ライフサイエンスコーパス: highly active antiretroviral therapy

1 nofovir disoproxil fumarate (TDF) as part of highly active antiretroviral therapy.

2 ount/mm(3) prior to widespread initiation of highly active antiretroviral therapy.

3 not correlate with CD4 cell count or use of highly active antiretroviral therapy.

4 l surgical procedures in patients undergoing highly active antiretroviral therapy.

5 he often incomplete neurological response to highly active antiretroviral therapy.

6 IV-positive patients after widespread use of highly active antiretroviral therapy.

7 including lipoatrophy associated with HIV or highly active antiretroviral therapy.

8 successful administration of life-prolonging highly active antiretroviral therapy.

9 serves the immune system and avoids lifetime highly active antiretroviral therapy.

10 fter immune reconstitution during receipt of highly active antiretroviral therapy.

11 al mortality rates since the introduction of highly active antiretroviral therapy.

12 of Lck was ameliorated following suppressive highly active antiretroviral therapy.

13 y infections, even after receiving effective highly active antiretroviral therapy.

14 different than that observed in patients on highly active antiretroviral therapy.

15 in Brazil and 170,000 patients are receiving highly active antiretroviral therapy.

16 A.HIVA) in HIV-1-infected patients receiving highly active antiretroviral therapy.

17 s and multiple CD8(+) T-cell epitopes during highly active antiretroviral therapy.

18 eficiency virus (HIV) disease and the use of highly active antiretroviral therapy.

19 dysfunction among HIV-infected men receiving highly active antiretroviral therapy.

20 emic HIV infection while they were receiving highly active antiretroviral therapy.

21 mm(3), whereas there was no association with highly active antiretroviral therapy.

22 bjects in whom HIV levels were suppressed by highly active antiretroviral therapy.

23 nment of complete response after DR-COP with highly active antiretroviral therapy.

24 CGRP plasma levels return to baseline after highly active antiretroviral therapy.

25 are a mounting problem despite the advent of highly active antiretroviral therapy.

26 During 4,054 person-years, 374 initiated highly active antiretroviral therapy, 211 developed acqu

27 Highly active antiretroviral therapy agents are notoriou

28 We highlight what is known about how and why highly active antiretroviral therapy agents can affect d

29 ibed hepatotoxins, new reports appeared with highly active antiretroviral therapy agents, herbal ther

30 There were 434 HIV-infected men receiving highly active antiretroviral therapy and 200 HIV-uninfec

31 d States in 1996, randomly assigned 577 to a highly active antiretroviral therapy and 579 to a largel

32 mphoma are improving with the routine use of highly active antiretroviral therapy and combination che

33 od of perinatally HIV-1-infected children on highly active antiretroviral therapy and compared them t

34 fects of age on the toxicity and efficacy of highly active antiretroviral therapy and death from AIDS

35 Acetaminophen, highly active antiretroviral therapy and drugs for tuber

36 Access to highly active antiretroviral therapy and healthcare disp

37 are challenges of drug interactions between highly active antiretroviral therapy and immunosuppressi

38 Control of HIV replication with highly active antiretroviral therapy and increased CD4 c

39 onocytes have been identified in patients on highly active antiretroviral therapy and may represent a

40 re incidence of these cancers: the effect of highly active antiretroviral therapy and the imminent ap

41 immunodeficiency virus (HIV)+ recipients on highly active antiretroviral therapy, and acute rejectio

42 mic patients, aviremic patients treated with highly active antiretroviral therapy, and HIV controller

43 cell ablative therapies, HIV patients under highly active antiretroviral therapy, and in the elderly

44 is disorder has increased despite the use of highly active antiretroviral therapy, and its underlying

45 Both patients were HIV-positive, receiving highly active antiretroviral therapy, and were closely m

46 avirus in HIV infection outline why, despite highly active antiretroviral therapy, anogenital tumors

47 up of 272 patients successfully treated with highly active antiretroviral therapy appears to be power

48 Since the introduction of highly active antiretroviral therapies (ART), the progno

49 is study was to determine whether initiating highly active antiretroviral therapy (ART) before concep

50 ether people living with HIV (PLHIV) ever on highly active antiretroviral therapy (ART) follow a patt

51 os of outcomes for time after HIV diagnosis, highly active antiretroviral therapy (ART) initiation, a

52 n in MSM studies conducted before the era of highly active antiretroviral therapy, as in the recent m

53 wo consecutively enrolled infants initiating highly active antiretroviral therapy at a median age of

54 e inhibitors (HIV-PIs) are key components of highly active antiretroviral therapy, but they have been

55 e year 2010, with just over 30% initiated on highly active antiretroviral therapy by 2011.

