ライフサイエンスコーパス: antiretroviral therapy

1 poor quality of life and poor adherence with antiretroviral therapy.

2 o, especially in the presence of combination antiretroviral therapy.

3 completion of chemotherapy in individuals on antiretroviral therapy.

4 latently infected cells that persist during antiretroviral therapy.

5 on-competent HIV in individuals on effective antiretroviral therapy.

6 rvoirs for latent HIV even in individuals on antiretroviral therapy.

7 V are living longer as a result of effective antiretroviral therapy.

8 aracteristics, CSF cytokines/chemokines, and antiretroviral therapy.

9 fected individuals despite fully suppressive antiretroviral therapy.

10 during human HIV infection in the absence of antiretroviral therapy.

11 nced by HIV RNA levels, CD4+ cell counts, or antiretroviral therapy.

12 s (HIV) disease and the use of highly active antiretroviral therapy.

13 imethoprim-sulfamethoxazole, and combination antiretroviral therapy.

14 T cell counts after virologically successful antiretroviral therapy.

15 th increased HIV diagnosis and initiation of antiretroviral therapy.

16 e (PoC) assays to monitor patients receiving antiretroviral therapy.

17 d and older HIV-infected adults on effective antiretroviral therapy.

18 k factors for CKD and nephrotoxic effects of antiretroviral therapy.

19 ting HIV-infected individuals on suppressive antiretroviral therapy.

20 s to persist in infected individuals despite antiretroviral therapy.

21 observed in HIV-1-infected individuals under antiretroviral therapy.

22 from HIV-infected individuals on suppressive antiretroviral therapy.

23 duals who are receiving clinically effective antiretroviral therapy.

24 omic site that is not effectively exposed to antiretroviral therapy.

25 stance patterns may influence the outcome of antiretroviral therapy.

26 oring of HIV-infected individuals undergoing antiretroviral therapy.

27 ency virus (HIV)-infected patients receiving antiretroviral therapy.

28 Baseline was initiation of antiretroviral therapy.

29 were receiving TDF as a part of combination antiretroviral therapy.

30 e in the suppression of HIV-1 during ongoing antiretroviral therapy.

31 grase inhibitor based regimens in first-line antiretroviral therapy.

32 us reservoirs that persist despite effective antiretroviral therapy.

33 of a long-acting, slow, effective release of antiretroviral therapy.

34 monitoring are feasible to detect suboptimal antiretroviral therapy.

35 Despite the development of antiretroviral therapy against HIV, eradication of the v

36 At prescription of antiretroviral therapy, all patients in 3 Mozambican hea

37 viral loads (VL) during tenofovir-containing antiretroviral therapy among patients with a replicating

38 Tat) protein continues to be present despite antiretroviral therapy and activates NF-kB, we hypothesi

39 for several years, despite widespread use of antiretroviral therapy and high rates of virological sup

40 ted to HIV infection that address concurrent antiretroviral therapy and immune status should be desig

41 infection is not eliminated with combination antiretroviral therapy and is possibly linked to microbi

42 for HIV-1 persists in CD4(+) T cells despite antiretroviral therapy and is the major barrier to cure.

43 ere HIV transcription is reactivated so that antiretroviral therapy and the immune system clear the i

44 g is recommended to help in the selection of antiretroviral therapy and to prevent virologic failure.

45 HIV-positive status, 76 (96.2%) were not on antiretroviral therapy, and 29 (36.7%) had viral loads o

46 er, had received 10 days or less of previous antiretroviral therapy, and had tested negative for the

47 imens dosed daily throughout, high uptake of antiretroviral therapy, and low prevalence of isoniazid

48 ed antiretroviral therapy retention, earlier antiretroviral therapy, and male circumcision as the bud

49 of existing interventions (condom promotion, antiretroviral therapy, and male circumcision) for key p

50 me of widespread availability of combination antiretroviral therapy, and mortality is reaching levels

51 viremic HIV-1-infected patients on long-term antiretroviral therapy, and their frequency in the circu

52 t uptake of HIV testing and thus coverage of antiretroviral therapy are much lower in older children

53 oad to undetectable levels in the absence of antiretroviral therapy, are unable to fully downregulate

54 posi sarcoma (KS) risk in adults who started antiretroviral therapy (ART) across the Asia-Pacific, So

55 to the initial HIV prevalence rate, PrEP and antiretroviral therapy (ART) adherence and initiation ra

