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1 and drives CD4 decline independently of the viral load.
2 gical sequelae at 6 months of age, or plasma viral load.
3 enes and gene sets for an influence on HIV-1 viral load.
4 ntiviral interferon expression and decreased viral load.
5 at any time during hospitalization, and high viral load.
6 ght loss, airway inflammation, and pulmonary viral load.
7 after RSV infection associated with reduced viral load.
8 with antiretroviral exposure and low plasma viral load.
9 HCV infection was defined by detectable HCV viral load.
10 on HBsAg testing and had an undetectable HBV viral load.
11 redictors of patient outcome, independent of viral load.
12 motor impairment, mortality, and spinal cord viral load.
13 group, calendar year, cohort, CD4 count, and viral load.
14 over time and correlated with the individual viral load.
15 f infected cells in the intestine and plasma viral load.
16 spiratory symptoms, lung function, and nasal viral load.
17 wed a significant, positive correlation with viral load.
18 s in infected mice and decreased spinal cord viral loads.
19 pairment, increased mortality, and increased viral loads.
20 iruses by lessening weight loss and lowering viral loads.
21 oxetine had no effect on motor impairment or viral loads.
22 (>50,000) or low (<10,000 HIV RNA copies/ml) viral loads.
23 th CD4 T cell counts and positively with HIV viral loads.
24 ive antiretroviral therapy with undetectable viral loads.
25 and HPS/CTM v2 in samples with quantifiable viral loads.
26 utations showed no significant difference in viral loads.
27 r BA, infants with GA5 infections had higher viral loads.
28 atients with CMV pneumonia had higher median viral loads (3.9 log10 IU/mL; interquartile range [IQR],
30 At baseline, 9 patients had a detectable HBV viral load, 7 had positive results on hepatitis B surfac
33 nical virology, and accurate quantitation of viral load among labs requires the use of international
35 ART, as reflected by a rapid drop in plasma viral load and a dramatic decrease in the levels of cell
36 disease severity and viral load (P = .994); viral load and adverse outcomes (P = .667; OR: 1.02; 95%
37 e breastfeeding; ART treatments can suppress viral load and are key to preventing transmission to the
38 Treg cells was analyzed and correlated with viral load and CD4(+) T-cell counts/percentages in 93 HI
42 prick blood samples, the Cepheid Xpert HIV-1 Viral Load and HIV-1 Qual cartridges were compared with
43 ody levels, ASCs and HAI titers with reduced viral load and inflammatory responses in the cVLP group.
44 ans was correlated positively with set-point viral load and negatively with duration of viral suppres
45 Importantly, it reveals that initial high viral load and neutralizing IgG response may function in
46 approved medications can reliably reduce the viral load and prevent the progression of liver diseases
47 lpha (IL-27RA) axis as a predictor of plasma viral load and proviral copy number in the peripheral bl
48 immune response and as robust correlates of viral load and proviral reservoir size in PBMC.IMPORTANC
49 conclusion, the correlation between patient viral load and replication kinetics of RSV patient isola
50 omatic cases in the relationship between the viral load and the response kinetics, emphasizing how mu
52 ness in which patients have high circulating viral loads and an exaggerated virus-induced immune resp
56 um is especially susceptible, harboring high viral loads and displaying marked neuropathology, with m
57 ETH users have been shown to have higher HIV viral loads and experience more severe neurological comp
60 -deficient mice had significantly higher CNS viral loads and mortality rates than wild-type animals.
61 yte (Hu-PBL)] mice by completely suppressing viral loads and preventing human CD4(+) T-cell loss.
62 s (HIV or SIV), respectively, express higher viral loads and progress more rapidly to AIDS than infec
63 graft removal, which led to decreasing serum viral loads and resolution of neurological symptoms.
