ライフサイエンスコーパス: antiretroviral

1 n vivo Finally, we reveal a SAMHD1-dependent antiretroviral activity of histone deacetylase inhibitor

2 metabolism between statins and commonly used antiretroviral agents.

3 ess than 200 copies per mL, or not receiving antiretrovirals and had a CD4 T-cell count of greater th

4 creening, patients were either receiving HIV antiretrovirals and had HIV RNA less than 200 copies per

5 We used data from the Breastfeeding, Antiretrovirals and Nutrition (BAN) clinical trial (cond

6 or more antiretrovirals, including screening antiretrovirals, and 169 (15%) had previous virological

7 of age, CD4 cell count, viral load (VL), and antiretroviral (ARV) drug use with risk of opportunistic

8 Mounting evidence implicates antiretroviral (ARV) drugs as potential contributors to

9 s type 1 (HIV-1)-infected women treated with antiretroviral (ARV) therapy.

10 erences in prevalence of linkage to care and antiretroviral (ARV) treatment among human immunodeficie

11 prevention research is focused on combining antiretrovirals (ARV) and progestin contraceptives to pr

12 Antiretrovirals (ARVs) affect bone density and turnover,

13 Research and development (R&D) for pediatric antiretrovirals (ARVs) is a lengthy process and lags con

14 Antiretroviral-based strategies for HIV prevention have

15 this process constitutes a major target for antiretroviral compounds.

16 the relationship between the microbiome and antiretroviral concentrations in the FGT.

17 aired cervicovaginal and plasma sampling for antiretroviral concentrations using high-performance liq

18 n FGT mCTs are associated with decreased FGT antiretroviral concentrations.

19 dimerization interface as a target site for antiretroviral drug development.

20 valuate the differential effect of different antiretroviral drug families on viral kinetics in semina

21 ion and persisted during 7 mo of combination antiretroviral drug therapy (cART).

22 To this end, hydrophobic antiretroviral drugs (ARVs) were recently developed for

23 options coalesce around a smaller number of antiretroviral drugs (ARVs), data are emerging on the dr

24 tive to the time horizon chosen, the cost of antiretroviral drugs (for treatment and PrEP), and the u

25 A reduction in the cost of antiretroviral drugs (including the drugs used for PrEP)

26 es because of the widespread availability of antiretroviral drugs and early testing for HIV.

27 Cabotegravir and rilpivirine are antiretroviral drugs in development as long-acting injec

28 l participants providing OMTs and tested for antiretroviral drugs to confirm HIV status.

29 Antiretroviral drugs with a lower potential to induce he

30 on, and probably replication, indicates that antiretroviral drugs with optimal penetration through th

31 nts because of poor adherence, resistance to antiretroviral drugs, or both.

32 in people who have had previous exposure to antiretroviral drugs.

33 Our results highlight the need of evaluating antiretroviral effects on genital wound healing in futur

34 ty may play a direct role in TF in long-term antiretroviral-experienced patients and that based on en

35 OQ conversion delay time was associated with antiretroviral exposure and low plasma viral load.

36 ological changes during pregnancy can reduce antiretroviral exposure.

37 being considered as partners for long-acting antiretrovirals for use in therapy or prevention of HIV

38 4 (58%) had previously received five or more antiretrovirals, including screening antiretrovirals, an

39 Long-acting injectable antiretroviral (LA-ARV) drugs with low toxicity profiles

40 dy highlights the design of PrEP not only as antiretroviral medication but as combination HIV/STI pre

41 ile range, 39-49), 85% were men, 74% were on antiretroviral medication, and 50% had plaque.

42 Maternal HIV infection and antiretroviral medication, including maternal receipt pr

43 In a cohort of 53 antiretroviral-naive HIV-infected subjects, the measure

44 samples were collected from 24 HIV-infected antiretroviral-naive, genetically and epidemiologically

45 at not only demonstrate drastically improved antiretroviral potency but also are characterized by an

46 regnancy and breastfeeding as well as infant antiretroviral prophylaxis lead to high rates of pretrea

47 nt pairs receiving all 3 recommended arms of antiretroviral prophylaxis or treatment (prenatal, intra

48 2-2005) and 94 (40.3%) (2010-2013) receiving antiretroviral prophylaxis or treatment during pregnancy

49 ns occur yearly, despite the availability of antiretroviral prophylaxis.

50 to retention of nanoparticles containing the antiretroviral protease inhibitor atazanavir.

51 of genital shedding were HIV disease stage, antiretroviral regimen, and genital ulcers or cervical t

52 mized, controlled, double-blinded study of 4 antiretroviral regimens used as PrEP.

53 n, determining optimal immunosuppressive and antiretroviral regimens, and elucidating the incidence o

54 for HIV infection, including the choices of antiretroviral regimens.

