ライフサイエンスコーパス: virus load

1 (odds ratio [OR], 1.31 per log10 increase in virus load).

2 a reduction in the magnitude and duration of virus load.

3 with elevated inflammatory markers and high virus load.

4 n have previously been associated with lower virus load.

5 infection and are inversely associated with virus load.

6 tis, who have a relatively high Epstein-Barr virus load.

7 arations and were not in proportion to local virus load.

8 , FTC produced a 1.7-log10 mean reduction in virus load.

9 vitro is a significant determinant of plasma virus load.

10 t of initial number of naive T cells and HIV virus load.

11 with a rise in cell-associated Epstein-Barr virus load.

12 wer CD4:CD8 ratio and a dramatic increase in virus load.

13 rkers of disease progression, in addition to virus load.

14 nd naive T cells and negatively with age and virus load.

15 o predict sustained long-term suppression of virus load.

16 duction is associated with decreased in vivo virus load.

17 with infant infection, independent of plasma virus load.

18 s, and demonstrated a trend toward decreased virus load.

19 contact to the index patient with high serum virus load.

20 c reproductive ratio of the virus, R(0), and virus load.

21 ed a typical maximum of 1.5 log reduction in virus load.

22 reactive, there was no measurable effect on virus load.

23 l [CI], 1.29-1.64) per 1 log(10) increase in virus load.

24 leads to a stable chronic infection at high virus load.

25 loads in treated adults who had undetectable virus loads.

26 develop slowly, even in the presence of high virus loads.

27 py (HAART) with undetectable (<50 copies/mL) virus loads.

28 the only predictor of achieving undetectable virus loads.

29 SHV peripheral blood mononuclear cell (PBMC) virus loads.

30 s and developed gross splenomegaly with high virus loads.

31 nt at inducing CD8 cell proliferation at low virus loads.

32 ls, which were partly dependent on increased virus loads.

33 V-PPR challenge and exhibited similar plasma virus loads.

34 nt for pathogenicity and maintenance of high virus loads.

35 del predicted that 95% of children had early virus loads 3.75-5.04 log10 copies/mL and slopes -0.07 t

36 in 145 of 978 maternal saliva samples (mean virus load, 488,450 copies/mL; range, 1550-660,000 copie

37 pt 1 were confirmed as HHV-6 variant A (mean virus load, 5066 copies/10(6) peripheral blood leukocyte

38 L) and in 12 of 43 breast-milk samples (mean virus load, 5800 copies/mL; range, 1550-12,540 copies/mL

39 d with every 10-fold increase in breast-milk virus load (95% confidence interval, 1.3-3.0; P<.001).

40 on was observed (odds ratio [OR], 2.20/1-log virus load; 95% confidence interval [CI], 1.15-4.18).

41 tal HIV detection was associated with plasma virus loads above 3.15 log(1)(0) copies/mL (95% confiden

42 9% of subjects had reproducible undetectable virus loads, according to repeat measurements (virologic

43 ved or maintained a >or=2 log10 reduction in virus load after 6 months.

44 ndetectable (<400 copies/mL) than detectable virus loads after the initiation of therapy.

45 Virus load, age, and malaria parasite coinfection play a

46 adjustment for pre-ART CD4(+) T-cell count, virus load, age, and sex, a higher month 12 KT ratio pre

47 or V3 populations, suggesting that the high virus loads allowed the env populations to reequilibrate

48 Virus load also declined more rapidly in carriers of bot

49 ely correlated with repeated measurements of virus load, although the significance was lost once the

50 ssion, the reasons for variability in plasma virus loads among infected individuals are not fully und

51 hat during periods of sustained undetectable virus loads among the case subjects themselves, if avail

52 t significant overlap in the range of plasma virus loads among transmitters and nontransmitters is of

53 High virus load and advanced immunosuppression correlated wit

54 This treatment can reduce virus load and ameliorate disease symptoms.

55 Virus load and antibody responses were also similar, alt

56 studies suggest that, after controlling for virus load and CD4 cell count, anemia is related to dise

57 Virus load and CD4 cell counts were not significantly al

58 (CVL) ADCC titers were compared with plasma virus load and CD4 cell number in 45 infected and 10 uni