56 n=9) and HIV-infected (n=10) women receiving highly active antiretroviral therapy, by use of multipar

57 sults in a chronic illness because long-term highly active antiretroviral therapy can lower viral tit

58 Highly active antiretroviral therapy can suppress plasma

59 Our findings suggest that HIV+ patients on highly active antiretroviral therapy can undergo success

60 nfected pregnant Kenyan women ineligible for highly active antiretroviral therapy (CD4 > 250 cells/mm

61 The existence of federally sponsored highly active antiretroviral therapy, clinicians and hea

62 ministration of targeted chemotherapies with highly active antiretroviral therapy could well impede t

63 models that incorporated HIV prevalence and highly active antiretroviral therapy coverage as covaria

64 se birth outcomes associated with the use of highly active antiretroviral therapy during pregnancy.

65 HIV-1 protease inhibitors are part of the highly active antiretroviral therapy effectively used in

66 Use of highly active antiretroviral therapy, either concomitant

67 or =18 years old and underwent LT during the highly active antiretroviral therapy era (starting Janua

68 IV-infected patients with sepsis in the post-highly active antiretroviral therapy era are conflicting

69 As HIV-infected patients in the highly active antiretroviral therapy era continue to hav

70 omavirus-related cancers remains high in the highly active antiretroviral therapy era, raising concer

71 nce of which appears to be increasing in the highly active antiretroviral therapy era.

72 complication of HIV infection in the current highly active antiretroviral therapy era.

73 t common non-AIDS defining malignancy in the highly active antiretroviral therapy era.

74 nd cancer incidence continues to rise in the highly active antiretroviral therapy era; however, data

75 Patients treated with highly active antiretroviral therapy exhibited a partial

76 Moreover, patients under highly active antiretroviral therapy frequently develop

77 S or death comparing always with never using highly active antiretroviral therapy from the marginal s

78 e been less common since the introduction of highly active antiretroviral therapy, globally, human im

79 munodeficiency virus (HIV) infection despite highly active antiretroviral therapies (HAART) and can n

80 increased from 6% before the introduction of highly active antiretroviral therapy (HAART) (before 199

81 : between admission to WIHS and the start of highly active antiretroviral therapy (HAART) (interval X

82 ng HIV-infected adults, 87.1% were receiving highly active antiretroviral therapy (HAART) (median dur

83 ong-term (2+ years) HIV-infected subjects on highly active antiretroviral therapy (HAART) (n = 134) a

84 of >10,000 copies/ml), and 10 individuals on highly active antiretroviral therapy (HAART) (VL of <75

85 rus type 1 (HIV-1) transmission and maternal highly active antiretroviral therapy (HAART) after infan

86 10 HIV-positive individuals before and after highly active antiretroviral therapy (HAART) and 10 non-

87 IV-related KS progressing after 11 months of highly active antiretroviral therapy (HAART) and 2 lines

88 (3)) before and up to 3 years after starting highly active antiretroviral therapy (HAART) and compare

89 rs of influenza vaccination for both the pre-highly active antiretroviral therapy (HAART) and HAART e

90 ndance at adult HIV clinics, eligibility for highly active antiretroviral therapy (HAART) and reasons

91 oirs of infected cells that are resistant to highly active antiretroviral therapy (HAART) and the imm

92 iciency virus-positive (HIV+) patients under highly active antiretroviral therapy (HAART) and their a

93 infected children, including those receiving highly active antiretroviral therapy (HAART) between 198

94 Highly active antiretroviral therapy (HAART) can control

95 Highly active antiretroviral therapy (HAART) can reduce

96 Highly active antiretroviral therapy (HAART) can reduce

97 nalysis of their dynamics prior to and after highly active antiretroviral therapy (HAART) could revea

98 Highly active antiretroviral therapy (HAART) decreases p

99 Highly active antiretroviral therapy (HAART) dramaticall

100 Antiretroviral Therapy (ART) including Highly Active Antiretroviral Therapy (HAART) drug regime

101 f this study was to determine the effects of highly active antiretroviral therapy (HAART) drugs on pu

