ライフサイエンスコーパス: HIV

1 HIV prevalence was 49%.

2 HIV test uptake in the incentivised groups was compared

3 HIV-1 drug resistance to older thymidine analogue nucleo

4 HIV-1 establishes chronic infection and stimulates vigor

5 HIV-1 infection and methamphetamine (METH) abuse frequen

6 HIV-1 is rare among viruses for having a low number of e

7 HIV-1 recruits human tRNA(Lys3) to serve as the reverse

8 HIV-1 transcription was quantified by measuring plasma H

9 HIV-associated dysregulation of adaptive immunity by dep

10 HIV-infected participants enrolled in a study of cerebro

11 Human immunodeficiency virus type 1 (HIV-1) drug resistance genotyping is recommended to help

12 of the human immunodeficiency virus type 1 (HIV-1) gp41 NHR trimer has been known as the classic dru

13 chronic human immunodeficiency virus type 1 (HIV-1) infection.

14 variant human immunodeficiency virus type 1 (HIV-1) nonnucleoside reverse transcriptase inhibitor (NN

15 onal study of matrix turnover in HIV type 1 (HIV-1)-infected and -uninfected TB patients and controls

16 improve human immunodeficiency virus type 1 (HIV-1)-specific immunity and increase clearance of HIV-1

17 tumor specimens from 23 HIV-positive and 17 HIV-negative patients (29 men and 11 women; mean [SD] ag

18 ibodies significantly correlated with tier 2 HIV-1 neutralization, and anti-H2A antibody clones were

19 levels in CSF and plasma specimens from 220 HIV-positive adults who were taking suppressive ART.

20 oximately half of 40 tumor specimens from 23 HIV-positive and 17 HIV-negative patients (29 men and 11

21 POCT detected all 30 HIV-infected neonates (sensitivity 100%; 95% CI 88.4-100

22 y selective TLR7 agonist, GS-9620, activated HIV from peripheral blood mononuclear cells isolated fro

23 etermine whether ART initiation during acute HIV infection would attenuate changes in these biomarker

24 omodulatory effect, rapamycin did not affect HIV-1 gene expression induced by T cell activation in th

25 rial elicited significant protection against HIV-1 acquisition, but the efficacy and immune memory we

26 criteria (ie, brain metastases, minimum age, HIV infection, and organ dysfunction and prior and concu

27 HIV-infected infants and 61.4 years for all HIV-exposed infants; clinical outcomes for truly infecte

28 ion of universal AC screening offered to all HIV-infected women.

29 Although HIV participants had slightly lower cognitive performanc

30 Among HIV-monoinfected patients, statin initiators had lower r

31 Among HIV-uninfected patients, mortality was associated with h

32 isk of future CHF events, particularly among HIV and hepatitis C infected people among whom cardiovas

33 ype differences in disease progression among HIV-1 subtypes; furthermore, we propose that the poorer

34 an immunodeficiency virus (HIV) status in an HIV-endemic setting.

35 a cluster-randomised controlled trial of an HIV test-and-treat strategy in 32 rural communities in U

36 ion can help guide the rational design of an HIV vaccine.

37 allow measurable clinical advances toward an HIV cure.

38 exploring the association between HSV-2 and HIV.

39 of Washington Virology Research Clinic) and HIV prevention trials (HIV Prevention Trials Network 039

40 of SVR12 in patients coinfected with HCV and HIV-1.

41 infections with hepatitis C virus (HCV) and HIV are highly prevalent in the USA and concentrated in

42 graphic characteristics, medical history and HIV-related clinical data were collected.

43 Among the 4,134 routine and HIV samples tested by the two automated assays, the perc

44 if this risk varies by sociodemographic and HIV-specific factors.

45 increased chemotaxis of both uninfected and HIV-infected human monocytes, suggesting a role for sPrP

46 By contrast, endemic diseases, such as HIV in 2017 and tuberculosis, struggle to maintain the s

47 .4mut-stabilized trimers may have utility as HIV-1 immunogens or in other antigen-specific contexts,

48 pable of blocking transmission of autologous HIV to the infant.

