the highest relative MOI of 400, survival was prolonged to 58+/-10 days.

279 rolongation was found at the lowest relative MOIs of 0.2 and 1, but there was dose-dependent prolonga

280 codes a yellow-fluorescent-protein (rHSV48Y; MOI = 1).

281 Similarly, MOI may bind in this substrate site.

282 r a low initial MOI or a high superinfecting MOI.

283 Our data demonstrate that MOI-dependent TLR2 activation of macrophages results in

284 (hydroxyethyl)ethacrynic acid indicates that MOI reacts in the active site region involving both the

285 allizable sequencing technologies means that MOI can be detected genome wide by considering the abund

286 These results show that MOI reacts preferentially with GST pi.

287 fold by S-methylglutathione, suggesting that MOI does not react entirely within the glutathione site.

288 OI), as well as the relationship between the MOI and the risk of subsequent malaria.

289 ild type is very sensitive to changes in the MOI (i.e., the degree of complementation) but depends li

290 critical factor in LOD-score analysis is the MOI at the linked locus, not that of the disease or trai

291 istinct antiviral responses depending on the MOI.

292 e increase was inversely proportional to the MOI.

293 h live organisms and was proportional to the MOI.

294 ore the relationship between the traditional MOI and F(WS) approaches.

295 adequacy of the approximate MOI for the true MOI.

296 (multiplicity of infection [MOI], 5), UVCP (MOI, 5), or cHSP60 for 24 h, and the expression of costi

297 The cells infected at the lower viral MOI induced the IFNAR2-dependent IFN-alpha subtypes 4, 6

298 esent the novel finding that different viral MOIs differentially activate JAK/STAT signaling through

299 Infection of CD34(+) progenitor cells with MOIs of 1 to 100 did not impair clonogeneic efficiency o

300 Prolonged survival with MOIs as low as 0.1 and 0.5 indicates that only a minorit