ライフサイエンスコーパス: HAART

1 HAART is very effective in suppressing HIV-1 replication

2 HAART receipt during pregnancy was associated with incre

3 HAART reduces but does not eliminate the risk of ARR.

4 HAART-treated adults with wild-type HIV were prospective

5 sed children to 860 echocardiograms from 140 HAART-unexposed but HIV-infected children from the Pulmo

6 the United States (pre-HAART era, 1987-1994; HAART era, 1997-2005).

7 The CHAART-2 (HAART-Associated Cardiotoxicity in HIV-Infected Children

8 ctively compared 148 echocardiograms from 74 HAART-exposed children to 860 echocardiograms from 140 H

9 ARV prophylaxis (prenatal zidovudine, 43.9%; HAART, 52.1%).

10 After HAART availability, non-infectious lung diseases were no

11 After HAART introduction , influenza-related mortality in adul

12 e interval [CI], 2.2-2.7; p<0.001) and after HAART availability (MACS, adjusted-OR, 1.5; 95%CI 1.3-1.

13 e severity of HIV infection before and after HAART.

14 immunoblastic histology has decreased after HAART.

15 gatibacter was significantly decreased after HAART.

16 over the six-month study period, even after HAART.

17 nses continue to shape HIV-1 evolution after HAART initiation, but the extent and rate at which this

18 icatella, and Atopobium were increased after HAART.

19 HLA-associated evolution in HIV-1 Pol after HAART initiation in a large, population-based observatio

20 Immune reconstitution after HAART initiation did not restore protective levels of me

21 ART era and evaluated mortality trends after HAART introduction in the United States.

22 had no detectable viremia for 9 years after HAART cessation.

23 otherapy in a group of grass pollen-allergic HAART-treated HIV-positive patients.

24 z-score for difference = 1.07; p = 0.02) and HAART exposure duration (z-score difference per year = 0

25 adjusted hazard, 0.34; 95% CI, .23, .49) and HAART (0.39 [0.31, 0.48]) decreased the hazard of all-ca

26 Comparing the HAART-exposed and HAART-unexposed groups, any HAART exposure was positivel

27 rates of HBV infection in the pre-HAART and HAART eras and to identify factors associated with incid

28 le response in the coinfected, non-HAART and HAART groups were 2.1 (95% confidence interval [CI], 1.7

29 We studied the impact of HIV and HAART on ARR among patients taking thrice-weekly antitub

30 of this study suggest that HIV infection and HAART can have significant effects on salivary microbial

31 iduals in both the pre-HAART (MACS only) and HAART eras; and adjusted Cox proportional hazard ratios

32 While both OST and HAART are life-saving treatments, joint administration i

33 Both OST and HAART independently protected against HIV-related death,

34 the independent and joint effects of OST and HAART on all-cause as well as drug- and HIV-related mort

35 the independent and joint effects of OST and HAART on mortality, by cause, within a population of HIV

36 components of highly active antiretroviral (HAART) therapy targeting HIV reverse transcriptase (RT).

37 AART-exposed and HAART-unexposed groups, any HAART exposure was positively associated with left ventr

38 LV mass was negatively associated with any HAART exposure (z-score difference = -0.64; p = 0.01) as

39 This study suggests that highly active ART (HAART) does not appear to impair heart function.

40 ed children were measles IgG seropositive at HAART initiation.

41 In the United States before HAART, influenza-related mortality rates in adults with

42 gible if they had an HIV diagnosis and began HAART between January 1, 1996 and June 30, 2010.

43 Associations between HAART exposure and echocardiographic measures were evalu

44 protection (IRR, 0.2 [CI, 0.1 to 0.5]), but HAART in those with HIV RNA levels of 400 copies/mL or g

45 ered by known atherogenic effects of chronic HAART or the prolonged inflammatory state associated wit

46 British Columbia HAART Observational, Medical Evaluation and Research coh

47 responses to long-term lamivudine-containing HAART were comparable between HIV-infected patients with

48 l other HIV-infected women, those continuing HAART from before pregnancy had higher odds of PTD (adju

49 LIT therapy in viro-immunological controlled HAART treated HIV positive patients was efficacious, saf

50 main common in HIV-infected persons, despite HAART, but whether anemia predicts HAND in the HAART era

51 -associated HIV-1 evolution continues during HAART to an extent that is inversely related to the viro

52 ricted CD8(+) T cell control develops during HAART treatment and then enters latent reservoirs in the

53 s were observed in 269 (43%) patients during HAART and occurred at 49 of 63 (78%) investigated immune

54 -competent forms of the virus persist during HAART, and when treatment is stopped, high rates of HIV-

55 copies/mL at an arbitrary time point during HAART (= T0), according to whether the actual, unreporte

56 eservoirs and reduce residual viremia during HAART.