55 n human PBMCs induces potent and long-acting antiretroviral response against several laboratory-adapt

56 MC-099 facilitates ARV sequestration and its antiretroviral responses by promoting the nuclear transl

57 ion of autophagy and the previously reported antiretroviral responses in HIV-1-infected humanized mic

58 odeficiency virus (HIV) drug resistance from antiretroviral roll-out programs remain a threat to long

59 ; 24% with previous exposure to short-course antiretrovirals), the median time of follow-up from VS w

60 tiviral activity but, as with small-molecule antiretrovirals, the issues of viral escape and resistan

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

104 Early antiretroviral therapy (ART) limits proviral reservoirs,

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

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

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

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

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

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

111 Antiretroviral therapy (ART) substantially decreases mor

112 Antiretroviral therapy (ART) suppresses viral replicatio

113 Antiretroviral therapy (ART) that enables suppression of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

158 Combination antiretroviral therapy (cART) suppresses plasma viremia

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

181 Antiretroviral therapy can suppress HIV replication to u

182 300 for black MSM) and was most sensitive to antiretroviral therapy costs.

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

184 The use of antiretroviral therapy during pregnancy is important for

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

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

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

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

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

190 Antiretroviral therapy has enabled people to live long l

191 Antiretroviral therapy has greatly reduced the incidence

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

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

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

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

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

197 Combination antiretroviral therapy initiated during acute infection

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

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

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

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

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

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

204 47 635 individuals initiated an antiretroviral therapy regimen between Jan 1, 2000, and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

238 us reservoirs that persist despite effective antiretroviral therapy.

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

240 monitoring are feasible to detect suboptimal antiretroviral therapy.

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

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

243 completion of chemotherapy in individuals on antiretroviral therapy.

244 latently infected cells that persist during antiretroviral therapy.

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

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

247 T cell counts after virologically successful antiretroviral therapy.

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

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

250 fected individuals despite fully suppressive antiretroviral therapy.

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

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

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

254 imethoprim-sulfamethoxazole, and combination antiretroviral therapy.

255 th increased HIV diagnosis and initiation of antiretroviral therapy.

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

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

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

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

260 Antiretroviral therapy; HIV-associated comorbidities, su

261 Antiretroviral tissue:blood penetration ratios were abov

262 ted control against HIV in stably suppressed antiretroviral-treated subjects.

263 fection (0.9%, 95% CI 0.4-2.5) and initiated antiretroviral treatment (0.2%, 0.2-0.3).

264 isoproxil fumarate (TDF) is commonly used in antiretroviral treatment (ART) and pre-exposure prophyla

265 Antiretroviral treatment (ART) is now recommended for al

266 Achieving effective antiretroviral treatment (ART) monitoring is a key deter

267 trial of HIV-infected individuals receiving antiretroviral treatment (ART) randomized to continue (t

268 Maternal antiretroviral treatment (ART) started before conception

269 s decline is attributable to the scale-up of antiretroviral treatment (ART), as previous models have

270 smitted drug resistance mutations (TDRMs) in antiretroviral treatment (ART)-naive patients can advers

271 rofile, which are only partially restored by antiretroviral treatment (ART).

272 crease cost because of earlier initiation of antiretroviral treatment (ART).

273 esting is a key barrier to the initiation of antiretroviral treatment (ART).

274 of pre-exposure prophylaxis (PrEP) and early antiretroviral treatment (ART).

275 ion and CD4 T cell recovery by highly active antiretroviral treatment (HAART), HIV-1 is still not cur

276 controllers [HIC]) or after progression and antiretroviral treatment (progressor patients [PP]).

277 V) can be reduced through services including antiretroviral treatment and prophylaxis.

278 f 1000 or more copies per mL and no previous antiretroviral treatment at 139 sites worldwide.

279 ta were obtained from the national web-based antiretroviral treatment database.

280 c tuberculosis notification data and HIV and antiretroviral treatment estimates to disaggregate the W

281 on and resumption of virus replication after antiretroviral treatment interruption.

282 The National Free Antiretroviral Treatment Program was implemented in Jian

283 emergence of HIV drug resistance (HIVDR) as antiretroviral treatment programs expand could preclude

284 oirs in infected individuals under effective antiretroviral treatment represents a major obstacle tow

285 , South Africa adopted a policy of providing antiretroviral treatment to everyone infected with HIV i

286 l as subjects before and after initiation of antiretroviral treatment, and they identify IL-27 and it

287 There are several regimens for starting antiretroviral treatment, but it remains unknown whether

288 for both antiretroviral treatment-naive and antiretroviral treatment-experienced patients, and highl

289 impact of DRMVs across drug classes for both antiretroviral treatment-naive and antiretroviral treatm

290 s (normally <2000 HIV-RNA copies/mL) without antiretroviral treatment.

291 ation, CD4 counts, inflammation, and type of antiretroviral treatment.

292 r implementation research around rapid start antiretroviral treatment.

293 92%) were white, and 25 (96%) were receiving antiretroviral treatment.

294 at baseline and at 12, 24, and 48 weeks post antiretroviral treatment.

295 cate HIV-1 infection or to safely deescalate antiretroviral treatment.IMPORTANCE The most relevant fe

296 hibitors (NRTIs) are the backbone of current antiretroviral treatments.

297 al NICHD HPTN 040 study (distinguished by no antiretroviral use before labor) was evaluated.

298 ted after adjustment for Hispanic ethnicity, antiretroviral use, and alcohol (0.10 FIB-4 units per ye

299 These findings are relevant for optimizing antiretrovirals used for biomedical HIV prevention in wo

300 Nevirapine (NVP), is an HIV-1 antiretroviral with treatment-limiting hypersensitivity