59 lost once the measurements were adjusted for virus load and CD4(+) cell count at baseline, by use of

60 These markers were related to clinical (virus load and CD4(+) cell count) and immunological (HIV

61 Plasma virus load and CD4+ and CD8+ T cell subsets were measure

62 Thai and US women were evaluated for tissue virus load and histologic makeup.

63 sessed the relationship between HIV-2 plasma virus load and immune system activation in a cross-secti

64 There was no correlation between virus load and M. avium load in coinfected lymph nodes,

65 vaccine on the basis of observed effects on virus load and other postinfection surrogate end points

66 e basis of the extent of the initial drop in virus load and the duration of virus load reduction.

67 In hepatitis C virus (HCV) infection, virus load and the risk for HCV-related end-stage liver

68 morbidity and death, higher set point plasma virus load and virus acquisition; thus, therapeutic agen

69 of antibodies to CD134 correlated with lower virus loads and a better overall health status in FIV(+)

70 s previously associated with distinct plasma virus loads and altered rates of disease progression; on

71 lowest postchallenge viremia generated high virus loads and an irreversible loss of CD4(+) T-cell lo

72 n of the respiratory tract, following higher virus loads and higher IFN production in Ifit2(-/-) lung

73 Higher early virus loads and higher slopes were each associated with

74 ponses, significant reductions in both acute virus loads and pathology and, most importantly, long-te

75 interleukin-2 in place of nef developed high virus loads and progressed to simian AIDS.

76 with recombinant MVA-SIV vaccines had lower virus loads and prolonged survival relative to control a

77 ts were comparable at T0 in age, CD4 counts, virus load, and B cell immunophenotypic characteristics.

78 ibody therapy on 5-year disease progression, virus load, and host immunity were explored.

79 ronic exercise resulted in reduced symptoms, virus load, and levels of inflammatory cytokine and chem

80 White ethnicity, higher pre-HAART virus load, and lower pre-HAART CD4 and CD8 cell counts

81 meters, syncytium-inducing phenotype, higher virus load, and mutation in HIV-1 pol encoding the T69D/

82 zed in relation to route of virus challenge, virus load, and neutralizing antibody (NAb) titers durin

83 urs mainly directly and scales linearly with virus load, and virulence or immune responses are neglig

84 udied the frequency of infected cells, total virus load, and virus load per infected cell in PBMCs fr

85 We compared the pathological lesions, virus loads, and distribution of virus and target cells

86 These data suggest that virus loads are the main reason for the increased streng

87 Models were combined using virus load as a parameter of infectivity.

88 the well-established and powerful effects on virus load at different stages of infection.

89 t for covariates (CD4(+) T cell lymphocytes, virus load at enrollment, level of neutropenia and antir

90 Virus load at study entry did not predict outcome, but p

91 Plasma virus loads at necropsy ranged from 11 to 28 copies of v

92 pregnant mice was not associated with higher virus load because equivalent virus titers and immunohis

93 Most subjects had several relatively stable virus loads before initiation of antiretrovirals, indica

94 group comparisons showed a mean decrease in virus load between hydroxyurea/didanosine versus didanos

95 ed CSF HIV RNA loads usually represented CSF virus load blips.

96 ted atazanavir [ATV]) with suppressed plasma virus loads, blood and cervicovaginal samples collected

97 adjustment for pre-ART CD4(+) T-cell count, virus load, body mass index, sex, and age, a higher pre-

98 fied viruses (10(8) RNA copies) and measured virus load by quantitative RT-PCR.

99 all of the controls, and showed undetectable virus loads by day 42 postchallenge.

100 apy and predict that individuals with a high virus load can be switched to a low-viremia state that w

101 protease can result in dramatic decreases in virus load, causing a contraction in the virus populatio

102 4(+) T cells while receiving HAART, baseline virus load, CD4(+) T cell count at the time therapy was

103 virus was used to mirror what may happen if virus-loaded cells pass through an epithelium or perhaps

104 In an individual patient, a CSF virus-load change >0.5 log(10) copies/mL may be clinical

105 terize, over time, cerebrospinal fluid (CSF) virus-load change in clinically stable patients, human i

106 change and sampling time interval, baseline virus load, change in virus load, or development of NNRT

107 ry, detection of additional viral types, and virus load changes during follow-up influence histologic

108 an inhibitor of iNOS, resulted in increased virus load compared to nontreated chickens.