57 enefit from focused efforts to promote early HAART initiation and adherence.

58 y HIV infection that persisted through early HAART and post-therapy interruption.

59 Effective HAART is associated with lower incidence of HBV infectio

60 d represent a secondary benefit of effective HAART.

61 urteen patients had been receiving effective HAART for at least 6 months (median, 1 year).

62 To achieve eradication, HAART must be combined with drugs that reactivate the do

63 Reversion of escape mutations following HAART initiation was extremely rare.

64 changes with immune reconstitution following HAART is unknown.

65 investigated immune reconstitution following HAART.

66 oinfected VATS subjects, after adjusting for HAART status, HIV RNA level, and CD4 cell count at basel

67 itive during pregnancy were not assessed for HAART eligibility during pregnancy or in the first four

68 attended an HIV clinic and been assessed for HAART eligibility.

69 ty-three HIV-1-infected patients, naive from HAART, were randomly assigned to HAART with dietary inte

70 The analysis examined the survival from HAART initiation to all-cause mortality or an AIDS event

71 sociated with hepatitis B e antigen (HBeAg), HAART <2 years, CD4 <200 cells/mm(3), detectable HIV RNA

72 However, HAART targets only actively replicating virus and is una

73 ncy virus (SIV) Gag escape mutation K165R in HAART-treated SIV-infected pigtailed macaques.

74 virus-induced uveitis should be suspected in HAART-naive, HIV-positive patients or in those in whom t

75 ea often has noninfectious causes, including HAART-related adverse events and HIV enteropathy.

76 A total of 13.1% of women who initiated HAART during pregnancy had detectable VL at delivery.

77 Initiating HAART at the antenatal clinic, improved counselling and

78 months in 3418 patients with HIV initiating HAART between November 2006 and November 2008 in 7 clini

79 a population of HIV-positive PWID initiating HAART.

80 epatomegaly were associated with no maternal HAART versus those with HAART (41% vs 6%; P < .05).

81 Prenatal maternal HAART was defined as triple antiretroviral therapy (ART)

82 neurocognitive impairment in a multicenter, HAART-era HIV cohort study (N = 1261), adjusting for pot

83 unfavorable response in the coinfected, non-HAART and HAART groups were 2.1 (95% confidence interval

84 -)TB(+)), 212 HIV patients not on HAART (non-HAART), and 116 HIV-infected patients on HAART.

85 of AIDS patients and 29% (95% CI, 22, 38) of HAART subjects and 3% (95% CI, 0.8, 7.2) and 42% (95% CI

86 After the administration of HAART, the intraocular inflammation disappeared entirely

87 Since the advent of HAART, patients with HIV infection have seen a significa

88 itiating virus replication upon cessation of HAART, thus leading to viral rebound.

89 the Evaluation of Metabolic Complications of HAART, with representatives from academia, patient commu

90 n has not been established in the context of HAART.

91 Duration of HAART exposure was negatively associated with LV end-sys

92 ameters narrowed with increasing duration of HAART, independently of age (167.83 microm <3 years of H

93 was conducted to characterize the effects of HAART and revaccination on measles immunoglobulin G (IgG

94 identify long-term cardiovascular effects of HAART in HIV-infected children.

95 analysis demonstrated beneficial effects of HAART on cervical SIL in HIV-positive women.

96 The increasing efficiency of HAART has helped to transform HIV/AIDS into a chronic di

97 In the era of HAART, diarrhea from opportunistic infections is uncommo

98 The goal of HAART may need to be revised to a lower cutoff than 50 c

99 of diagnosis, late diagnosis, and history of HAART.

100 mmune reconstitution following initiation of HAART (P=.003).

