ライフサイエンスコーパス: HIV

1 HIV drug resistance is a major threat to achieving long-

2 HIV encodes an aspartyl protease that is activated durin

3 HIV infection (24.4%, 74/303) was not associated with ot

4 HIV migration was more frequent from San Diego county to

5 HIV pol sequences sampled across China were used to iden

6 HIV surveillance data were used to assess demographic, c

7 HIV transmission via genital and colorectal mucosa are t

8 HIV-negative, non-pregnant Rwandan BV patients were rand

9 Human immunodeficiency virus type 1 (HIV-1) exploits a number of specialized microtubule (MT)

10 Human immunodeficiency virus 1 (HIV-1) is a life-threatening pathogen that still lacks a

11 nfected with human immunodeficiency virus 1 (HIV-1).

12 Among 119 HIV-seronegative inpatients, 46 (39%) had culture-positi

13 BV/KSHV co-infection (OR = 5.71(1.58-7.12)), HIV positivity (OR = 2.22(1.32-3.73)) and living in a mo

14 In total, 485 HEU children and 2495 HIV-unexposed controls were included.

15 Of 3259 HIV-negative MSM, 19% were currently using PrEP, 6% had

16 ses were performed on stool samples from 405 HIV-infected and 111 uninfected participants of the Cope

17 We studied 1123 men (589 HIV+ and 534 HIV-) from MACS (Multicenter AIDS Cohort Study), using t

18 years, 586 of whom were HIV-negative and 535 HIV-positive.

19 We studied 1123 men (589 HIV+ and 534 HIV-) from MACS (Multicenter AIDS Cohort St

20 viral load) were virally suppressed, and 673 HIV-negative men (40% of 1673) were circumcised in inter

21 For the early-treated cohort (83 HIV-1 adult patients treated within 3 months after infec

22 vention interventions, are needed to achieve HIV epidemic control.

23 gs are susceptible to high rates of acquired HIV drug resistance (HIVDR), but few studies include chi

24 ch consortium, which investigates adolescent HIV prevention and treatment in seven LMICs: Brazil, Ken

25 ical treatment interruption (ATI) may affect HIV persistence research.

26 orm curative and preventive measures against HIV/AIDS.

27 represent a novel therapeutic target against HIV-1 infection and HIV-associated neurological complica

28 fness measured with TE was similar among all HIV, LD+, LD-, and control patients and between the LD+

29 of knowledge regarding mechanisms that allow HIV-infected cells to persist in individuals during comb

30 igated 3 rapid urine tests in 372 ambulatory HIV-negative individuals suspected of having TB in South

31 Among HIV-infected, model of end-stage liver disease (aHR, 1.0

32 and HSILs were common during follow-up among HIV-positive MSM without dysplasia at baseline.

33 onfirmatory assay in 12.0% (10/83) and in an HIV rapid test in 31.3% (26/83).

34 s the implementation science framework of an HIV/AIDS program in the United States.

35 cally evolving viral reservoir along with an HIV-1-specific immune response seems to be key for the s

36 both safe and efficacious against HSV-2 and HIV-1 infections in vivo.

37 prominent roles in development, cancer, and HIV, the chemokine receptor CXCR4 and its ligand CXCL12

38 ation in vitro and autophagosome closure and HIV-1 release in human cells.

39 a large cohort of HIV/HTLV-1-coinfected and HIV-monoinfected individuals on combination antiretrovir

40 condom use with clients, and depression and HIV infection.

41 erapeutic target against HIV-1 infection and HIV-associated neurological complications.

42 istics, outpatient prescription, kidney, and HIV databases.

43 ment of both haematological malignancies and HIV.

44 rug resistant mutations (DRMs), subtypes and HIV-1 diversity estimations were completed.