109 However, in multivariate analyses, elevated virus load continued to be the predominant risk factor f

110 did not predict outcome, but pre-study-exit virus load correlated with a histologic outcome of any C

111 istologic outcome of any CIN, and changes in virus load correlated with risk for an outcome of CIN2/3

112 d by a "shoulder phase" (4-28 days) in which virus load decays slowly or remains constant, and a thir

113 sists of a first phase (1-2 days) with rapid virus load decline, followed by a "shoulder phase" (4-28

114 e in the method of efavirenz administration, virus loads declined again and remained undetectable in

115 BK virus load decreased in 3 of 3 patients after the reduct

116 Upper and lower respiratory tract virus load, duration of virus shedding, select mucosal c

117 ection was associated with greater change in virus load during follow-up.

118 n the same immunized macaques, a decrease in virus load during primary infection (P = 0.0078) and pro

119 with rate of initial HIV clearance (P=.002), virus load during set point (P=.008), and CD4(+) cell co

120 Thalidomide therapy did not affect virus load, even though none of the children was receivi

121 Subjects with a strong initial drop in virus load exhibited a loss of heterogeneity in the env

122 ntrast, subjects with a weak initial drop in virus load exhibited little to no loss of heterogeneity

123 the infected respiratory tract slowed at low virus loads following challenge of naive and previously

124 rus neutralizing antibodies, confers reduced virus loads following challenge with two heterologous is

125 The mean+/-SEM CD4(+) T lymphocyte count and virus load for all patients were 237+/-41 cells/mm(3) an

126 nts (control subjects), who had undetectable virus loads for 3 consecutive months, and (2) that durin

127 y be influenced by the elevated Epstein-Barr virus load found in rheumatoid arthritis patients and ma

128 ction by day 30 and 1 mouse had undetectable virus load from day 6 onward.

129 ratio inversely correlated with the cellular virus load from the corresponding compartment.

130 re not associated with effects on mortality, virus load, genital shedding, or transmission in this co

131 progressors have higher plasma and lymphoid virus loads, greater CD38 expression in CD8(+)/HLA-DR(+)

132 detected among 11 of 13 patients carrying a virus load >100 copies/10(5) lymphocytes.

133 s the first of 2 consecutive measurements of virus load >500 human immunodeficiency virus RNA copies/

134 with CD4 cell counts >/=50 cells/microL and virus loads >/=500 copies/mL.

135 y detected 54 to 100% of spiked samples with virus loads >10,000 copies/ml and 68% of the clinical sa

136 eficiency virus (HIV)-infected patients with virus loads >5000 and <100,000 copies/mL who were naive

137 Children with high respiratory syncytial virus loads (>/=3.16 x 10(7) copies/ml) experienced incr

138 The plasma virus load had been approximately the same for 16 years

139 TL, followed by a decline to low levels once virus load has been significantly suppressed.

140 ect escape mutations concurrent with falling virus load in acute infection.

141 g HIV-1 infection are capable of suppressing virus load in blood to undetectable levels, and result i

142 Antibody to IFN-gamma resulted in increased virus load in both B6 and B6-lpr mice and eliminated the

143 e explains much of the variability in plasma virus load in chronic HIV-1 infection.

144 The polytropic virus load in coinoculated mice was markedly enhanced, w

145 Within women who breast-fed, median virus load in colostrum/early milk was significantly hig

146 Two subjects had an increasing virus load in consecutive CSF samples, representing poss

147 rrelation was found between IP-10 levels and virus load in CSF (r2=.777; P=.0007).

148 f rhinovirus-induced asthma exacerbation and virus load in experimentally infected human volunteers.

149 retroviral therapy and techniques to monitor virus load in humans have demonstrated that the early st

150 infection, which correlated with a decreased virus load in mice infected with MHV68-IkappaBalphaM com

151 rvation is in contrast to the relatively low virus load in milk compared to that in plasma of SIV-inf

152 ated antiviral activity is linked to reduced virus load in multiple lymphoid tissues.