101 gh school diploma; P = 0.013), initiation of HAART in the third trimester (23.9% vs. 12.3% and 8.6% i

102 Whereas early initiation of HAART should improve immunosurveillance and reduce the i

103 Interruption of HAART leads to a rapid rebound of viremia, so life-long

104 spiratory diseases after the introduction of HAART, and infectious respiratory diseases were associat

105 In this Review we discuss the management of HAART pharmacotherapy in relation to cytotoxic chemother

106 stand the potential pathogenic mechanisms of HAART-associated NeuroAIDS and design effective adjuvant

107 ions in semen in the absence and presence of HAART, and suggest further studies.

108 HAART) (interval X) and between the start of HAART and the most recent WIHS visit (interval Y), and e

109 Despite the success of HAART in reducing mortality, resistant strains continue

110 Despite the overall success of HAART in slowing the progression to AIDS in HIV-infected

111 and lead to discontinuation or switching of HAART regimens.

112 However, there is no fundamental theory of HAART.

113 The timing of HAART initiation and prenatal care, along with medicatio

114 ependently of age (167.83 microm <3 years of HAART vs. 158.89 microm >6 years, p-trend = 0.02), and w

115 oviral therapy (HAART), 21% were formerly on HAART, and 24% were HAART-naive.

116 oup 1 (G1) consisted of patients with HIV on HAART (n = 176), Group 2 (G2) consisted of patients with

117 on HAART (32.6%) than those patients not on HAART (17.9%) (p<0.05).

118 nsisted of patients with HIV who were not on HAART (n = 48), and Group 3 (G3) consisted of controls w

119 ients (HIV(-)TB(+)), 212 HIV patients not on HAART (non-HAART), and 116 HIV-infected patients on HAAR

120 ients without HIV or with HIV who are not on HAART.

121 r manifestation was higher among patients on HAART (32.6%) than those patients not on HAART (17.9%) (

122 e reconstitution in HIV-infected patients on HAART for 12 months was poor despite a marked reduction

123 strategies targeting CD8+ Tcm in patients on HAART might provide hosts with expanded, long-lasting im

124 the response of CD8+ cells from patients on HAART.

125 c T lymphocytes (CTLs) from most patients on HAART.

126 non-HAART), and 116 HIV-infected patients on HAART.

127 they are subject to high FRR in subjects on HAART or with AIDS.

128 Those on HAART and protease inhibitor (PI)-based treatment had si

129 , and Thailand, the majority of whom were on HAART at study entry, were prospectively followed semian

130 h HIV regardless of whether patients were on HAART.

131 a HIV viral load >10,000 copies/mL while on HAART (p = 0.05).

132 After 1 year on HAART, HIV BAL contained an increased abundance of Prevo

133 dietary intervention (diet group, n = 43) or HAART without dietary intervention (control group, n = 4

134 Among HIV-positive participants, HAART increased the likelihood of regression (from prese

135 % changes in nadir CD4(+) T-cell percentage, HAART was not associated with measles IgG seroconversion

136 tal CMV rates did not differ by time period, HAART use, or infant HIV infection status.

137 CMV among HIV-exposed infants pre- and post- HAART.

138 l lymphomas (AR-DLBCLs) in the pre- and post-HAART era.

139 lated and compared between the pre- and post-HAART era.

140 were compared between the pre-HAART and post-HAART era.

141 ongenital CMV rates did not change, the post-HAART era showed reduced P/EP CMV and occurrence of rela

142 IV patients who underwent biopsy in the post-HAART era was 225 days (90-2446).

143 lysis was performed for patients in the post-HAART era.

144 ss rate was significantly higher in the post-HAART than the pre-HAART era (97.5% vs 91.9%, p=0.047).

145 e antiretroviral therapy (HAART) versus post-HAART era via meta-analysis.

146 ore incident respiratory infections both pre-HAART (MACS, odds ratio [adjusted-OR], 2.4; 95% confiden

147 Among HIV-infected children pre-HAART, Attenuvax at 6 months was well tolerated and immu

148 infected vs. HIV-uninfected participants pre-HAART (hazard ratio [adjusted-HR] 2.9; 95%CI, 1.02-8.4;

149 frica (1998-2005) and the United States (pre-HAART era, 1987-1994; HAART era, 1997-2005).