56 Urgent antiretroviral therapy (ART) among hospitalised HIV-infe

57 The interactions between antiretroviral therapy (ART) and high-risk human papillo

58 y virus (HIV)-infected individuals receiving antiretroviral therapy (ART) and may contribute to HIV p

59 antibodies decline in patients on long-term antiretroviral therapy (ART) and may not be sufficient t

60 een the incidence of HIV and the scale-up of antiretroviral therapy (ART) and medical male circumcisi

61 Antiretroviral therapy (ART) and retention in care are e

62 pe 1 (HIV) in semen occurs despite effective antiretroviral therapy (ART) and suppressed blood HIV-1

63 n immunodeficiency virus (HIV) infection and antiretroviral therapy (ART) are associated with bone lo

64 hese B cell abnormalities can be reversed by antiretroviral therapy (ART) are limited.

65 ized-trial data on the risks and benefits of antiretroviral therapy (ART) as compared with zidovudine

66 (VL) suppression<400 c/mL among patients on antiretroviral therapy (ART) at transfer were assessed u

67 Second-line antiretroviral therapy (ART) based on ritonavir-boosted

68 s type 1 (HIV-1) infection despite effective antiretroviral therapy (ART) can fuel rebound viremia af

69 The global intensification of antiretroviral therapy (ART) can lead to increased rates

70 While antiretroviral therapy (ART) can reduce HIV-1 to undetec

71 or human immunodeficiency virus (HIV) during antiretroviral therapy (ART) complicates investigation o

72 stance in people initiating or re-initiating antiretroviral therapy (ART) containing non-nucleoside r

73 irological failure of first-line combination antiretroviral therapy (ART) containing the modern nucle

74 Their frequency after antiretroviral therapy (ART) correlated with HIV viremia

75 l human immunodeficiency virus (HIV) without antiretroviral therapy (ART) cost-effective.

76 ical model to time trends in HIV prevalence, antiretroviral therapy (ART) coverage, and tuberculosis

77 ates of adults (aged >15 years) with HIV and antiretroviral therapy (ART) coverage.

78 Plasma, duodenal, and rectal tissue antiretroviral therapy (ART) drug concentrations, human

79 om Rakai District, Uganda, who had initiated antiretroviral therapy (ART) during chronic infection.

80 ment failure because nonsuppressive maternal antiretroviral therapy (ART) during pregnancy and breast

81 Africa has undergone multiple expansions in antiretroviral therapy (ART) eligibility from an initial

82 risk among HIV-infected people in the modern antiretroviral therapy (ART) era is essential given thei

83 risk extends to different types of HF in the antiretroviral therapy (ART) era.

84 Cross-resistance after first-line antiretroviral therapy (ART) failure is expected to impa

85 iving with HIV (PLHIV) ever on highly active antiretroviral therapy (ART) follow a pattern where morb

86 The 2015 WHO recommendation of antiretroviral therapy (ART) for all immediately followi

87 Current antiretroviral therapy (ART) for HIV/AIDS slows disease

88 Optimal laboratory monitoring of antiretroviral therapy (ART) for human immunodeficiency

89 , and PrEP+screen with enhanced provision of antiretroviral therapy (ART) for individuals who become

90 ual to 350 cells per muL who were initiating antiretroviral therapy (ART) from two HIV/AIDS clinics i

91 It remains controversial whether current antiretroviral therapy (ART) fully suppresses the cycles

92 iency virus (HIV)-infected persons beginning antiretroviral therapy (ART) has been incompletely chara

93 While antiretroviral therapy (ART) has improved the quality of

94 Antiretroviral therapy (ART) has rendered HIV-1 infectio

95 V-1 transmission in pediatric populations by antiretroviral therapy (ART) have been highly successful

96 asuring HIV-1 persistence during suppressive antiretroviral therapy (ART) have been reported, a simpl

97 As access to antiretroviral therapy (ART) in Africa has increased dra

98 Antiretroviral therapy (ART) in combination with IFN-I b

99 ief (PEPFAR) supports aggressive scale-up of antiretroviral therapy (ART) in high-burden countries an

100 itor (NNRTI) resistance in people initiating antiretroviral therapy (ART) in low-income and middle-in

101 ciency virus (HIV)-infected women initiating antiretroviral therapy (ART) in pregnancy are increasing

102 ons of HIV-infected people worldwide receive antiretroviral therapy (ART) in programmes using WHO-rec

103 A severe complication of antiretroviral therapy (ART) in these patients is neurol

104 thout hepatitis B virus (HBV) coinfection on antiretroviral therapy (ART) in Zambia.