153 The virus load in one of these two animals rebounded; virus

154 model, it lowered the viremia level and the virus load in organs and normalized levels of cell-damag

155 The virus load in PB2-E158G-infected mouse lungs was 1,300-f

156 although there was no consistent decrease in virus load in peripheral-blood mononuclear cells.

157 The maximum CMV virus load in plasma was >1 log(10) higher among case pa

158 sue (LT) to account for virus production and virus load in plasma.

159 ype 1 require continuous nondetectability of virus load in serum for 36 and 32 weeks, to attain 90% a

160 trolled viremia caused an increase in tissue virus load in some animals, suggesting a role for CD8(+)

161 Assessment of cell-associated virus load in T cell subsets in multiple anatomic compar

162 Pre-treatment geometric mean Ebola virus load in the 14 TKM-130803 recipients was 2.24 x 10

163 ion and transmission in ducks, increased the virus load in the ferret nasal cavity early during infec

164 infection while simultaneously reducing the virus load in the lungs.

165 Virus load in the plasma was monitored along with combin

166 is associated with an eightfold increase in virus load in the seminal plasma compartment.

167 cell content, was correlated inversely with virus load in the thymus and blood.

168 The longer reduction of virus load in these subjects may have allowed for improv

169 s a sequence-independent means of monitoring virus loads in HIV-1 group O-infected patients.

170 Virus loads in plasma at the set point were significantl

171 to the (-)-FTC therapy induced a decrease in virus loads in plasma, these loads eventually returned t

172 se brain tissue revealed significantly lower virus loads in SPBNGAN-GAK- and SPBNGAK-GAN-infected bra

173 tract, liver, and kidney sustain high plasma virus loads in the absence of CD4(+) T cells.

174 e primary EBV exposure carry relatively high virus loads in the B-cell, but not the NK- or T-cell, co

175 g persistent infection characterized by high virus loads in the central nervous system (CNS) in the a

176 allenge and reduced pathological changes and virus loads in the lungs at early times after infection.

177 Three controller macaques had chronic phase virus loads in the range of 1 x 10(3) RNA copies/ml, whe

178 loped a real-time PCR assay to quantitate BK virus loads in the setting of renal transplantation, and

179 ansplant recipients who developed persistent virus loads in their peripheral blood lymphocytes after

180 tudinal, clonal genotypic analysis of plasma virus loads in treated adults who had undetectable virus

181 virus (EBV) have a unique ability to amplify virus loads in vivo through latent growth-transforming i

182 Ebola virus RNA levels (virus load) in PBMC specimens were found to be much high

183 us type 1 (HIV-1) acquisition and subsequent virus loads, in a prospective cohort study of women in M

184 Irrespective of virus load, incidence of ESLD was marginally increased 2

185 on was 4.46 log10 copies/mL, and the average virus load increase during subsequent follow-up was 0.00

186 As the virus load increased above this threshold, the magnitude

187 three animals after 36 weeks of therapy, and virus loads increased rapidly.

188 Virus loads increased slightly between 12 and 16 weeks o

189 cle dysfunction was associated with a higher virus load, increased mRNA expression of the macrophage

190 Virus load increment with HIV or HTLV-II infection was h

191 The rate of progression of fibrosis and virus load inversely correlated with intrahepatic HCV-sp

192 ion between lymphoproliferative response and virus load is established early during HIV-1 infection a

193 The results show that virus load is highest in B cells.

194 eded in order to ensure virus clearance when virus load is reduced by the immune system.

195 but also bring into question the notion that virus load is regulated predominantly by the virus-speci

196 age, sex, genital ulcer, and index partner's virus load) known to influence transmission of HIV-1 sel

197 ter of 400 was significantly correlated with virus load late in infection.

198 Co-infection with HIV increases HCV virus load, liver-related mortality, and the risk of sex

199 des evidence of strong relationships between virus load, lower airway virus-induced inflammation and

200 Higher maternal plasma virus load, lower maternal CD4 T cell count, and detecti

201 n the virus load was below a threshold (peak virus load < 225 genomes per mL, or integrated virus loa

202 rus load < 225 genomes per mL, or integrated virus load < 400 genome days per mL), the magnitude of t

203 ter cumulative proportion of time spent with virus load <400 copies/mL was associated with a more fav

204 each extra 10% cumulative time spent with a virus load <400 copies/mL) (P<.0001).