45 e modeling of concurrent treatment of TB and HIV to potentially reduce the risk of reactivation of TB

46 revious studies of murine leukemia virus and HIV-1, we hypothesized that unpaired guanosines in the 5

47 at baseline, 30% at the follow-up visit) and HIV-positive (27% at baseline, 35% at the follow-up visi

48 he Data Collection on Adverse Events of Anti-HIV Drugs (DAD) study has reported an increased risk of

49 Persons who are HIV positive and taking ART and persons taking PrEP to p

50 As HIV incidence and mortality continue to increase in east

51 y rollout among at-risk populations, such as HIV-serodiscordant couples, adolescent girls and young w

52 of the JCI, Chaillon and coworkers assessed HIV-infected cells from various anatomic compartments ob

53 y of the qSVS assay in quantifying authentic HIV minority variants, and support the use of this appro

54 Antiretroviral therapies efficiently block HIV-1 replication but need to be maintained for life.

55 te Type IV-B, was the most prevalent in both HIV-negative (38% at baseline, 30% at the follow-up visi

56 although the gut microbiome is influenced by HIV infection and may contribute to altered immunity, th

57 Nevertheless, candidate HIV interventions for men advance to clinical trials wit

58 ated invariant T (MAIT) cell loss in chronic HIV-1 infection is a significant insult to antimicrobial

59 Inclusion criteria were confirmed HIV infection and age > 18 years.

60 aracterize the cellular factors that control HIV multiplication in these reservoir cells.

61 In both high- and low-income countries, HIV-negative children born to HIV-positive mothers (HIV

62 Curing HIV infection will require the elimination of a reservoi

63 We defined HIV PrEP utilization as the number of people taking teno

64 infected CD4+ T cells that persists despite HIV-specific cytotoxic T cell (CTL) responses.

65 among black patients, those with detectable HIV RNA, and those with lower CD4 cell counts (all P < .

66 We applied the methods to determine HIV prevalence in men having sex with men in Brazilian c

67 Countries should consider incorporating dual HIV and syphilis rapid diagnostic tests as the first tes

68 these responses play a role in driving early HIV-1 viral evolution.IMPORTANCE HIV-1 has exceptionally

69 to explore these areas to develop effective HIV cure strategies.

70 Efficacious HIV-1 vaccination requires elicitation of long-lived ant

71 atent Mtb infection supported more efficient HIV-1 transcription, release, and replication.

72 random sample was assessed for eligibility (HIV+, age >= 14 years, on ART >6 months, not acutely ill

73 To this end, HIV-1 patients on antiretroviral therapy who are reporte

74 treatment interventions, including enhanced HIV testing, earlier antiretroviral therapy (ART), and s

75 dependent modulation of T(fh) cells enhances HIV-1 vaccine-induced antienvelope (anti-Env) antibody r

76 tivate the HIV-1 LTR promoter and facilitate HIV-1 viral replication in the nucleus.

77 nhibitor-sensitive immune response following HIV-1 infection.

78 sitive people in South Africa, adjusting for HIV treatment outcomes.

79 d present an opportunity to improve care for HIV-2-infected individuals.

80 t Through a Comprehensive Care Continuum for HIV-affected Adolescents in Resource Constrained Setting

81 he greatest obstacle to obtaining a cure for HIV infection, as these cells can persist despite decade

82 ve, antiretroviral therapy is not a cure for HIV infection.

83 Developing a cure for HIV is a global priority.

84 To get a cure for HIV, it is important to identify and characterize the ce

85 ofovir disoproxil fumarate/emtricitabine for HIV prevention.

86 were injection drug use as a risk factor for HIV acquisition (aOR, 2.2; 95% CI, 1.3-3.9), hepatitis C

87 NRS IPERGAY trial with on demand TDF/FTC for HIV prevention and the impact of doxycycline post-exposu

88 tabine and tenofovir disoproxil fumarate for HIV prevention, as the upper limit of the 95% CI of the

89 Kidney transplant (KT) outcomes for HIV-infected (HIV+) persons are excellent, yet acute rej

90 ally from test-and-treat recommendations for HIV.

91 studied for HIV-1, has not been reported for HIV-2 and could present an opportunity to improve care f

92 identified 11 cellular pathways required for HIV-1 reactivation as druggable targets.

93 who were HIV-uninfected and at low-risk for HIV, were randomly assigned (3:1) to long-acting injecta

94 be considered when designing strategies for HIV prevention for PWID.

95 drug resistance testing, widely studied for HIV-1, has not been reported for HIV-2 and could present

96 o vaccines, including candidate vaccines for HIV.