102 tment, have become increasingly important in highly active antiretroviral therapy (HAART) due to thei

103 t harbor inducible infectious HIV even after highly active antiretroviral therapy (HAART) during preg

104 Highly active antiretroviral therapy (HAART) enables lon

105 ed patients with non-Hodgkin lymphoma in the highly active antiretroviral therapy (HAART) era approac

106 virus (HIV)/tuberculosis coinfection, in the highly active antiretroviral therapy (HAART) era, needs

107 sociated cervical cancer have changed in the highly active antiretroviral therapy (HAART) era.

108 tations associated with HIV infection in the highly active antiretroviral therapy (HAART) era.

109 rialized settings, both in the pre- and post-highly active antiretroviral therapy (HAART) era.

110 ass I-restricted cytotoxic T lymphocytes and highly active antiretroviral therapy (HAART) exert stron

111 181 +/- 59 in 33 patients who were receiving highly active antiretroviral therapy (HAART) for a media

112 Since the introduction of highly active antiretroviral therapy (HAART) for prevent

113 NNRTIs are recommended components of highly active antiretroviral therapy (HAART) for the tre

114 udy was to determine if patients with HIV on highly active antiretroviral therapy (HAART) had any dif

115 ndividuals who control HIV-1 viremia without highly active antiretroviral therapy (HAART) had stronge

116 RNA decay dynamics during the initiation of highly active antiretroviral therapy (HAART) has been a

117 The use of highly active antiretroviral therapy (HAART) has been as

118 Although highly active antiretroviral therapy (HAART) has convert

119 Highly active antiretroviral therapy (HAART) has dramati

120 Highly active antiretroviral therapy (HAART) has dramati

121 In the last decade, highly active antiretroviral therapy (HAART) has improve

122 Highly active antiretroviral therapy (HAART) has led to

123 90s, and their subsequent incorporation into highly active antiretroviral therapy (HAART) has profoun

124 The use of highly active antiretroviral therapy (HAART) has resulte

125 Highly active antiretroviral therapy (HAART) has substan

126 Since patients on highly active antiretroviral therapy (HAART) have a high

127 ple have decreased since the introduction of highly active antiretroviral therapy (HAART) in 1996.

128 Interruption of suppressive highly active antiretroviral therapy (HAART) in HIV-infe

129 birth outcomes are associated with maternal highly active antiretroviral therapy (HAART) in pregnanc

130 everse transcriptase inhibitor (NNRTI)-based highly active antiretroviral therapy (HAART) including e

131 whether good nutrition can delay the time to highly active antiretroviral therapy (HAART) initiation

132 Screening for tuberculosis prior to highly active antiretroviral therapy (HAART) initiation

133 Highly active antiretroviral therapy (HAART) is able to

134 immunodeficiency virus (HIV) infection with highly active antiretroviral therapy (HAART) is effectiv

135 Although highly active antiretroviral therapy (HAART) is effectiv

136 nt residual viremia in patients on prolonged highly active antiretroviral therapy (HAART) is not clea

137 counts in HIV-infected individuals receiving highly active antiretroviral therapy (HAART) is not full

138 Immune-reconstitution after highly active antiretroviral therapy (HAART) is often in

139 mmune reconstitution following initiation of highly active antiretroviral therapy (HAART) is poorly u

140 Highly active antiretroviral therapy (HAART) is recommen

141 hether this outcome holds true in the era of highly active antiretroviral therapy (HAART) is unclear.

142 s analysis considered the effects of HIV and highly active antiretroviral therapy (HAART) on HPV pers

143 Data on the effect of highly active antiretroviral therapy (HAART) on incident

144 t to determine the role of HIV infection and highly active antiretroviral therapy (HAART) on lung can

145 The effect of highly active antiretroviral therapy (HAART) on the inci

146 We evaluated the effect of highly active antiretroviral therapy (HAART) on the inci

147 The impact of highly active antiretroviral therapy (HAART) on the natu

148 s (HIV)-infected children who were beginning highly active antiretroviral therapy (HAART) or changing

149 nucleoside-backbone component of their first highly active antiretroviral therapy (HAART) regimen hav

150 Recent treatments with highly active antiretroviral therapy (HAART) regimens ha

151 Highly active antiretroviral therapy (HAART) suppresses

152 Highly active antiretroviral therapy (HAART) suppresses

153 The most effective highly active antiretroviral therapy (HAART) to prevent

154 Most HIV+ individuals require lifelong highly active antiretroviral therapy (HAART) to suppress

155 The development of highly active antiretroviral therapy (HAART) to treat in

156 iency virus (HIV)-infected individuals after highly active antiretroviral therapy (HAART) treatment.