49 Th cells accumulate in the blood of aviremic HIV-1-infected patients on long-term antiretroviral ther

50 e constructed to assess associations between HIV and food insecurity and changes in body composition

51 MMP activity differed between HIV-1-infected and -uninfected TB patients and correspon

52 At birth, HIV-exposed newborns had a similar length and weight as

53 were also more effective than WQ in blocking HIV-1 Env-mediated membrane fusion and had higher levels

54 SAMHD1 potently blocks HIV-1 replication in DCs, although the underlying mechan

55 es as well as resting T-cells, SAMHD1 blocks HIV-1 infection through this dNTP triphosphohydrolase ac

56 ovide sufficient antigenic stimulus to boost HIV-1-specific functional antibodies that can eliminate

57 ability to screen, isolate, and characterize HIV-specific antibodies have led to the identification o

58 he Congo (DRC) is a reservoir of circulating HIV strains exhibiting high levels of diversity and reco

59 ult, HIV-associated nephropathy, the classic HIV-driven kidney lesion among individuals of African de

60 xvirus vector NYVAC expressing clade C(CN54) HIV-1 Env(gp120) and Gag-Pol-Nef antigens (NYVAC-C) show

61 and age-specific approaches to confidential HIV testing with linkage to HIV services.

62 kely plays an important role in constraining HIV-1 transmission and contributes to defining subsequen

63 e HIV-specific CD8(+) T cells in controlling HIV-1 replication.

64 Failure of OFOQ to detect HIV-1 infection was frequent and multifactorial in origi

65 mber of patients in 3 cohorts with different HIV disease progression phenotypes.

66 nonuclear, SupT1, and THP-1 cells diminishes HIV-1 replication.

67 ssors supports the crucial role of effective HIV-specific CD8(+) T cells in controlling HIV-1 replica

68 Previous work has suggested that efficient HIV entry also depends on intracellular signaling, but t

69 rticipants from a TB-endemic setting, either HIV-infected or uninfected and with latent or active TB

70 fic functional antibodies that can eliminate HIV-1-infected cells.

71 Different methods to estimate HIV reservoirs exist, but there is currently no optimal

72 integration of fungal diseases into existing HIV infection, tuberculosis infection, diabetes, chronic

73 of 7% of proviruses (range: 2-18%) expressed HIV RNA.

74 mine the requirement of Vpr for facilitating HIV-1 infection of monocyte-derived dendritic cells (MDD

75 Lifetime CVD risk was 64.8% for HIV-infected males compared to 54.8% for males in the US

76 Using an ex vivo assay for HIV-1 mRNA, we demonstrated that despite this immunomodu

77 the application of a standardized assay for HIV-1 RNA in multiple specimen types.

78 which should serve as a useful benchmark for HIV-1 vaccine developers.

79 Maraviroc (MVC) is a candidate drug for HIV preexposure prophylaxis (PrEP).

80 fections; and lifestyle are risk factors for HIV-associated atherosclerosis.

81 ndomized trial of behavioral weight loss for HIV-infected patients (n = 40).

82 Models for HIV-related eligibility criteria in National Cancer Inst

83 to PrEP, the efficacy of daily oral PrEP for HIV prevention did not differ significantly among women

84 eceptors CD4 and CCR5, that are required for HIV infection yet are dispensable for cellular prolifera

85 The risk for HIV-associated opportunistic infections increases as cir

86 minance of Vlambda pairing with human VH for HIV-1 Env V2 recognition resulted in human VH pairing wi

87 confirmatory testing, LE was 26.2 years for HIV-infected infants and 61.4 years for all HIV-exposed

88 d mononuclear cells in six samples from four HIV-infected donors (one with viremia and not on ART and

89 f infection events per cell during cell-free HIV-1 infection follows a negative-binomial distribution

90 n in peripheral blood mononuclear cells from HIV-infected ART-treated individuals in response to M. t

91 in T-cells exposed to exosomes derived from HIV-1 infected DCs.

92 pheral blood mononuclear cells isolated from HIV-infected individuals with suppressed infection.

93 Lessons learned from HIV should be shared to support progress in developing p

94 e infected cells following reactivation from HIV-1 latency.

95 (+) T cells from elite controllers than from HIV-1 progressors supports the crucial role of effective

96 Healthy, HIV-uninfected adults were randomized to receive 4 mg of

97 g assay can be used to explore in detail how HIV-1 splicing is regulated and, with moderate throughpu

98 However, HIV-positive blacks continue to have much higher rates o

99 s Network 039 and Partners in Prevention HSV/HIV Transmission Study) in the US, Africa, and Peru with

100 s Affairs Clinical Case Registry to identify HIV/HCV GT1-coinfected veterans initiating 12 weeks of L

101 domain but at the same time markedly impair HIV-1 replication capacity.