105 rates of testing uptake, result return, and antiretroviral therapy (ART) initiation (100%).

106 0 copies per mL or higher at 12 months after antiretroviral therapy (ART) initiation (among those who

107 We estimated joint effects of antiretroviral therapy (ART) initiation and depressive s

108 in uninfected controls, before and after HIV antiretroviral therapy (ART) initiation and during inter

109 he time of an HIV-positive test, accelerated antiretroviral therapy (ART) initiation for treatment-el

110 rition during the period from HIV testing to antiretroviral therapy (ART) initiation is high worldwid

111 Correlates of death soon after antiretroviral therapy (ART) initiation remain unclear.

112 ficiency virus (HIV)-positive persons before antiretroviral therapy (ART) initiation to the costs of

113 ctancy of HIV-positive individuals receiving antiretroviral therapy (ART) is approaching that of HIV-

114 ryptococcus) shortly after the initiation of antiretroviral therapy (ART) is approximately 10%.

115 e homeostasis and HIV/SIV persistence during antiretroviral therapy (ART) is critical to effectively

116 Although lifelong combination antiretroviral therapy (ART) is recommended for all indi

117 load (VL) monitoring for patients receiving antiretroviral therapy (ART) is recommended worldwide.

118 reastfeeding in HIV-infected women receiving antiretroviral therapy (ART) is unknown.

119 Suppression of viremia by antiretroviral therapy (ART) leads to quantitative and q

120 Early antiretroviral therapy (ART) limits proviral reservoirs,

121 is unknown if extremely early initiation of antiretroviral therapy (ART) may lead to long-term ART-f

122 uman immunodeficiency virus (HIV) initiating antiretroviral therapy (ART) may reduce cryptococcal dis

123 The impact of antiretroviral therapy (ART) on herpes simplex virus typ

124 analysed the effect of immediate combination antiretroviral therapy (ART) on viraemia and immune resp

125 Botswana has a well-developed antiretroviral therapy (ART) program that serves as a re

126 inform the level of attention to be given by antiretroviral therapy (ART) programs to HIV drug resist

127 human immunodeficiency virus (HIV)-infected antiretroviral therapy (ART) recipients.

128 Whether TDF-containing antiretroviral therapy (ART) reduces HSV-2 acquisition i

129 (HIV)-infected individuals despite effective antiretroviral therapy (ART) reflects ongoing immune act

130 cur in HIV positive individuals on different antiretroviral therapy (ART) regimens are important to u

131 ica, more than 50,000 patients have received antiretroviral therapy (ART) since the inception of this

132 confidence interval, 1.64-5.48) and time to antiretroviral therapy (ART) start (adjusted odds ratio

133 Women are under-represented in HIV antiretroviral therapy (ART) studies.

134 Antiretroviral therapy (ART) substantially decreases mor

135 Antiretroviral therapy (ART) suppresses viral replicatio

136 Antiretroviral therapy (ART) that enables suppression of

137 rnal HIV-1 vaccine that could synergize with antiretroviral therapy (ART) to eliminate pediatric HIV-

138 erized cohort of HIV-infected individuals on antiretroviral therapy (ART) with a history of prior TB

139 c subgroups are present among individuals on antiretroviral therapy (ART) with access to care.

140 The length of time that people with HIV on antiretroviral therapy (ART) with viral load suppression

141 tment failure among patients with HIV taking antiretroviral therapy (ART) would improve appropriate a

142 n HIV-positive individuals receive sustained antiretroviral therapy (ART), and 90% of individuals on

143 eir status, 90% of these receiving sustained antiretroviral therapy (ART), and 90% of those having vi

144 rapy (OST), HIV counselling and testing, HIV antiretroviral therapy (ART), and condom distribution pr

145 ir status, for 90% of those aware to receive antiretroviral therapy (ART), and for 90% of those on tr

146 , 110 (75%) had primary VL, 57 (40%) were on antiretroviral therapy (ART), and the median CD4 count w

147 Universal antiretroviral therapy (ART), as per the 2015 WHO recomm

148 ends viral load (VL) monitoring for those on antiretroviral therapy (ART), availability in low-income

149 ILC numbers were preserved by antiretroviral therapy (ART), but only if initiated duri

150 ) of human immunodeficiency virus (HIV) with antiretroviral therapy (ART), continued access to ART th