205 risk ratio, 8.8 and 51.5 among patients with virus loads < or =2860 and >2860 copies/10(6) peripheral

206 resume treatment and continued to have a low virus load (<1080 HIV-1 RNA copies/mL) and persistent an

207 a significant, although modest, decrease in virus loads (maximum median, -0.86 log(10)) and increase

208 We propose that increasing virus load may contribute to systemic immune activation

209 aried with cytologic findings at the time of virus load measurement.

210 l CD4 cell counts and human immunodeficiency virus load measurements.

211 model was fitted to sequential quantitative virus load measurements.

212 antigen after in vitro coculture with highly virus-loaded monomyeloid precursors from the patients.

213 Neither dichotomized human immunodeficiency virus loads nor dichotomized CD4 counts predicted either

214 ame for 16 years when a 100-fold increase in virus load occurred in years 17 and 18.

215 Of 21 children with a transient decrease in virus load of > or = 0.7 log(10) HIV RNA copies/mL from

216 A CSF-associated virus load of >20 copies/mL was associated with higher C

217 ctively; 84%, 84%, and 80% of subjects had a virus load of <400 copies/mL during the same periods.

218 us suppression (i.e., time since achieving a virus load of <400 HIV RNA copies/mL) among both the nuc

219 response defined as significant decrease of virus load of at least 2-logs10.

220 on by sexual contact, but the association of virus load of hepatitis C virus (HCV) with risk of HCV t

221 There was no decrease in the virus load of KSHV in peripheral blood mononuclear cells

222 At 24 hours after infection, the virus load of RV-B (RV-B52, RV-B72, or RV-B6) in adheren

223 It also decreased the virus load of the BECs.

224 <10,000 RNA copies/ml and all 29 with plasma virus loads of >10,000.

225 say detected 100% of the spiked samples with virus loads of >250,000 copies/ml and 61% of the clinica

226 lifiable, including 8/11 (72.7%) with plasma virus loads of <10,000 RNA copies/ml and all 29 with pla

227 oncurrently, 92 (83%) achieved or maintained virus loads of <50 copies/mL, and 99 (89%) achieved or m

228 pies/ml and 61% of the clinical samples with virus loads of 219 to 288,850 copies/ml.

229 CD8(+) T-cell responses when present during virus-loading of DCs or for the time of the DC-T-cell co

230 mothers through vaccination may reduce milk virus load or protect against virus transmission in the

231 ime interval, baseline virus load, change in virus load, or development of NNRTI resistance.

232 ations at baseline had greater reductions in virus load over time than did children who did not.

233 KT ratio was associated with a higher plasma virus load (P < .001) and lipopolysaccharide level (P =

234 uring the chronic phase (1.7 log decrease in virus load, P = 0.009).

235 Sputum virus load peaked on Days 5-9 and bacterial load on Day

236 ncy of infected cells, total virus load, and virus load per infected cell in PBMCs from men coinfecte

237 IVmac bearing M184V achieved high, sustained virus loads, perhaps with a compensatory effect of the P

238 ZIKV infection was associated with maternal virus load, prior dengue antibodies, or abnormal pregnan

239 3 beta-herpesviruses was more significant by virus load quantitation than by qualitative detection of

240 is suppression, HIV-1 infection persists and virus load quickly rebounds when therapy is interrupted.

241 T-cell response correlated strongly with the virus load (R(2) approximately 0.63).

242 Mean virus loads ranged from 3 to 330 copies per infected PBM

243 ibited little to no loss of heterogeneity at virus load rebound in either region of env examined.

244 d further resistance mutations subsequent to virus load rebound, no changes were observed in V1/V2 or

245 a loss of heterogeneity in the env region at virus load rebound; in contrast, subjects with a weak in

246 The duration of virus load reduction also affected env populations.

247 mens and that early viral dynamics or week 1 virus load reduction measurements may be useful in evalu

248 itial drop in virus load and the duration of virus load reduction.

249 Week 24 virus load reductions and CD4 cell changes were similar

250 rrelated with baseline RNA levels and week 1 virus load reductions.