157 Protease inhibitor (PI)-based highly active antiretroviral therapy (HAART) use in preg

158 istance to NVP and may reduce the ability of highly active antiretroviral therapy (HAART) used for pr

159 e of brain biopsy in HIV patients in the pre-highly active antiretroviral therapy (HAART) versus post

160 The median duration of lamivudine-containing highly active antiretroviral therapy (HAART) was 2.80 ye

161 aposi's sarcoma (KS) diagnosed in the era of highly active antiretroviral therapy (HAART) was based o

162 xis and growth factor support were required; highly active antiretroviral therapy (HAART) was discret

163 /muL), levels declined regardless of whether highly active antiretroviral therapy (HAART) was include

164 ity of HBV vaccination in children receiving highly active antiretroviral therapy (HAART) was investi

165 e calendar periods as an imperfect proxy for highly active antiretroviral therapy (HAART) when estima

166 ously reported that in patients treated with highly active antiretroviral therapy (HAART) who achieve

167 mplantation, 55% of patients were prescribed highly active antiretroviral therapy (HAART), 21% were f

168 nts treated with infusional chemotherapy and highly active antiretroviral therapy (HAART), 68 survive

169 ficiency virus type 1 (HIV-1) infection with highly active antiretroviral therapy (HAART), a combinat

170 Despite the use of highly active antiretroviral therapy (HAART), AIDS-relat

171 ghty-five percent of patients were receiving highly active antiretroviral therapy (HAART), and HIV RN

172 In patients receiving highly active antiretroviral therapy (HAART), antiretrov

173 Before the introduction of highly active antiretroviral therapy (HAART), cardiac mo

174 positive subjects, before and 6 months after highly active antiretroviral therapy (HAART), compared w

175 Before highly active antiretroviral therapy (HAART), congenital

176 Tregs were functional in ES and patients on highly active antiretroviral therapy (HAART), ES maintai

177 sure changes in measles serostatus following highly active antiretroviral therapy (HAART), exposure t

178 achieve viral loads of <50 copies/ml during highly active antiretroviral therapy (HAART), low levels

179 th HIV-1 protease inhibitors, a component of highly active antiretroviral therapy (HAART), often resu

180 mmunodeficiency virus type 1 (HIV-1) load by highly active antiretroviral therapy (HAART), recovery o

181 ve individuals and men receiving suppressive highly active antiretroviral therapy (HAART), summarize

182 for HIV-infected patients is treatment with highly active antiretroviral therapy (HAART), suppressio

183 PURPOSE OF REVIEW: In the present era of highly active antiretroviral therapy (HAART), the challe

184 nd increases in the number of individuals on highly active antiretroviral therapy (HAART), the epidem

185 During the era of highly active antiretroviral therapy (HAART), the preval

186 Before the availability of highly active antiretroviral therapy (HAART), there was

187 iption, RT is a key target of currently used highly active antiretroviral therapy (HAART), though RT

188 common in the developed world in the era of highly active antiretroviral therapy (HAART), while it h

189 sociated with improved survival for the 2107 highly active antiretroviral therapy (HAART)-experienced

190 f incident TB on mortality was similar among highly active antiretroviral therapy (HAART)-exposed wom

191 cterized the CD8(+) T-cell responses of nine highly active antiretroviral therapy (HAART)-naive B 270

192 Highly active antiretroviral therapy (HAART)-related hep

193 ally infected progressors (CPs; n = 18), and highly active antiretroviral therapy (HAART)-suppressed

194 it was not found differentially modulated in highly active antiretroviral therapy (HAART)-treated HIV

195 -negative persons but different from that of highly active antiretroviral therapy (HAART)-treated ind

196 ies/mL is regarded as the optimal outcome of highly active antiretroviral therapy (HAART).