151 Despite years of fully suppressive antiretroviral therapy (ART), HIV persists in its hosts

152 In the era of antiretroviral therapy (ART), HIV-1 infection is no long

153 Despite the immune-reconstitution with antiretroviral therapy (ART), HIV-infected individuals r

154 HIV-infected persons on suppressive antiretroviral therapy (ART), including those receiving

155 Before antiretroviral therapy (ART), LTs contained >98% of the

156 ar is high to improve on current combination antiretroviral therapy (ART), now highly effective, safe

157 atent or subclinical reservoir of HIV during antiretroviral therapy (ART), potentially for many of th

158 radoxically is intensified by HIV-associated antiretroviral therapy (ART), resulting in an increased

159 of 64 (25%) had a stroke soon after starting antiretroviral therapy (ART), suggesting an immune recon

160 Africa transitions to a new era of universal antiretroviral therapy (ART), up-to-date assessments of

161 ts of human immunodeficiency virus-infected, antiretroviral therapy (ART)-naive adults who started AR

162 e of superinfection in a well-characterized, antiretroviral therapy (ART)-naive, primary infection co

163 tain control of HIV spread in the absence of antiretroviral therapy (ART).

164 its use as functional delivery vehicles with antiretroviral therapy (ART).

165 to realize the full benefits of combination antiretroviral therapy (ART).

166 mmunodeficiency virus (HIV) suppression with antiretroviral therapy (ART).

167 We included African women on antiretroviral therapy (ART).

168 IV-1 RNA in cerebrospinal fluid (CSF) during antiretroviral therapy (ART).

169 emia or individuals on long-term suppressive antiretroviral therapy (ART).

170 y and mortality among HIV-infected adults on antiretroviral therapy (ART).

171 is high among HIV patients not yet receiving antiretroviral therapy (ART).

172 rolonged suppression of viral replication by antiretroviral therapy (ART).

173 common AIDS-defining condition in the era of antiretroviral therapy (ART).

174 icipants receiving virologically suppressive antiretroviral therapy (ART).

175 immunodeficiency virus (PWHIV) on effective antiretroviral therapy (ART).

176 sult in lost opportunities to provide timely antiretroviral therapy (ART).

177 control viral replication in the absence of antiretroviral therapy (ART).

178 ent viral reservoir in individuals receiving antiretroviral therapy (ART).

179 ative HIV virus load (VL) testing to monitor antiretroviral therapy (ART).

180 ent HIV replication in individuals receiving antiretroviral therapy (ART).

181 resistance (TDR) may compromise response to antiretroviral therapy (ART).

182 g at diagnosis to guide initial selection of antiretroviral therapy (ART).

183 nd 376 with viral suppression on combination antiretroviral therapy (ART).

184 matory syndrome (C-IRIS), upon initiation of antiretroviral therapy (ART).

185 common AIDS-defining condition in the era of antiretroviral therapy (ART).

186 oinfected patients on stable, DRV-containing antiretroviral therapy (ART).

187 rienced (ie, with >/=9 months on combination antiretroviral therapy [ART] and at risk of viral reboun

188 esentation of 0.260 x 109 cells/L, universal antiretroviral therapy [ART] eligibility, and 5-year ret

189 ) and three clinical stages (eligibility for antiretroviral therapy [ART], initiation of ART, and the

190 Access to combination antiretroviral therapy, as well as health resources, has

191 was conducted among HIV-infected patients on antiretroviral therapy at 20 AIDS clinics.

192 imethoprim-sulfamethoxazole, and combination antiretroviral therapy at enrollment.

193 IDS and tuberculosis mortality, despite free antiretroviral therapy being made available from public

194 We observed that irrespective of combination antiretroviral therapy, both short- and long-length vira

195 Although potent combination antiretroviral therapy can effectively block viral repli

196 le to prevent HIV transmission, and although antiretroviral therapy can prevent disease progression,

197 Antiretroviral therapy can suppress HIV replication to u

198 Although antiretroviral therapy can suppress HIV-1 infection to u

199 The widespread use of combinational antiretroviral therapies (cART) in developed countries h

200 ients with AIDS after initiating combination antiretroviral therapy (cART) and the role of an immune

201 TANCE HIV patients who interrupt combination antiretroviral therapy (cART) eventually experience vira

202 Combination antiretroviral therapy (cART) has reduced HIV-1-related

203 ng protease inhibitor (PI)-based combination antiretroviral therapy (cART) have lower levels of proge

204 raditional CKD risk factors, and combination antiretroviral therapy (cART) may all contribute.