102 tifies "exhausted" CD8 T cells with impaired HIV-specific effector functions, but its role on CD4 T c

103 sid-host interactions that promote or impede HIV-1 infection may provide unique insight to exploit fo

104 htened inflammation and immune activation in HIV-1+ infants did not alter IgA responses associated wi

105 conjunction with T cell-activating agents in HIV-1 cure strategies.

106 unctions, but its role on CD4 T cells and in HIV-infected children is poorly understood.

107 Deaths in HIV-positive people have decreased since the introductio

108 advances and decrease racial disparities in HIV rates.

109 H- exacerbated neurocognitive dysfunction in HIV-infected patients.

110 rimeric symmetry has ushered in a new era in HIV-1 vaccination.

111 utes to the MHC-B downregulation function in HIV-1 subtype C and show that carriage of Nef variants w

112 out interferon for treatment of acute HCV in HIV-1 infected individuals (SWIFT-C) is an open-label, 2

113 pecific CD4 T cells was markedly impaired in HIV-infected individuals, compared with HIV-uninfected i

114 While the extent of proviral integration in HIV-1-infected MDDCs was unaffected by the absence of Vp

115 ributes to loss of immune control of LTBI in HIV-infected individuals, although the precise mechanism

116 ce associated with the Tyr181Cys mutation in HIV-1 RT has been a key roadblock in the discovery of no

117 t the possible cause of neurodegeneration in HIV-1-seropositive patients, which engages the ability o

118 s the abnormalities in B cells that occur in HIV infection both in the peripheral blood and lymphoid

119 th interferon-free regimens, particularly in HIV-coinfected individuals, remains unknown.

120 Blocking this pathway in HIV-1-producing cells resulted in less infectious progen

121 f pneumonia cases were due to pneumococci in HIV-infected South African adults.

122 e regulatory role of IFN-induced proteins in HIV-1 infection.

123 function, measured by sj/beta-TREC ratio, in HIV disease progression by analyzing a large number of p

124 o optimal assay to measure HIV reservoirs in HIV eradication interventions.

125 HC-B-restricted cellular immune responses in HIV-infected individuals.

126 to timely linkage and sustained retention in HIV care in Mozambique.

127 cross-sectional study of matrix turnover in HIV type 1 (HIV-1)-infected and -uninfected TB patients

128 nd had achieved high levels of ART uptake in HIV-diagnosed individuals from 2004 onwards.

129 se-escalating study of BMS-936559, including HIV-1-infected adults aged >18 to <70 years on suppressi

130 ch visit, clinical and laboratory (including HIV) assessments were done.

131 8(+) T cells in elite controllers to inhibit HIV infection.IMPORTANCE The greater ex vivo antiviral i

132 he viral restriction factor SERINC5 inhibits HIV-1 infection via unknown mechanisms.

133 As expected, only Ser5-001 strongly inhibits HIV-1 infectivity, whereas the other Ser5 isoforms and m

134 inhibitors (INSTIs) as components of initial HIV therapy.

135 osomes from uninfected cells activate latent HIV-1 in infected cells and that true transcriptional la

136 tify inducible, replication-competent latent HIV-1.

137 with implications for elimination of latent HIV-1 infection by T cell-based vaccines.

138 Establishment of latent HIV-1 infection in CD4(+) T could be inhibited by viral-

139 ng (ATAC-seq) data, we found that the latent HIV-1 promoter phenotypically resembles endogenous long

140 The development of an effective maternal HIV-1 vaccine that could synergize with antiretroviral t

141 ere is currently no optimal assay to measure HIV reservoirs in HIV eradication interventions.

142 Using a single-copy assay, we measured HIV-1 RNA levels in CSF and plasma specimens from 220 HI

143 Outcome Measures: HIV transmissions and deaths, years of life, and budgeta

144 cosylation profile at every site in multiple HIV-1 Env trimers, accomplishing two goals.

145 s a randomised controlled trial in ART-naive HIV-positive patients with CD4 cell count of more than 5

146 The program addressed National HIV/AIDS Strategy goals 2 through 4 including steps with

147 circulating CD4+ cells in the HIV-negative (HIV-) brain-dead donor (BDD) is not known.

148 H2A antibody clones were found to neutralize HIV-1.

149 ne immunodeficiency virus (BIV) Vif, but not HIV-1 Vif, interfered with HIV-1 production and viral in

150 orts from the Collaboration of Observational HIV Epidemiological Research Europe (COHERE).

151 male circumcision and risk of acquisition of HIV and sexually transmitted infections in women.