197 comes, including dementia, in the era before highly active antiretroviral therapy (HAART).

198 on and HIV disease markers in the context of highly active antiretroviral therapy (HAART).

199 act of discordancy on treatment responses to highly active antiretroviral therapy (HAART).

200 infected individuals and is not affected by highly active antiretroviral therapy (HAART).

201 arding these relationships in patients using highly active antiretroviral therapy (HAART).

202 l morbidity despite the wide spread usage of highly active antiretroviral therapy (HAART).

203 and blood before and after the initiation of highly active antiretroviral therapy (HAART).

204 cell activation, in individuals treated with highly active antiretroviral therapy (HAART).

205 barrier to virus eradication in patients on highly active antiretroviral therapy (HAART).

206 not been achieved with the prolonged use of highly active antiretroviral therapy (HAART).

207 nfected individuals treated effectively with highly active antiretroviral therapy (HAART).

208 Is) have been shown to be a key component of highly active antiretroviral therapy (HAART).

209 ntidepressants, before and during the era of highly active antiretroviral therapy (HAART).

210 ppressed by the continuous administration of highly active antiretroviral therapy (HAART).

211 portant prognostic indicator for patients on highly active antiretroviral therapy (HAART).

212 ological and virological responses following highly active antiretroviral therapy (HAART).

213 rate of preterm delivery is associated with highly active antiretroviral therapy (HAART).

214 tion of the virus in patients on suppressive highly active antiretroviral therapy (HAART).

215 blems in HIV-positive (HIV+) women receiving highly active antiretroviral therapy (HAART).

216 All received highly active antiretroviral therapy (HAART).

217 namics was noted in relation to CD4 count or highly active antiretroviral therapy (HAART).

218 tality in HIV-positive persons not receiving highly active antiretroviral therapy (HAART).

219 f age enrolled in a trial of ritonavir-based highly active antiretroviral therapy (HAART).

220 dividuals with HIV-1 infection in the era of highly active antiretroviral therapy (HAART).

221 tion of the gut mucosal immune system during highly active antiretroviral therapy (HAART).

222 early one-half of the infected population on highly active antiretroviral therapy (HAART).

223 various degrees of viral control on and off highly active antiretroviral therapy (HAART).

224 uppressors and HIV-1-positive individuals on highly active antiretroviral therapy (HAART).

225 uman immunodeficiency virus (HIV) undergoing highly active antiretroviral therapy (HAART).

226 le HBV DNA in HIV-HBV-coinfected subjects on highly active antiretroviral therapy (HAART).

227 )T cells from virally suppressed subjects on highly active antiretroviral therapy (HAART).

228 (HIV)-1-infected patients who are started on highly active antiretroviral therapy (HAART).

229 us (HIV)-infected children in the absence of highly active antiretroviral therapy (HAART).

230 rden in sub-Saharan Africa and the impact of highly active antiretroviral therapy (HAART).

231 nd mortality among individuals not receiving highly active antiretroviral therapy (HAART); however, t

232 lity risk and improves the odds of accessing highly active antiretroviral therapy (HAART); however, t

233 smaller CRAE and larger CRVE with history of highly active antiretroviral therapy (HAART; P < .001);

234 e mortality among persons in care during the highly-active antiretroviral therapy (HAART) era.

235 Highly-active antiretroviral therapy (HAART) has led to

236 man immunodeficiency virus (HIV) patients on highly-active antiretroviral therapy (HAART) or multiple

237 ssessed in 341 (25% women, 52% white, 74% on highly active antiretroviral therapy [HAART]) participan

238 cline prior to April 1996 (before the era of highly active antiretroviral therapy [HAART]).

239 Highly active antiretroviral therapy has been used to ef

240 The introduction of highly active antiretroviral therapy has dramatically re

241 renal disease (ESRD) and the introduction of highly active antiretroviral therapy has indicated that

242 Highly active antiretroviral therapy has led to a dramat

243 Although highly active antiretroviral therapy has led to improved

244 Highly active antiretroviral therapy has limited benefit

245 Highly active antiretroviral therapy has the potential t

246 AIDS-defining illnesses after the advent of highly active antiretroviral therapy, HIV-associated non

247 y has been slow to recognize the efficacy of highly active antiretroviral therapy in changing the cou

248 eficiency syndrome or death comparing use of highly active antiretroviral therapy in the prior 2 year