205 tion and CD4 T-cell dynamics and combination antiretroviral therapy (cART) onset were analyzed using

206 of patients receiving long-term combination antiretroviral therapy (cART) present with CCR5 (R5)-tro

207 voirs in infected individuals under combined antiretroviral therapy (cART) represents a major obstacl

208 IMPORTANCE Although developments in combined antiretroviral therapy (cART) strategies have successful

209 Combination antiretroviral therapy (cART) suppresses plasma viremia

210 ted pigtailed macaques receiving combination antiretroviral therapy (cART) was conducted.

211 ion with number of vaccinations, combination antiretroviral therapy (cART), and HIV status.

212 H) who are receiving suppressive combination antiretroviral therapy (cART), but their pathophysiology

213 plication that can be achieved with combined antiretroviral therapy (cART), low levels of type I inte

214 e immune reconstitution promoted by combined antiretroviral therapy (cART), lymphomas still represent

215 1.SIGNIFICANCE STATEMENT Despite combination antiretroviral therapy (cART), neurocognitive disorders

216 o analyzed effects of initiating combination antiretroviral therapy (cART).

217 xpression and effectively resist combination antiretroviral therapy (cART).

218 infection that is responsive to combination antiretroviral therapy (cART).

219 h increased longevity in the era of combined antiretroviral therapy, chronic inflammation with underl

220 With suppression of HIV replication by antiretroviral therapy, circulating CD4(+) Tcell numbers

221 was an effect modifier for both adherence to antiretroviral therapy (coefficient estimate -0.43, 95%

222 spontaneously control HIV in the absence of antiretroviral therapy ("controllers").

223 300 for black MSM) and was most sensitive to antiretroviral therapy costs.

224 sons who achieve undetectable viral loads on antiretroviral therapy currently have near-normal lifesp

225 Simultaneously, innovations in antiretroviral therapy, diagnostic approaches, and vacci

226 sis" [EID]) followed by prompt initiation of antiretroviral therapy dramatically reduces mortality.

227 ase management (1.65; 1.36-1.99), receipt of antiretroviral therapy during incarceration (1.39; 1.11-

228 The use of antiretroviral therapy during pregnancy is important for

229 can target HIV reservoirs.IMPORTANCE Though antiretroviral therapies effectively suppress viral repl

230 dations are made to limit their influence on antiretroviral therapy efficacy.

231 TERPRETATION: In our large HIV cohort in the antiretroviral therapy era, we found evidence that dysfu

232 odeficiency virus (HIV) patients in the post-antiretroviral therapy era.

233 at HIV fusion inhibitors intended for use as antiretroviral therapies extended the survival of HIV-in

234 per muL and HIV-1 RNA <200 copies per mL) on antiretroviral therapy for at least 6 months and dyslipi

235 ervoir of latently infected T cells prevents antiretroviral therapy from eliminating HIV-1 infection.

236 ermine if patients with HIV on highly active antiretroviral therapy (HAART) had any difference in the

237 In the last decade, highly active antiretroviral therapy (HAART) has improved the immune f

238 ased since the introduction of highly active antiretroviral therapy (HAART) in 1996.

239 Before the introduction of highly active antiretroviral therapy (HAART), cardiac mortality and mo

240 of the infected population on highly active antiretroviral therapy (HAART).

241 e, 397-820) cells/mm(3) ; most (97%) were on antiretroviral therapy, had HIV RNA <20 copies/mL (87%),

242 The introduction of combined antiretroviral therapy has changed the overall prognosis

243 Antiretroviral therapy has enabled people to live long l

244 Antiretroviral therapy has greatly reduced the incidence

245 odeficiency virus (HIV) that is treated with antiretroviral therapy have improved longevity but face

246 Raltegravir and efavirenz-based initial antiretroviral therapy have similar 4-year clinical effe

247 developed countries, remarkable advances in antiretroviral therapy have transformed HIV infection in

248 spirituality', 'Beliefs and Attitudes about Antiretroviral Therapy', 'Healthcare providers', 'Signif

249 mission category, nadir CD4(+) T-cell count, antiretroviral therapy, HIV RNA, liver fibrosis, HCV gen

250 Despite antiretroviral therapy, HIV-1 persists in memory CD4(+)

251 Antiretroviral therapy; HIV-associated comorbidities, su

252 gative serum cryptococcal antigen initiating antiretroviral therapy in a resource-limited setting.