251 rthermore, our data suggest that, if the CSF virus load reflects the size of the reservoir of infecte

252 s could be infected in BAFF-R(-/-) mice, but virus loads remained low.

253 Patients with virus loads remaining >400 RNA copies/mL plasma were cla

254 The relationship between the pattern of virus load response to highly active antiretroviral ther

255 -2 before and after storage, suggesting that virus-loaded scaffolds may be convenient for application

256 iency virus type 1 (HIV-1)-infected persons, virus load (serum/plasma level of HIV) predicts outcome.

257 ag may be important for the establishment of virus load set point.

258 -189) epitope correlated negatively with the virus load set point.

259 Postchallenge pulmonary virus loads show that these vectors provide sterilizing

260 d METH(-)Tox- subjects'; cerebrospinal fluid virus loads showed a similar but nonsignificant trend.

261 he value of R(0) and the predictions for the virus loads, so the effects on the infection dynamics ar

262 Moreover, in the 13 treated monkeys, plasma virus loads subsequently declined to undetectable levels

263 Importantly, 10E8V2.0/iMab reduced virus load substantially in HIV-1-infected humanized mic

264 However, a long-term relatively high virus load, such as that in SM E041, is consistent with

265 during pro gene sequence transitions at high virus load suggests that recombination is active in defi

266 ich allows us to incorporate measurements of virus load, target cells, and virus-specific immunity an

267 HIV-1 RNA quantitation in plasma, or virus load testing, is the primary method by which the r

268 6A-infected cats consistently carried higher virus loads than FRA-infected cats.

269 This study identifies a relative cutoff virus load that predicts subsequent development of CMV d

270 Five of the infected monkeys maintained high virus loads; the sixth, which was infected with the E89G

271 e 10-1074 antibody caused a rapid decline in virus load to undetectable levels for 4-7 days, followed

272 Virus load trends have been characterized in adults and

273 Virus load trends in 22 male children with hemophilia wh

274 In conclusion, those subjects had virus load trends similar to those in adults.

275 Virus loads varied greatly among cohort individuals but,

276 We show that: (i) the plateau virus load (VL) reached after STIs correlated with pretr

277 Mechanisms that underly discordant CD4+ cell/virus load (VL) responses in patients who receive highly

278 tive analyte for lower-cost quantitative HIV virus load (VL) testing to monitor antiretroviral therap

279 ible pattern was found in changes of vaginal virus loads (VVLs) during the menstrual cycle.

280 Compared with HIV(-)/HTLV-II(-) subjects, virus load was 0.50, 0.22, and 0.56 log(10) higher in HI

281 e for detection of CIN-3 on the basis of the virus load was 0.70 (95% CI, 0.61-0.78).

282 Median initial pretreatment plasma virus load was 25,800 copies/mL (range, undetectable-262

283 When the virus load was below a threshold (peak virus load < 225

284 Semen virus load was more variable, 1.3 log(10) lower and mode

285 ith other SIV isolates, we observed that the virus load was not significantly lower in Mamu-A*01-posi

286 esized that the longer the duration that the virus load was rendered undetectable in serum, the bette

287 Virus load was significantly lower in infected pups born

288 In asthmatic, but not normal, subjects virus load was significantly related to lower respirator

289 antiretroviral therapy (HAART) revealed that virus loads were higher only in those Tox+ subjects who

290 In some individuals, mean virus loads were less than 10 genomes per infected cell,

291 Early virus loads were lower than those in vertically infected

292 BK virus loads were measured in urine, plasma, and kidney b

293 Provirus and RNA virus loads were obtained, the samples were screened for

294 Virus loads were only different after 10 days postinfect

295 Tox+ subjects' plasma virus loads were significantly higher than METH(+)Tox- a

296 lude a lengthened incubation period; reduced virus load, which acts to lower infectiousness; reduced

297 breast-feeding is influenced by breast-milk virus load, which is highest early after delivery.

298 The loss of CTL did not affect plasma virus load, which remained elevated for both groups.

299 cient at inducing CD8 cell expansion at high virus loads, while the CD4-APC-CD8 pathway is more effic

300 al transplantation, and we correlated the BK virus load with clinical course and with the presence of