64 of clinical signs for 2 years, despite high viral loads and the accumulation of large intracellular
65 DENV2 infection on the basis of undetectable viral loads and the lack of an anamnestic antibody respo
66 (HBsAg) testing and had an undetectable HBV viral load, and 3 had negative results on HBsAg testing
67 eloped more-severe immunosuppression, higher viral load, and a broader range of clinical signs typica
68 ltivariable analysis, age, historical plasma viral load, and ART regimen changes prior to interruptio
69 eristics, neuroimaging abnormalities, plasma viral load, and audiological and neurological outcomes o
72 60 after adjusting for age, tobacco smoking, viral load, and traditional risk factors (odds ratio [OR
73 tegrated next generation sequencing, patient viral load, and viral replication analysis with surveill
74 the blood-brain barrier (BBB), higher brain viral loads, and higher brain inflammatory cytokine and
75 lerated viral suppression, further decreased viral loads, and reduced the persistently infected HIV r
81 in serum and plasma by the Cepheid Xpert HCV Viral Load assay in comparison to the Abbott RealTime HC
83 rnal quality assessment panel, the Xpert HCV Viral Load assay results (quantified in log10 IU per mil
84 e evaluated the performance of the Xpert HCV Viral Load assay with venepuncture and finger-stick capi
86 ed virologic response as defined as negative viral load at 12 weeks postcompletion of therapy and all
91 the fraction of variation in HIV-1 set point viral load attributable to viral or human genetic factor
93 were significantly higher in patients with a viral load below 800 000 (100% vs 83.9%, P value = 0.022
96 ciency virus (SHIV), we observe a lower peak viral load but an unchanged viral set point during viral
97 d the EVGcobi groups reached an undetectable viral load but only 58.3% in the DRVrtv arm (P = .003).
98 associated with mean CD4 cell counts or HIV viral load but was associated with younger maternal age
99 ior to ART did not correlate with HIV plasma viral load, but positively associated with plasma sCD14
100 % of those on treatment to have a suppressed viral load by 2020, with each individual target reaching
102 with a lethal dose of Ebola virus suppressed viral loads by more than 5 logs and protected animals fr
103 use showed no significant associations with viral load, CD4 counts, AIDS, cancer, or mortality in bo
104 Traditional cardiovascular risk factors, HIV viral load, CD4 lymphocyte count, statin use, antihypert
105 te with HIV disease progression, measured by viral load, CD4 percentage, CD4:CD8 T-cell ratio, and im
106 ated with markers of viral disease activity (viral load, CD8+ T cells, and CD4/CD8 ratio) and CD4+ T-
109 ficient for the virus to evolve intermediate viral loads consistent with maximising transmission, as
115 However, there was substantial overlap in viral load distribution of cases and controls for all vi
116 ammation whose expression is associated with viral load during experimental rhinovirus infection of a
117 g revealed that patients with higher initial viral loads during the acute phase of illness had poor p
118 d used to measure CD4 cell count and HIV RNA viral load every 3-6 months (when below the threshold) o
119 models of character evolution describing how viral load evolves on the phylogeny of whole-genome vira
120 research showing the benefits of suppressed viral load for the individual and the whole population.
123 icipants with virological rebound (confirmed viral load >/=50 copies per mL or premature discontinuat
124 mL or premature discontinuations, with last viral load >/=50 copies per mL) cumulative through week
125 esentation: 40 of 43 patients (93.0%) with a viral load >/=7.0 log10 copies/mL serum developed the ex
127 ernal hepatitis B e-antigen (HBeAg) and high viral load have been noted to be the most important risk
129 ablated interferon production and increased viral load; however, the heightened immunopathology and
130 can predict CD4 decline independently of the viral load (HR = 2.9; P = 0.004) or protective HLA allel
132 eck") that includes stabilising selection on viral load; (iii) we controlled for covariates, includin
134 tent reservoir size and the relationships to viral load in acute HIV infection, measurements of the l
139 related to an increase in RABV mRNA and live viral load in the brain, as well as to an accelerated sp
141 fp683-dependent liver ILC1 lead to increased viral load in the presence of intact adaptive and innate
142 dence of causality of pneumonia, we compared viral load in the URT of children with World Health Orga
143 t was low, despite a significantly lower HIV viral load in those recently started on treatment (P < .