150 o HIV-uninfected individuals in both the pre-HAART (MACS only) and HAART eras; and adjusted Cox propo

151 incidence rates of HBV infection in the pre-HAART and HAART eras and to identify factors associated

152 Outcomes were compared between the pre-HAART and post-HAART era.

153 cantly higher in the post-HAART than the pre-HAART era (97.5% vs 91.9%, p=0.047).

154 antly lower in the HAART era than in the pre-HAART era among HIV-infected (IRR, 0.2 [CI, 0.1 to 0.4])

155 outh Africa and the United States in the pre-HAART era and evaluated mortality trends after HAART int

156 an in those of similar children from the pre-HAART era but did decline over time.

157 ng ocular complication compared with the pre-HAART era.

158 ate is reduced from that observed in the pre-HAART era.

159 ilar to that in the United States in the pre-HAART era.

160 tiating antiretroviral therapy in pregnancy, HAART use (vs zidovudine) was associated with higher odd

161 ndings underscore the importance of prenatal HAART for all HIV-infected pregnant women.

162 ere observed in the percentage of prescribed HAART, the percentage who achieved a suppressed HIV VL,

163 less than 200/muL, and 92 patients received HAART during chemotherapy.

164 CONCLUSION In adults receiving HAART, use of high-dose multivitamin supplements compare

165 ents with lung cancer who are also receiving HAART.

166 oprotection and memory in children receiving HAART.

167 isolated from infected individuals receiving HAART and were found to exhibit potent induction activit

168 fected children 2 to <19 years old receiving HAART and with HIV loads <30,000 copies/mL, CD4% >/=15,

169 had >200 CD4 T cells/muL; 98% were receiving HAART at baseline.

170 Twenty-six patients were receiving HAART; viral load was <100 copies per mL in 12 patients.

171 In multivariate regression, HAART and PI use were positively associated with Lp-PLA2

172 t HIV progression by 6 months after starting HAART.

173 ferences remain up to 3 years after starting HAART.

174 n individuals with high discordancy starting HAART, but there was no association with subsequent HIV

175 Long-term HAART appears to be cardioprotective for HIV-infected ch

176 However, patients staying on long-term HAART still develop various HIV-associated neurological

177 of influenza-related complications and that HAART alone may not circumvent this risk in AIDS patient

178 chronic, untreated HIV-1 infection and that HAART had a restorative effect on this subset.

179 terested in the alternative possibility that HAART critically contributes to the neuroinflammation in

180 Our results suggest that HAART restores a normal frequency of CD8(+) T(SCM) and t

181 Comparing the HAART-exposed and HAART-unexposed groups, any HAART expo

182 In both cohorts during the HAART era, median ages at time of non-AIDS-related death

183 nfected persons with lung disease during the HAART era.

184 therapy (HAART) (before 1996) to 53% in the HAART era (P < 0.01); the median age of persons who died

185 , vinblastine, and dacarbazine (ABVD) in the HAART era according to HIV serostatus to establish wheth

186 d red blood cell indices predict HAND in the HAART era and may contribute to risk assessment.

187 of death in people diagnosed with HIV in the HAART era compared with the general population.

188 ART, but whether anemia predicts HAND in the HAART era is unknown.

189 to 2.4]) and was significantly lower in the HAART era than in the pre-HAART era among HIV-infected (

190 HIV-infected participants in the HAART era with respiratory infections had an increased r

191 at risk for developing CMV retinitis in the HAART era, although the incidence rate is reduced from t

192 incidence has decreased substantially in the HAART era, cytomegalovirus (CMV) retinitis remains an im

193 dence of HBV infection; however, even in the HAART era, incidence of HBV infection remains high among

194 tality among HIV-positive individuals in the HAART era, independent of study cohort.

195 In the HAART era, systemic anti-CMV therapy, while there is imm

196 lammation and lung complications seen in the HAART era.

197 During 11 years of follow-up, in the HAART-exposed group, LV mass and LV end-diastolic septal

198 shortening were higher when compared to the HAART-unexposed group.