152 Analysis of HIV-1 isolates bearing defined mutations in the capsid p

153 ly, we reported that membrane association of HIV-1 Gag, as well as purified Rous sarcoma virus (RSV)

154 ectancy and trends in the residual burden of HIV mortality after the roll-out of a public sector ART

155 ibute to the increased antiviral capacity of HIV-specific CD8(+) T cells in elite controllers to inhi

156 ed ITRIs were shorter with each new class of HIV tests, ranging from 5.9 to 24.8 days.

157 -specific immunity and increase clearance of HIV-1-expressing cells.

158 f genotype/phenotype analyses in a cohort of HIV-1 subtype C-infected patients (n = 168), together wi

159 cells harbored the highest concentrations of HIV-1 RNA and highest levels of Ki67 expression.

160 In bulge-stem-loop constructs of HIV-1 transactivation response element (TAR) RNA, we ach

161 , had virological suppression (<50 copies of HIV-1 RNA per mL) on a stable regimen for at least 6 mon

162 lar trafficking and decreased degradation of HIV-1 in cocaine treated DCs.

163 offer a new strategy for the development of HIV inhibitors.

164 lence and population prevalence estimates of HIV, HCV, and HBV among homeless veterans nationally.

165 , and mRNA synthesis.IMPORTANCE The fates of HIV-1 reverse transcription products within infected cel

166 These findings allow for identification of HIV-1-controllers at risk for immunologic progression, a

167 ded to achieve the full beneficial impact of HIV treatment.

168 N2/UNC84B are potent or modest inhibitors of HIV-1 infection, respectively, and that suppression corr

169 need for assumptions concerning knowledge of HIV status and ART coverage among adults not consenting

170 ed DCs revealed increased co-localization of HIV-1 with endosomal or multi vesicular body (MVB) marke

171 The matrix domain (MA) of HIV-1 Gag protein is N-myristoylated and plays an import

172 Developing in vitro models of HIV-1 latency that recapitulate the characteristics of l

173 tem allows stable labeling and monitoring of HIV genomic DNA within infected cells during cytoplasmic

174 We aimed to trace the geographic origin of HIV-1 infection for migrants who inject drugs and to inv

175 owed an increased risk to female partners of HIV-infected men resuming sex early after male circumcis

176 The prevalence of HIV, HCV, and HBV among homeless veterans nationally is

177 itutions inhibited proteolytic processing of HIV-1 polyproteins Gag and Gag-Pol, resulting in immatur

178 Thus, the proliferation of HIV-1-infected cells may play a role in viral persistenc

179 suppression, as indicated by the quantity of HIV-1 DNA and replication-competent-virus-producing cell

180 d tumor cell PD-L1 expression, regardless of HIV status.

181 plied to other PrEP approaches and routes of HIV acquisition, accelerating clinical implementation of

182 y and motor function with advanced stages of HIV infection suggests that these two domains are most s

183 Intracellular trafficking studies of HIV-1 in cocaine treated DCs revealed increased co-local

184 controls, and a prospective cohort study of HIV-1-infected TB patients at risk of TB immune reconsti

185 lope glycoproteins (Envs) on the surfaces of HIV-1 particles are targeted by host antibodies.

186 and scalable approaches to promote uptake of HIV testing among youths at risk is critical.

187 adults not consenting to the intervention or HIV testing, although our conclusions were robust in sen

188 unity to cytosolic bacteria, DNA viruses, or HIV.

189 les to the development of active and passive HIV-1 vaccines.

190 Pathogenic HIV or lymphocytic choriomeningitis virus chronic infect

191 roviral therapy (ART) to eliminate pediatric HIV-1 infection will require the characterization of mat

192 ancy to achieve the elimination of pediatric HIV infections.

193 ed, and pound628 874 (434 902-4 740 724) per HIV transmission averted.

194 racteristics, including receipt of perinatal HIV testing, treatment, and prophylaxis.

195 counts >350 cells/muL and detectable plasma HIV-1 RNA by single-copy assay.

196 scription was quantified by measuring plasma HIV-1 RNA during MGN1703 administration.