144 A single dose of N6-LS suppressed plasma viral loads in 4 out of 5 animals at day 7, while the co
145 , adjuvanted G protein significantly reduced viral loads in both the lungs and nose at early time poi
146 ness of fit test based on the correlation of viral loads in cherries of the phylogenetic tree, showin
147 ted the role of RSV subtypes, genotypes, and viral loads in disease severity and host transcriptional
150 ased morbidity-including fever, viremia, and viral loads in spinal cord and testes-and increased mort
152 hat in five cases of asymptomatic infection, viral loads in the blood were as high as those in patien
153 strate that N6-LS potently suppressed plasma viral loads in the majority of animals but that the comb
154 es concurrently in 11 patients, with average viral loads in urine a log higher than those in serum.
155 Interestingly, in another case with a higher viral load, in which T and NK cell responses were undete
156 not detected in pretransplant serum, however viral loads increased with time, peaking during the heig
162 to be receiving effective antiviral therapy (viral load <100 IU/mL); antiviral therapy was not requir
163 redicted-active NRTIs had viral suppression (viral load <400 copies per mL) at week 144, compared wit
164 nt-experienced and virologically suppressed (viral load <50 copies per mL for >/=2 months; one viral
167 We examined time to LTC (defined as first viral load measurement after release) and viral suppress
168 WHO-defined virological failure (one or more viral load measurement of >/=1000 copies per mL) and swi
169 as defined as the occurrence of at least one viral load measurement of 51-999 copies per mL during AR
172 ere therapeutic drug monitoring and/or close viral load monitoring are feasible to detect suboptimal
175 pact of HIVDR: (1) routine access to routine viral load monitoring in all settings; (2) optimization
178 agnosis of HIV from dried blood spots (DBS), viral load monitoring with this system is not practical
184 rhesus macaques with regards to reduction of viral load, morbidity, or survival highlighting the chal
185 24 month risk ratios of virological failure (viral load more than 200 copies per mL) were 2.01 (1.17-
188 oir size, with the evolution of intermediate viral loads observed only when the within-host dynamics
189 g both elite controllers (ie, persons with a viral load of </=40 copies/mL) and noncontrollers, antib
190 ebig stage I infection with a median initial viral load of 2.97 log10 copies per mL (IQR 2.42-3.85).
191 enrolment, the proportion who died or had a viral load of 400 copies/mL or higher at 12 months post-
192 load <50 copies per mL for >/=2 months; one viral load of 50-200 copies per mL was allowed within 12
194 IV-infected veterans, time-updated HIV-1 RNA viral load of at least 500 copies/mL compared with less
195 the magnitude, function, and relation to the viral load of HIV-specific CD4(+) T cell responses in a
199 iral rebound was defined as the first single viral load of more than 200 copies per mL or treatment i
200 69%) were defined by measurement of a single viral load of more than 200 copies per mL, and 1414 (31%
201 trols for some viruses, the utility in using viral load of URT specimens to define viral pneumonia wa
203 men aged 18 years or older who had HIV-1 RNA viral loads of 500 copies per mL or greater, had receive
204 n the protease inhibitor plus NRTI group had viral loads of less than 400 copies per mL compared with
205 itor monotherapy group, 292 (78%) of 375 had viral loads of less than 400 copies per mL; p=0.003 vers
206 of 247 in the atazanavir group had HIV-1 RNA viral loads of less than 50 copies per mL (mean differen
207 he proportion of participants with HIV-1 RNA viral loads of less than 50 copies per mL at week 48 in
209 IV-infected persons who achieve undetectable viral loads on antiretroviral therapy currently have nea
210 t women with confirmed EVD had similar Ebola viral loads on presentation to nonpregnant women, as mea
212 CI, 2.5-151.3) and higher maternal HIV log10 viral load (OR, 2.8; 95% CI, 1.3-6.3) were also signific
214 reexposure prophylaxis (P = .01), low plasma viral load (P < .02), and time to kit expiration (P < .0
215 val [CI]: 0.796-1.270); disease severity and viral load (P = .994); viral load and adverse outcomes (
