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1 of protection (>1,500-fold reduction in lung virus titer).
2 There was no effect of carrageenan on virus titer.
3 rrespond to the 1- to 2-log-unit decrease in virus titer.
4 onsible for an early rapid decrease in HSV-2 virus titer.
5 ndent upon the duration of APC infection and virus titer.
6 n nasal-lavage specimens, or on quantitative-virus titer.
7 n the G tract had little or no effect on the virus titer.
8 d of the PPT and determined their effects on virus titer.
9 re complex mutations had stronger effects on virus titer.
10 V-activated CD4(+) T-cell blasts reduced the virus titer.
11 ent resulting in > or =100-fold reduction in virus titer.
12 (10- to 50-fold) in viral RNA packaging and virus titer.
13 gnal mutants has defects in RNA packaging or virus titer.
14 the 627K mutant, but it did enhance the lung virus titer.
15 xpression of IFIT3 resulted in a decrease of virus titer.
16 ectedly, anti-IL-22-treated mice had reduced virus titers.
17 lung tissue correlated with the reduction of virus titers.
18 , including a drastic reduction in challenge virus titers.
19 ut do not ultimately control cell-associated virus titers.
20 n-deficient mice contained similar influenza virus titers.
21 ducing a 10- to 1,000-fold reduction in peak virus titers.
22 matic increase in viral RNA accumulation and virus titers.
23 .0 +/- 0.3 days; p < 0.02) despite increased virus titers.
24 and were positively correlated with tracheal virus titers.
25 eter and a 51-fold decrease in extracellular virus titers.
26 ated with severe illness and higher vaccinia virus titers.
27 ection domain generally had small effects on virus titers.
28 the R-peptide yet does not adversely affect virus titers.
29 nes, while anti-F antibody treatment reduced virus titers.
30 rus production onset, and (iii) reduced peak virus titers.
31 s virus (WHV) induces a transient decline in virus titers.
32 nt reduction of viral protein expression and virus titers.
33 g but altered neither antibody responses nor virus titers.
34 alpha-globin mRNA per copy) without reducing virus titers.
35 rotein levels in viral pellets or infectious virus titers.
36 ttC or dptB showed a significant increase in virus titers.
37 lded at least a 1 log decrease in infectious virus titers.
38 Lesion expression did not correlate with virus titers.
39 ologic changes, reflecting reduced levels of virus titers.
40 t a 12-fold increase in encephalomyocarditis virus titers.
41 related to preexisting antibody or to higher virus titers.
44 I1 and HI8), (ii) particles with a decreased virus titer (1 log) but normal infectivity (HI4), and (i
45 was delivered to >80% of cells and inhibited virus titers 10- to 100-fold in a sequence-specific and
46 Treatment on day 0 reduced peak pulmonary virus titers 10- to 100-fold, reduced the severity of vi
48 n (>10 h postinfection [p.i.]) after maximal virus titers (150 to 200 PFU/cell) have been reached, wi
49 RNA displayed widespread eGFP expression and virus titers 16-fold higher than dsbetagal controls afte
50 ces a massive recall response, which reduces virus titers 2-3 days earlier than in nave controls.
51 e vaginal mucosa; 2) had significantly lower virus titers; 3) had decreased overt signs of genital he
54 ment of IRF-3(-/-) BMDCs resulted in reduced virus titers, a far greater reduction was seen after IFN
55 l result in a drastic decrease in infectious virus titers, a reduction in the amount of packaged vira
56 uced EHV-1 production by 23-fold compared to virus titers achieved in cells transfected with the empt
57 ions at Y501 have been shown to decrease the virus titer and affect the specificity of RNase H cleava
61 ed mice exhibited a significant reduction in virus titer and improvement in survival that is associat
64 th a approximately 10-fold reduction in lung virus titer and protection against weight loss when comp
66 n using 2-bromopalmitate (2-BP) affected the virus titer and the interaction of UL20 and gK but did n
69 s could be a major factor in determining the virus titer and, by extension, viral fitness, which coul
70 ulted in a 6-fold reduction of extracellular virus titers and a 13% reduction of plaque diameters, wh
71 selected until after the initial decrease in virus titers and after the development of immune respons
72 e severe pulmonary inflammation, higher lung virus titers and greater weight loss compared with mice
73 assessed by the quantification of infectious virus titers and HCMV genome copies and the detection of
74 vival rates associated with markedly reduced virus titers and immune pathology in the brain but norma
75 l NSV-induced encephalomyelitis, we compared virus titers and immune responses in adult B6 and Bc mic
76 ed with higher virus load because equivalent virus titers and immunohistochemical staining were obser
77 and blockade of PD-L1 in vivo led to reduced virus titers and increased CD8(+) T cell numbers in high
78 able Mcl-1-knockdown cells led to restricted virus titers and increased physical to infectious partic
79 accination decreased postchallenge tear film virus titers and ocular disease incidence and severity w
80 virus, resulted in significant reductions in virus titers and pathological lesions in the liver compa
81 d systemic infection in the ducks, with high virus titers and pathology in multiple organs, particula
85 at this stimulatory effect is independent of virus titers and RSV-induced inflammation; that it is as