197 ts with less than 50 copies per mL of plasma HIV-1 RNA at week 48 (by the US Food and Drug Administra

198 s discuss viral load monitoring for pregnant HIV-positive women and those breastfeeding; ART treatmen

199 This site has been neglected in previous HIV-1 vaccine studies.

200 ivity of study sites to India, lack of prior HIV/HCV diagnosis confirmation with clinic records, and

201 demonstrate that IFN-inducible LY6E promotes HIV-1 entry and replication and highlight a positive reg

202 18 089 adults receiving HIV medical care who participated in the Medical Monitor

203 Tenofovir reduced HIV incidence by 61% (P = 0.013) in Lactobacillus-domina

204 The prevalence of resistant HIV in Aruba has increased to alarming levels, compromis

205 As a result, HIV-associated nephropathy, the classic HIV-driven kidne

206 monstrated safety in human trials of an rVSV/HIV-1 vaccine.

207 More than one third of U.S. HIV patients had missed opportunities to initiate hepati

208 one of the populations with the most severe HIV epidemics in the world.

209 irus (HIV) RNA levels and the risk of sexual HIV transmission.

210 t that the potent antiviral capacity of some HIV-specific CD8(+) T cells is a consequence of factors

211 ned genetic markers able to segregate stable HIV-1-controllers from those who experience CD4(+)T-cell

212 t's Emergency Plan for AIDS Relief-supported HIV clinic.

213 ood was collected from 70 virally suppressed HIV-1-infected individuals from Rakai District, Uganda,

214 l study in which 15 virologically suppressed HIV-1-infected individuals on antiretroviral therapy rec

215 icipants maintained virological suppression (HIV-1 RNA <50 copies per mL) at week 24.

216 ith a replicating HDV infection in the Swiss HIV Cohort Study.

217 y (cryo-EM) structure of the core tetrameric HIV-1 STC and a higher-order form that adopts carboxyl-t

218 tinue to have much higher rates of ESRD than HIV-positive whites, which could be attributed to the AP

219 However, we recently established that HIV-1 can infect kidney transplant epithelial cells in t

220 Our findings indicate that HIV infection and replication rely on a limited set of h

221 etween lysyl-tRNA synthetase (LysRS) and the HIV-1 Gag polyprotein.

222 nctionally replace the HIV-1 CA CTD, but the HIV-1 CA NTD cannot replace the HTLV-1 CA CTD, indicatin

223 nt guidance to therapeutic approaches in the HIV cure agenda.

224 the numbers of circulating CD4+ cells in the HIV-negative (HIV-) brain-dead donor (BDD) is not known.

225 We identify five factors, including the HIV co-receptors CD4 and CCR5, that are required for HIV

226 prevent replenishment or repopulation of the HIV reservoir.

227 We sought to investigate the effect of the HIV-1 auxiliary protein, Nef, which is suspected of extr

228 e sought to restrict the conformation of the HIV-1 Env trimer to its prefusion-closed state as this s

229 nts an intermediate during maturation of the HIV-1 virus.

230 e HTLV-1 CA NTD can functionally replace the HIV-1 CA CTD, but the HIV-1 CA NTD cannot replace the HT

231 Importantly, we find that the HIV-1 Vif-A3H interface is distinct from the Vif-A3G and

232 rminants of Lv2 susceptibility mapped to the HIV-2 envelope (Env) and capsid (CA).

233 In parallel, direct exposure to the HIV-related proteins Tat or gp120 induces TREM-1 express

234 Of these, 117 711 (89.2%) had their HIV status established, of whom 11 964 (10.2%) were HIV

235 Antiretroviral therapy; HIV-associated comorbidities, such as dyslipidemia, drug

236 over how the multifunctional nature of these HIV-1 regulatory and accessory proteins, and in particul

237 iving with HIV who accessed services through HIV/AIDS sentinel hospital-based and ART service deliver

238 Plasma and tissue HIV RNA correlated at baseline and when 9-month declines

239 RV144 induced antibodies to HIV that were partially protective against infection, as

240 w broadly neutralizing antibodies (bnAbs) to HIV envelope (Env) develop during natural infection can

241 A significant challenge to HIV eradication is the elimination of viral reservoirs i

242 e status of chromatin largely contributes to HIV latency.

243 TREM-1 silencing in macrophages exposed to HIV-related proteins led to increased caspase 3 activati

244 sient activation of viral replication led to HIV-1 reservoir reduction after viremia resuppression, a

245 to confidential HIV testing with linkage to HIV services.

246 show that TFR cells are highly permissive to HIV-1 both ex vivo and in vivo The expression of Ki67, a

247 cell clones segregated based on responses to HIV-1-infected and peptide-loaded target cells.

248 sal ganglia are preferentially vulnerable to HIV-1.