199 pite highly active antiretroviral therapies (HAART) and can negatively affect patient quality of life

200 ion of highly active antiretroviral therapy (HAART) (before 1996) to 53% in the HAART era (P < 0.01);

201 art of highly active antiretroviral therapy (HAART) (interval X) and between the start of HAART and t

202 eiving highly active antiretroviral therapy (HAART) (median duration, 58 months), their median CD4 co

203 cts on highly active antiretroviral therapy (HAART) (n = 134) and subjects with low CD4 counts (AIDS

204 after highly active antiretroviral therapy (HAART) and 10 non-HIV-infected control individuals.

205 ths of highly active antiretroviral therapy (HAART) and 2 lines of conventional chemotherapy (pegylat

206 arting highly active antiretroviral therapy (HAART) and compared with 22 uninfected control subjects.

207 ty for highly active antiretroviral therapy (HAART) and reasons for lack of attendance.

208 under highly active antiretroviral therapy (HAART) and their association with cluster of differentia

209 Highly active antiretroviral therapy (HAART) decreases plasma viremia below the limits of dete

210 luding Highly Active Antiretroviral Therapy (HAART) drug regimens is widely considered to be one of t

211 in the highly active antiretroviral therapy (HAART) era approaches that of the general population whe

212 in the highly active antiretroviral therapy (HAART) era, needs evaluation.

213 d post-highly active antiretroviral therapy (HAART) era.

214 es and highly active antiretroviral therapy (HAART) exert strong selective pressures on human immunod

215 ion of highly active antiretroviral therapy (HAART) for prevention of mother-to-child transmission of

216 nts of highly active antiretroviral therapy (HAART) for the treatment of HIV-1.

217 HIV on highly active antiretroviral therapy (HAART) had any difference in their IOP compared with pat

218 though highly active antiretroviral therapy (HAART) has converted HIV into a chronic disease, a reser

219 Highly active antiretroviral therapy (HAART) has dramatically decreased mortality from HIV-1 i

220 ecade, highly active antiretroviral therapy (HAART) has improved the immune function and life expecta

221 Highly-active antiretroviral therapy (HAART) has led to some reduction in influenza-related co

222 nts on highly active antiretroviral therapy (HAART) have a high risk of developing hypertension and d

223 ion of highly active antiretroviral therapy (HAART) in 1996.

224 essive highly active antiretroviral therapy (HAART) in HIV-infected patients leads to increased HIV r

225 ternal highly active antiretroviral therapy (HAART) in pregnancy, particularly in resource-limited se

226 -based highly active antiretroviral therapy (HAART) including efavirenz is recommended as a 1(st)-lin

227 Highly active antiretroviral therapy (HAART) is able to suppress human immunodeficiency virus

228 ion of highly active antiretroviral therapy (HAART) is poorly understood.

229 era of highly active antiretroviral therapy (HAART) is unclear.

230 IV and highly active antiretroviral therapy (HAART) on HPV persistence and cervical squamous intraepi

231 ect of highly active antiretroviral therapy (HAART) on incident HBV infection in HIV-infected and HIV

232 ect of highly active antiretroviral therapy (HAART) on the incidence of herpes zoster (HZ) in human i

233 nts on highly-active antiretroviral therapy (HAART) or multiple sclerosis patients treated with natal

234 Highly active antiretroviral therapy (HAART) suppresses HIV-1 replication but cannot eliminate

235 Highly active antiretroviral therapy (HAART) suppresses HIV-1 replication, transforming the ou

236 he pre-highly active antiretroviral therapy (HAART) versus post-HAART era via meta-analysis.

237 aining highly active antiretroviral therapy (HAART) was 2.80 years (interquartile range, 1.73-5.92 ye

238 uired; highly active antiretroviral therapy (HAART) was discretionary.

239 hether highly active antiretroviral therapy (HAART) was included with the anti-tuberculosis regimen.

240 cribed highly active antiretroviral therapy (HAART), 21% were formerly on HAART, and 24% were HAART-n

241 use of highly active antiretroviral therapy (HAART), AIDS-related lymphoma remains common.

242 eiving highly active antiretroviral therapy (HAART), and HIV RNA was undetectable in the plasma of 75

243 ion of highly active antiretroviral therapy (HAART), cardiac mortality and morbidity were common in H

244 after highly active antiretroviral therapy (HAART), compared with that for 10 HIV-seronegative subje

245 Before highly active antiretroviral therapy (HAART), congenital cytomegalovirus (CMV) rates were high

246 lowing highly active antiretroviral therapy (HAART), exposure to measles virus, and revaccination amo

247 essive highly active antiretroviral therapy (HAART), summarize the data on the detection and localiza

248 t with highly active antiretroviral therapy (HAART), suppression of viral replication in these patien

249 era of highly active antiretroviral therapy (HAART), the challenges that HIV/AIDS patients face with

250 als on highly active antiretroviral therapy (HAART), the epidemic burden continues to be high.