90 lted in a significant reduction in pulmonary virus titers, and largely reduced virus-induced lung pat
92 C-CX3CR1 binding and chemotaxis, reduce lung virus titers, and prevent body weight loss and pulmonary
93 influenza-associated morbidity and influenza virus titers, and that these changes in disease severity
96 strategies for retroviral transduction, the virus titers are relatively high and stable and can be f
97 s difference in inflammatory damage, cardiac virus titers are similar between C57BL/6 and Bl.Tg.Ealph
98 corneal infection were found to have ocular virus titers as much as 10(5)-fold higher than that seen
101 o a glycine resulted in a modest decrease in virus titer but a substantial decrease (1 log order) in
103 wn of IFITMs by RNA interference reduced the virus titer by about 100-fold on day 8 postinfection, ac
105 he adjacent region caused a reduction in the virus titer by blocking virus release, and some affected
106 yping contributed to the elevated polytropic virus titer by increasing the efficiency of packaging an
107 diately, evidenced by a 30-fold reduction in virus titer by week 2, declining to a nonquantifiable le
108 inhibitors that block HSP70 function reduces virus titers by up to 1,000-fold, suggesting that this i
109 at 14 days postinfection, a period when the virus titer comes primarily from reactivated latent geno
110 on shutoff (100-fold or greater reduction in virus titer compared to that at 37 degrees C) at 39 degr
112 NP show approximately 100-fold reductions in virus titers compared to controls, while mice immunized
113 mice showed a complete reduction in vaccinia virus titers compared to HCV DNA prime/boost- and mock-i
114 otent antiretroviral therapy and that plasma virus titers correlate, albeit in a nonlinear fashion, w
121 ced morbidity but had no effect on pulmonary virus titers during primary H1N1 infection compared to p
124 ice to SARS-CoV was associated with elevated virus titers, enhanced vascular leakage, and alveolar ed
125 ons caused an initial increase of infectious virus titer followed by a decrease with a longer duratio
127 51g rescued virus (51gR) but yielded reduced virus titers following infection of permissive bovine ce
130 ic relief in addition to reducing infectious virus titers, FST-100 should be a valuable addition to t
131 els in HuH-7 cells significantly affects HCV virus titers, further demonstrating the requirement for
137 verse transcriptase PCR (RT-PCR) analysis of virus titer in L1 thrips revealed a significant increase
139 of mice with 100 PFU of group 1 viruses, the virus titer in lungs was 10(7) PFU/g or 3 log units high
140 that eosinophil deficiency had no impact on virus titer in PVM Ag-vaccinated mice, nor on weight los
142 t there is a significant correlation between virus titer in the bloodstream of infected individuals a
144 e is no absolute correlation between primary virus titer in the eye and TG and the level of viral DNA
145 with CX4C had a 0.7 to 1.2 log10-fold lower virus titer in the lung at 5 days postinfection (p.i.) a
147 tion mutant in terms of disease severity and virus titer in vaginal swabs and central nervous system
150 It may be reasonable to obtain West Nile Virus titers in any patient presenting with the above fi
151 ignificant reduction of dengue and West Nile virus titers in cell-based assays of virus replication,
155 y of these siRNAs significantly reduced lung virus titers in infected mice and protected animals from
156 the CNS of infected mice, it does not affect virus titers in infected mice thymi, spleens or infected
157 na, and this delay correlated with decreased virus titers in infected tissues, compared with mice inf
159 ic reductions in weight loss, mortality, and virus titers in lung and bronchoalveolar lavage fluid af
161 ction, and a 100- to 1,000-fold reduction in virus titers in lymphoid tissue and bone marrow were obs
162 o doses of MVA prevented illness and reduced virus titers in mice who were challenged with either vSC
163 ociated with a broad tissue tropism and high virus titers in multiple organs, including the brain.
164 cation kinetics were assessed by determining virus titers in nasal swabs and respiratory tissues, whi
166 n only day 5, but E caused more reduction of virus titers in old than in young mice (25-fold vs. 15-f
167 of 1 and 10 mg/kg/day significantly reduced virus titers in organs and provided 60% and 80% survival
172 at 5 days postinfection (peak of infectious virus titers in the central nervous system) compared to
175 delayed until 2 and 4 days after infection, virus titers in the eye were analogous to those in the c
176 even after corneal scarification, had lower virus titers in the eye, had less latency in the TG, and
177 avirulent (KOS and RE) strains of HSV-1, and virus titers in the eyes and TG during primary infection
178 s, (ii) virus antigen shedding or infectious virus titers in the feces or intestinal contents measure
179 the liver, there was no correlation between virus titers in the gut and detection of virus in the li
180 / SA11-Cl4 reassortants and determination of virus titers in the gut and liver revealed that the extr
181 CVB3 resulted in approximately 50-fold-lower virus titers in the heart and approximately 6-fold-lower
183 tion with RSV showed substantially decreased virus titers in the lung and decreased inflammation and
184 nza virus resulted in dramatically increased virus titers in the lung and intranasal cavity of mutant
186 ein gene and PEI87 resulted in a 94% drop of virus titers in the lungs of influenza-infected animals.