253 iral load testing for individuals undergoing antiretroviral therapy in low-resource settings is a glo

254 fection consistently recommend initiation of antiretroviral therapy in patients with hepatitis C viru

255 vorinostat) to HIV-1-infected individuals on antiretroviral therapy induces a significant increase in

256 Combination antiretroviral therapy initiated during acute infection

257 tion level could enhance linkage to care and antiretroviral therapy initiation and substantially decr

258 ement, early HIV diagnosis, linkage to care, antiretroviral therapy initiation, and durable viral sup

259 scade of HIV care adapted to WHO-recommended antiretroviral therapy irrespective of CD4 cell count.

260 High adherence to antiretroviral therapy is crucial to the success of HIV

261 t similar levels of spending to when earlier antiretroviral therapy is included; however, PrEP for MS

262 h depression, but receipt of efavirenz-based antiretroviral therapy is not.

263 Without antiretroviral therapy, lifetime CVD risk for HIV-infect

264 resistance mutations (DRM), including among antiretroviral therapy-naive HIV-infected individuals.

265 and computed tomography in 35 asymptomatic, antiretroviral-therapy-naive, HIV-1-infected adults with

266 The effects of antiretroviral therapy on risk of severe bacterial infec

267 The Highly Active Antiretroviral Therapy Oversight Committee.

268 Treg depletion combined with combination antiretroviral therapy provides a novel strategy for HIV

269 affect patients' adherence to highly active antiretroviral therapy, psychological health, and qualit

270 ied rCD4s from HIV-1-infected individuals on antiretroviral therapy, rapamycin treatment downregulate

271 lly suppressed HIV-1-infected individuals on antiretroviral therapy received 60 mg MGN1703 subcutaneo

272 47 635 individuals initiated an antiretroviral therapy regimen between Jan 1, 2000, and

273 trengthened to minimize interruptions as new antiretroviral therapy regimens are introduced and to fa

274 rventions that aimed to improve adherence to antiretroviral therapy regimens in populations with HIV.

275 sk variants in the context of HIV infection, antiretroviral therapy-related nephrotoxicity, and devel

276 al persistence in individuals on suppressive antiretroviral therapy, remains unclear.

277 and MSM in particular, followed by improved antiretroviral therapy retention, earlier antiretroviral

278 from HIV-1-infected individuals treated with antiretroviral therapy significantly increased viral rea

279 enrolled in the Strategies for Management of Antiretroviral Therapy (SMART) trial robustly boosted HI

280 ptase inhibitor therapy prior to combination antiretroviral therapy, stavudine exposure was independe

281 HIV-1-infected patients receiving long-term antiretroviral therapy suggests that some host-related f

282 eatment for tuberculosis (especially without antiretroviral therapy) than in those without HIV.

283 ive study of treatment-naive PLWH initiating antiretroviral therapy, the score for the depression sca

284 longer, largely attributable to combination antiretroviral therapy, there is concern about the effec

285 Thus, IL-7 therapy in antiretroviral therapy-treated patients induces sustaine

286 are the 5-year mortality risk under observed antiretroviral therapy treatment plans to the 5-year mor

287 He remained aviremic off antiretroviral therapy until ATI day 288, when a low-lev

288 ted (n = 150) men by age, calendar year, and antiretroviral therapy use (HIV-infected men only).

289 r age, CD4 cell counts, last HIV viral load, antiretroviral therapy use, and AIDS-defining infection,

290 ng Mozambican HIV-positive patients starting antiretroviral therapy was 10%, with limited rifampicin

291 demic occurred in 1995-1996 when combination antiretroviral therapy was introduced, effectively block

292 After 1 participant taking antiretroviral therapy was observed to have a false nega

293 ency-reversing agents (LRAs) and combination antiretroviral therapy was proposed as a means to eradic

294 with HIV-1 coinfection, of whom 71% received antiretroviral therapy) were recruited.

295 onically HIV-infected patient on suppressive antiretroviral therapy who underwent allo-SCT for treatm

296 mononuclear cells from HIV-infected women on antiretroviral therapy who were HSV-2 seropositive or se

297 We evaluated HIV-infected adults on antiretroviral therapy who were LTFU (>90 days late for

298 adults aged >18 to <70 years on suppressive antiretroviral therapy with CD4+ counts >350 cells/muL a

299 NSTIs) are recommended components of initial antiretroviral therapy with two nucleoside reverse trans

300 ls from HIV-infected patients on suppressive antiretroviral therapy with undetectable viral loads.