97 mmune responses in affording protection from HIV.IMPORTANCE CD40-CD40 ligand (CD40L) interaction is c

98 id conditions at time of LTBI testing (e.g., HIV, diabetes, chronic kidney disease, etc.) were identi

99 NAIDS 90-90-90 targets to monitor the global HIV response, highlighting a need to address the holisti

100 Demographic data, TBM severity grade, HIV co-infection status, and clinical endpoints by 3 mon

101 cause of morbidity and mortality in the HBV/HIV co-infected patient population.

102 se, there were 246 children living with HIV (HIV+) who were initiated on ART before 3 years of age in

103 However, little is known about how HIV-1 latency affects their function.

104 iving early HIV-1 viral evolution.IMPORTANCE HIV-1 has exceptionally high sequence diversity, much of

105 of HIV replication in macrophages.IMPORTANCE HIV continues to be a major public health problem worldw

106 e mechanism limiting viral spread.IMPORTANCE HIV infection modulates the surface expression of Tim-3,

107 In HIV-uninfected patients, nonalcoholic fatty liver diseas

108 articipants of the Copenhagen Comorbidity in HIV Infection (COCOMO) study.

109 rebrospinal fluid (CSF) by flow cytometry in HIV-infected adults with cryptococcal (n = 31) and noncr

110 However, the true magnitude of difference in HIV-related mortality between men and women receiving an

111 ortality associated with mental disorders in HIV-positive people in South Africa, adjusting for HIV t

112 persons with and without TB at enrollment in HIV care, starting 9 months after clinic enrollment.

113 obes is important to consider, especially in HIV infection where gut-intestinal barrier dysfunction c

114 an early acting endosomal factor involved in HIV-1 budding from the cells.

115 mide (TAF) improves renal tubular markers in HIV-infected individuals but the impact on estimated glo

116 veillance and prevention of LRTIs and PTB in HIV+ adolescents.

117 ady contributed to substantial reductions in HIV-1 incidence and mortality in eSwatini.

118 y (BMD) and biomarkers of bone remodeling in HIV/HCV coinfected patients.

119 initiation in the hospital and retention in HIV care and viral suppression over a 12-month period.

120 gh its capacity to predict mortality risk in HIV-HCV-coinfected patients has never been investigated.

121 search on key populations and their roles in HIV implementation and sustainable scale-up is needed in

122 e as biomarkers for anal cancer screening in HIV+ and at-risk HIV-negative women.

123 to achieving long-term viral suppression in HIV-positive individuals.

124 Our results suggest that timing of TI in HIV-infected children has a long-term and measurable imp

125 TB amongst those with HIV who are not yet in HIV care, and who would thus be ineligible for a LAM tes

126 as those with underlying diseases including HIV/AIDS and cystic fibrosis.

127 Tim-3 knockdown and Tim-3 blockade increased HIV-1 replication in primary CD4(+) T cells, thereby sug

128 violence (IPV) is associated with increased HIV risk and other adverse health and psychosocial outco

129 y transplant (KT) outcomes for HIV-infected (HIV+) persons are excellent, yet acute rejection (AR) is

130 ts treated within 3 months after infection), HIV-1 diagnosis was not obtained in at least 1 confirmat

131 red to present the ectodomains of influenza, HIV, and RSV viral glycoprotein trimers.

132 We show that SP rapidly inhibits HIV-1 transcription by reducing RNAPII recruitment to th

133 nd such interventions can be integrated into HIV-care programs in low-income settings.

134 ion-based data from ~22,000 persons of known HIV status to characterize migratory patterns and their

135 The viral protein Gag selects full-length HIV-1 RNA from a large pool of mRNAs as virion genome du

136 tors driving the dispersal of pathogens like HIV as they have difficulties capturing linkages between

137 dy included 185 women (128 with longstanding HIV infection, 88% under antiretroviral therapy; and 57

138 We evaluated the impact of maternal HIV infection on the burden of RSV among mothers and the

139 In high and medium HIV prevalence settings in South Africa and Uganda, comm

140 approach to examine the impacts of minority HIV variants on virologic response and clinical outcome.