189 d lower at 2 days post-RacL11 challenge than virus titers in the lungs of nonimmunized mice, indicati
191 gher virus excretion via the nose and higher virus titers in the nasal turbinates than intratracheal
193 ociated with lethality, significantly higher virus titers in the respiratory tract, virus disseminati
196 Topical drug treatment markedly reduced virus titers in the skin and snout, whereas parenteral t
197 Immunized ferrets had significantly lower virus titers in the upper respiratory tract and less-sev
201 yet retained growth dynamics, stability, and virus titers in vitro that were similar to those of the
204 irus initially replicated to low titers, but virus titer increased significantly after mutations appe
206 l of intravenous JEV infection, we show that virus titers increased exponentially in the brain from 2
208 ion of mouse cells with 16/L leads to higher virus titers, increased production of RNA, and total cyt
209 s among healthy, full-term infants; however, virus titers, inflammation, and Th2 bias are proposed ex
211 ce were euthanized 5 days postinfection, and virus titers, levels of neutralizing antibodies, and num
212 e non-1 (75% vs. 56%) and in patients with a virus titer < 2 x 10(6) copies/mL (93% vs. 43%).
213 and had no significant reductions in tissue virus titers observed on day 5 post-H5N1 virus challenge
214 erefore, based on the analysis of CIT50, the virus titer of a given sample can be determined from the
216 were similar for Ncal99 and Sw30, with peak virus titers of 10(5.1) 50% tissue culture infectious do
220 ed 30 ppm of E had significantly higher lung virus titers on days 2 and 7 after infection than young
221 SV-2 strain resulted in significantly higher virus titers on days 3 to 7 but only slightly delayed re
224 here were no differences among the groups in virus titers or the route and timing of virus spread in
225 progression, hematology, serum biochemistry, virus titers, or lethality in nonhuman primates infected
231 l cell shedding accelerated the reduction of virus titers, presumably by clearing virus-infected cell
234 ical serum specimens (genotypes 1 to 6, with virus titers ranging from 15.1 to 2.1 x 10(7) IU/ml) sho
237 e observed a log-linear relationship between virus titer reduction and the number of rPMP molecules i
239 edia of infected cells has demonstrated that virus titers released from the apical surface are about
241 different methods available for determining virus titers such as plaque assays end-point dilution, q
242 although this mutation significantly reduced virus titer, suggesting that removing three nucleotides
244 cided with a 100- to 1,000-fold reduction in virus titer, supporting the hypothesis that the HPIV1 C
245 fectious progeny for weeks, producing higher virus titers than late-gestation cells that varied by do
246 tro and the SSTT mutation resulted in higher virus titers than were observed for the parental rOka st
248 replicate in primary fibroblasts, attaining virus titers that were 2 to 3 orders of magnitude lower
249 ated in all animals with a 2-log decrease in virus titer, the timing occurred approximately 2 weeks l
250 ere characterized by a continual decrease in virus titer, the titers in the persistent infections rea
252 virulent HSV-2 strain resulted in a rise in virus titers to levels comparable to those of nonimmune
256 iameter change data were used to compute the virus titer using a statistical method called the method
259 inoculation with poliovirus, no increase in virus titer was detected in the feces of TgFABP-PVR mice
261 was competent for virion formation, but the virus titer was reduced 4.5-fold relative to that of the
262 on and binding to the receptor; however, the virus titer was reduced 5- to 45-fold, indicating a post
267 mal cell damage in rat myocytes if the SERCA virus titer were maintained within 1 to 4 plaque-forming
270 f resistant lines carrying Ty-1 or Ty-3, low virus titers were detected concomitant with the producti
272 ected monkeys secreted virus, while marginal virus titers were detected in tracheal lavage fluid cell
278 the heart; in the absence of such signaling, virus titers were markedly elevated by day 3 postinfecti
279 In the absence of an intact ISG15 system, virus titers were markedly elevated by postinfection day
281 with the parental virus (pH1N1/NS1-wt), yet virus titers were not significantly increased in cell cu
286 us were treated with the 5'End or 3'CSI PMO, virus titers were reduced by approximately 5 to 6 logs a
287 Consistent with antibody responses, lung virus titers were significantly higher in obese mice tha
288 n the lungs of both Nu/Nu and Nu/+ mice, but virus titers were significantly higher in T cell-deficie
289 erforin and Fas or neither perforin nor Fas, virus titers were significantly lower than in control mi
292 ry steps of the virus life cycle because the virus titers were similarly inhibited from infected cell
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
300 egulation decreases extracellular infectious virus titers with little effect on intracellular RNA con
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