251 y used highly active antiretroviral therapy (HAART), though RT inhibitors offer generally a poor resi

252 era of highly active antiretroviral therapy (HAART), while it has emerged as a major public health pr

253 ted in highly active antiretroviral therapy (HAART)-treated HIV-infected subjects or in elite control

254 als on highly active antiretroviral therapy (HAART).

255 rgoing highly active antiretroviral therapy (HAART).

256 cts on highly active antiretroviral therapy (HAART).

257 cts on highly active antiretroviral therapy (HAART).

258 ted on highly active antiretroviral therapy (HAART).

259 nce of highly active antiretroviral therapy (HAART).

260 act of highly active antiretroviral therapy (HAART).

261 ome of highly active antiretroviral therapy (HAART).

262 ext of highly active antiretroviral therapy (HAART).

263 ion on highly active antiretroviral therapy (HAART).

264 ses to highly active antiretroviral therapy (HAART).

265 before highly active antiretroviral therapy (HAART).

266 nd off highly active antiretroviral therapy (HAART).

267 essing highly active antiretroviral therapy (HAART); however, the relative effects of these treatment

268 eiving highly active antiretroviral therapy (HAART); however, the safety and efficacy of such supplem

269 ory of highly active antiretroviral therapy (HAART; P < .001); and larger CRAE with lower CD4+ T lymp

270 iving highly active anti-retroviral therapy (HAART) or had clinical or laboratory evidence, or both,

271 74% on highly active antiretroviral therapy [HAART]) participants of a cohort with detailed character

272 These data support increased access to HAART and influenza vaccination for HIV-infected adults.

273 , single-item question measured adherence to HAART over the past 4 weeks.

274 asing retention in HIV care and adherence to HAART, and ultimately HIV suppression.

275 ences retention in HIV care and adherence to HAART, which in turn serve as key determinants of HIV su

276 ts on retention in HIV care and adherence to HAART.

277 naive from HAART, were randomly assigned to HAART with dietary intervention (diet group, n = 43) or

278 perinatally HIV-infected children exposed to HAART than in those of similar children from the pre-HAA

279 -infected women, comparisons were limited to HAART exposure status at conception, and those with simi

280 associated with increased HIV load prior to HAART (P=.005) and poor immune reconstitution following

281 virologic, but not immunologic, response to HAART was associated with increased risk of immune escap

282 s, or virologic and immunologic responses to HAART.

283 y of highly active antiretroviral treatment (HAART), a large proportion of human immunodeficiency vir

284 y by highly active antiretroviral treatment (HAART), HIV-1 is still not curable due to the persistenc

285 ring highly active antiretroviral treatment (HAART).

286 ion demonstrates that HIV+ individuals under HAART presents a high prevalence of mild to moderate per

287 Individuals with HIV undergoing HAART, compared with individuals without HIV, had no sta

288 in HIV-infected patients with KS undergoing HAART, KS improvement may be partly explained by immune

289 T), 21% were formerly on HAART, and 24% were HAART-naive.

290 ed mortality, which declines with widespread HAART introduction but does not disappear.

291 hrice-weekly throughout the study along with HAART in one of the groups.

292 inal arteriolar diameters is associated with HAART duration and viral load, and may reflect heightene

293 Diarrhea associated with HAART is typically caused by protease inhibitors (eg, ri

294 , diet prevents dyslipidemia associated with HAART.

295 therapeutics to be used in combination with HAART to slow or reverse this deterioration.

296 se reservoirs, when used in combination with HAART, could thus provide a strategy for the eradication

297 Differences improved with HAART, but still persisted up to 3 years after starting

298 rvention for HIV-1-infected individuals with HAART-related dyslipidemia, but there is no evidence fro

299 ted with no maternal HAART versus those with HAART (41% vs 6%; P < .05).

300 by treatment of tuberculosis with or without HAART.