249 t has not been fully described in the era of highly active antiretroviral therapy in the United State

250 ncer has increased since the introduction of highly active antiretroviral therapy in this population

251 8, the proportion of participants prescribed highly active antiretroviral therapy increased by 9 perc

252 Whether highly active antiretroviral therapy influences these mi

253 The role of early highly active antiretroviral therapy initiation in patie

254 AIDS-defining cancers in patients who are on highly active antiretroviral therapy is an open and comp

255 ug interaction between immunosuppression and highly active antiretroviral therapy is increasingly rec

256 One of the major limitations of highly active antiretroviral therapy is its inability to

257 proxil fumarate (TDF), a drug widely used in highly active antiretroviral therapy, is associated with

258 eveloped countries since the introduction of highly active antiretroviral therapy, Kaposi's sarcoma i

259 Since the advent of highly active antiretroviral therapy, liver disease has

260 Highly active antiretroviral therapy may not have had a

261 atitis C virus-coinfected patients receiving highly active antiretroviral therapy (n = 12).

262 Highly active antiretroviral therapy, nutritional supple

263 of MSM conducted before the introduction of highly active antiretroviral therapy (odds ratio, 0.47;

264 is a paucity of recent data on the effect of highly active antiretroviral therapy on human papillomav

265 man papillomavirus infections; the effect of highly active antiretroviral therapy on human papillomav

266 imate the net effect of imperfectly measured highly active antiretroviral therapy on incident acquire

267 resource-rich areas, including the impact of highly active antiretroviral therapy on the incidence of

268 on, the authors estimate the total effect of highly active antiretroviral therapy on time to acquired

269 shed in 1993, treating time to initiation of highly active antiretroviral therapy or to clinical dise

270 The Highly Active Antiretroviral Therapy Oversight Committee

271 In the era of highly active antiretroviral therapy, patients with HIV-

272 vate latent provirus may, in the presence of highly active antiretroviral therapy, permit clearance o

273 Longer duration of highly active antiretroviral therapy (PR, 1.09 [CI, 1.02

274 302 person-years) before the introduction of highly active antiretroviral therapy (pre-1996) to 6.1 (

275 OS) and uninfected (NEG) children in the pre-highly active antiretroviral therapy (pre-HAART) period.

276 two percent of HIV-infected patients were on highly active antiretroviral therapy prior to admission,

277 Highly active antiretroviral therapy prolongs the life o

278 Highly active antiretroviral therapy prolongs the lives

279 antiretroviral therapy (ART), also known as highly active antiretroviral therapy, provides clinical

280 may negatively affect patients' adherence to highly active antiretroviral therapy, psychological heal

281 In many instances, highly active antiretroviral therapy remains the corners

282 (CD4 cell counts, HIV viral load, and use of highly active antiretroviral therapy), sexual orientatio

283 Highly active antiretroviral therapy should be used with

284 xpressed genes of CD4(+) memory T cells from highly active antiretroviral therapy-suppressed patients

285 Since the introduction of highly active antiretroviral therapy, survival rates for

286 a to better understand and predict potential highly active antiretroviral therapy-targeted therapy in

287 In an era of highly active antiretroviral therapies, the authors need

288 With the advent of highly active antiretroviral therapy, the epidemiology o

289 re we show that, following the initiation of highly active antiretroviral therapy, the immediate decl

290 ) copies/ml TAR RNA in the serum exosomes of highly active antiretroviral therapy-treated patients or

291 l health outcomes were exacerbated among non-highly active antiretroviral therapy users.

292 talizations dropped markedly after 1995 when highly active antiretroviral therapy was introduced; how

293 Among HIV-infected subjects, highly active antiretroviral therapy was negatively asso

294 deficiency virus thresholds and adherence to highly active antiretroviral therapy were inconsistent.

295 ed anal intercourse, older age, and being on highly active antiretroviral therapy were independently

296 d declined rapidly in subjects who initiated highly active antiretroviral therapy, whereas NK cell ac

297 ibitors (HIV PIs) are the core components of highly active antiretroviral therapy, which has been suc

298 Despite the development of highly active antiretroviral therapy, which has effectiv

299 Highly active antiretroviral therapy with HIV RNA levels

300 an a log lower than that seen in patients on highly active antiretroviral therapy with undetectable v