216 her pre-ART CD4 count (p=0.0008) and pre-ART viral load (p=0.0003) were associated with viral rebound
223 stic regression analyses suggested that high viral load, receipt of high-dose steroids, and myeloabla
225 s well tolerated and resulted in substantial viral load reduction in all treated patients within 4 we
226 2 oligonucleotide, resulted in a significant viral load reduction in patients with chronic HCV infect
228 anel for HEV genotypes (code 8578/13) showed viral load results falling within the result ranges gene
232 in PBMC correlated directly with both plasma viral load (Rho = 0.3531; P = 0.0218) and the proviral c
233 iew we propose a new framework to accelerate viral load scale-up and ensure equitable access to this
234 ytic immune response that impacts the plasma viral load set point and the rate of progression to AIDS
237 rimary infections have very high circulating viral loads similar to those in patients during the acut
238 l infectivity, correlates with the set point viral load (Spearman r = 0.346; P = 0.045) and that repl
240 ith HIV on antiretroviral therapy (ART) with viral load suppression will be able to continue before d
244 rforms well compared to a market-leading HCV viral load test and should be considered for instances w
246 sensitivity and specificity of the Xpert HCV Viral Load test for HCV RNA detection by venepuncture an
247 CV antibody-reactive patients, 435 completed viral load testing (82%), of whom 301 (69%) were chronic
249 016, and July 27, 2016, 150 participants had viral load testing results for the three assays tested.
250 countries that have just started to scale up viral load testing, lessons can be learnt from countries
251 IV screening and CD4 counts, and in-parallel viral load testing, to promote fast and complete diagnos
252 would improve interlaboratory agreement for viral load testing; however, insufficient data are avail
254 nd patients, which will be vital in ensuring viral load tests are appropriately used to improve the q
256 y severe pneumonia cases did not have higher viral load than less severe cases for most viruses.
257 ssion, as is observed, and not the very high viral loads that previous models have predicted, an effe
259 , we show that IFNL4 genotypes determine HCV viral load through a mechanism dependent on a specific a
260 strongly with both neutralization titers and viral load titers in the nose and lungs post-viral chall
262 ter detection, which limited the median peak viral load to 4.22 log10 copies per mL (3.27-4.83) and t
263 ntrollers (EC), with the ability to suppress viral load to undetectable levels in the absence of anti
267 ontrast to previous studies, (i) we measured viral loads using standardized assays on a sample collec
268 people with observed viral rebound, the next viral load value after rebound was 50 copies per mL or l
271 that the median time to undetectable plasma viral load (VL) can be reduced from approximately 5 d to
275 rs associated with higher CD4 cell count and viral load (VL) suppression<400 c/mL among patients on a
276 ens through 12 months postpartum for batched viral load (VL) testing separate from routine care.
278 bout the association of age, CD4 cell count, viral load (VL), and antiretroviral (ARV) drug use with
281 itis B virus and hepatitis delta virus (HDV) viral loads (VL) during tenofovir-containing antiretrovi
282 ither cerebrospinal fluid (CSF) discordance (viral load [VL] in CSF 0.5 log10 copies HIV-1 RNA greate
283 asma human immunodeficiency virus (HIV) RNA (viral load [VL]) testing; however, its availability is v
286 three timepoints (months 5, 10, and 15), log viral load was 1.26 times higher (95% CI 1.04-1.52) in t
294 t infection as well as in reducing the nasal viral load when administered via the subcutaneous route.
295 must quantify the heritability of set-point viral load, which is the fraction of variation in this p
298 be useful for guiding the implementation of viral load with the aim of achieving the new global HIV
299 ospectively and retrospectively to track the viral load within the patient blood, urine, CSF, and kid
300 he key blood sample had high cell-associated viral loads without a marked CD8 lymphocytosis or NK cel
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