249 munologic interventions to prevent and treat HIV-1 infection, standardized reference reagents are a c

250 Research Clinic) and HIV prevention trials (HIV Prevention Trials Network 039 and Partners in Preven

251 T itself mediates the reduction of X4-tropic HIV-1.

252 st detailed case report suggesting wild-type HIV-1 infection despite good adherence, evidenced by rep

253 To better understand HIV-1 pathogenesis and the evolution of the viral popula

254 Lymph node cells from untreated HIV-infected individuals revealed that TFR cells harbore

255 irus (HCV) and human immunodeficiency virus (HIV) are at high risk of liver disease progression.

256 during treated human immunodeficiency virus (HIV) disease in Ugandans as compared to US-based populat

257 During human immunodeficiency virus (HIV) disease, chronic immune activation leads to T-cell

258 for novel anti-human immunodeficiency virus (HIV) drug development.IMPORTANCE The Vpr and its paralog

259 s emergence of human immunodeficiency virus (HIV) drug resistance has tremendously decreased, and tra

260 archeology of human immunodeficiency virus (HIV) emergence following human exposures to simian immun

261 patients with human immunodeficiency virus (HIV) infection.

262 of undiagnosed human immunodeficiency virus (HIV) infections among persons who inject drugs (PWID) wa

263 icenter of the human immunodeficiency virus (HIV) pandemic, the Democratic Republic of the Congo (DRC

264 modulate local human immunodeficiency virus (HIV) RNA levels and the risk of sexual HIV transmission.

265 or an unknown human immunodeficiency virus (HIV) status in an HIV-endemic setting.

266 ls living with human immunodeficiency virus (HIV) worldwide.

267 s of TDR among human immunodeficiency virus (HIV)-infected PWUD, and assessed its impacts on first-li

268 in a cohort of human immunodeficiency virus (HIV)/hepatitis C virus (HCV)-coinfected patients treated

269 d by different human immunodeficiency virus (HIV)/simian immunodeficiency virus (SIV) lentiviruses.

270 ] of whom were human immunodeficiency virus [HIV]+) were analyzed.

271 membrane-ordering effect of influenza virus, HIV, and Dengue virus FPs has been consistently observed

272 tus established, of whom 11 964 (10.2%) were HIV positive.

273 able by ET at 5-days post-infection, whereas HIV-1-infected cells surrounded by pools of free virions

274 als, although the precise mechanisms whereby HIV infection impedes successful T cell-mediated control

275 To investigate whether HIV infection increases the risk of future HFrEF and HFp

276 y was to assess risk factors associated with HIV/AIDS progression.

277 evidence shows a protective association with HIV, it was categorised as low consistency, because one

278 tio is substantially higher in children with HIV receiving treatment for tuberculosis (especially wit

279 d in HIV-infected individuals, compared with HIV-uninfected individuals.

280 antiretroviral therapy (ART) correlated with HIV viremia, CD4(+) T-cell counts, and immune activation

281 airment caused by ageing in individuals with HIV.

282 forms strong hydrogen-bond-interactions with HIV-1 protease (PR) active-site amino acids and is bulki

283 BIV) Vif, but not HIV-1 Vif, interfered with HIV-1 production and viral infectivity even in the absen

284 defined as (1) number of people living with HIV in the country by end of 2013; (2) proportion of sta

285 Women living with HIV on ART had lower prevalence of high-risk HPV than di

286 ghts into the outcomes of people living with HIV who accessed services through HIV/AIDS sentinel hosp

287 P compared with patients without HIV or with HIV who are not on HAART.

288 We followed up participants with HIV from the Veterans Aging Cohort Study for a minimum o

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

290 this study was to determine if patients with HIV on highly active antiretroviral therapy (HAART) had

291 This association was found in patients with HIV regardless of whether patients were on HAART.

292 76), Group 2 (G2) consisted of patients with HIV who were not on HAART (n = 48), and Group 3 (G3) con

293 Purpose People with HIV infection have an elevated risk of anal cancer.

294 he treatment of dyslipidaemia in people with HIV.

295 idities in reducing mortality in people with HIV.

296 ned aviremic for 7.4 months, rebounding with HIV RNA of 36 copies/mL that rose to 59,805 copies/mL 6

297 METHODS AND People with and without HIV infection participating in HSV-2 natural history stu

298 d Group 3 (G3) consisted of controls without HIV (n = 176).

299 imilar length and weight as newborns without HIV exposure, but their head circumference was smaller (

300 in their IOP compared with patients without HIV or with HIV who are not on HAART.

301 ntiretroviral therapy) than in those without HIV.