141 ative children born to HIV-positive mothers (HIV exposed, uninfected [HEU]) are more susceptible to s

142 hat viremia rebounded despite the absence of HIV-1 adaptation to VRC01 and an average VRC01 trough of

143 Because of HIV's vast sequence diversity, the ability of the CD8 T-

144 ntrast, SERINC5 did not alter the capture of HIV-1 particles bearing the SERINC5-resistant Env protei

145 inal humoral response to KSHV in a cohort of HIV-infected Zambian mothers without KS and identify pot

146 ated with survival time in a large cohort of HIV/HTLV-1-coinfected and HIV-monoinfected individuals o

147 fficacy of immunotherapies in the context of HIV and cancer, and opportunities for novel applications

148 Relative control of HIV-1 infection has been linked to genetic and immune ho

149 bit early steps of the replicative cycles of HIV-1 and EV-A71 by interacting with their respective vi

150 mate the global and regional distribution of HIV-1 recombinant forms during 1990-2015.

151 However, the vast diversity of HIV-1 is a major challenge for both active and passive i

152 and multiplexed identification of dozens of HIV drug-resistance mutations.

153 Known duration of HIV diagnosis does not seem to be a criterion for select

154 cans on the envelope glycoproteins (Envs) of HIV-1.

155 However, eradication of HIV is a major challenge due to cellular and anatomical

156 r that targets and reduces the expression of HIV Env.

157 ble of transcribing novel unspliced forms of HIV-RNA transcripts with competent open reading frames (

158 ective viral surfaces (glycoprotein gp120 of HIV and the fivefold axis of the EV-A71 capsid).

159 al association between the implementation of HIV PrEP and the growing incidence rates of sexually tra

160 thway by AZD5582 results in the induction of HIV and SIV RNA expression in the blood and tissues of A

161 Overall, our data show that inhibition of HIV-1 maturation by BVM involves changes in structure an

162 complex blockade to monitor the kinetics of HIV-1 nuclear import and define the biochemical staging

163 ver, the impact and underlying mechanisms of HIV Tat in KSHV-infected endothelial cells undergoing vi

164 care to support efforts to eliminate MTCT of HIV and syphilis.

165 mparison were used to detect the presence of HIV superinfection.

166 an cities and confirmed a high prevalence of HIV in these populations from 3.8% to 22.1%.

167 Whereas the process of HIV membrane fusion can be tracked by fluorescence micro

168 ntly, we demonstrate Vpr-dependent rescue of HIV-1 replication in human macrophages from inhibition b

169 lular degradation, leading to restriction of HIV replication in macrophages.

170 lin L2 expression, leading to restriction of HIV replication in macrophages.IMPORTANCE HIV continues

171 erventions are effective in reducing risk of HIV and sequelae of injection and other drug use, and th

172 d be no more than one period at high risk of HIV infection during the follow-up period when not takin

173 raction occurring during the early stages of HIV infection.

174 CD4(+) T cells of patients at all stages of HIV-1 infection.

175 A hallmark of the initiation step of HIV-1 reverse transcription, in which viral RNA genome i

176 Multiple phylogenetic studies of HIV in sub-Saharan Africa have shown that mobility-drive

177 he need for early diagnosis and treatment of HIV infection.

178 activities associated with the treatment of HIV-associated comorbidities with 92% mean accuracy was

179 Use of HIV preexposure prophylaxis (PrEP) has increased nationw

180 he effect of antiretroviral therapy (ART) on HIV suppression, immune activation, and quality of life

181 Limited data are available on HIV-related clinical indicators among transgender women.

182 (RM) model to study the impact of opioids on HIV reservoirs.

183 ing the UNAIDS 90-90-90 treatment targets on HIV-1 incidence and mortality, and to assess whether the

184 People with HIV should receive ongoing HIV prevention counselling and partner services data sho

185 Only HIV-negative or HCV-negative participants not on medicat

186 prenorphine maintenance therapy, to optimise HIV outcomes.

187 e health (29 [48%]), violence (26 [43%]), or HIV (18 [30%]).

188 YPHIVs aged >=18 years in the Pediatric HIV/AIDS Cohort Study (PHACS) AMP Up cohort approaching

189 paucity of relevant animal models of penile HIV infection.

190 cipants who initiated PrEP and had perceived HIV risk during follow-up reported taking PrEP, but one-

191 nrolled 323 women, of whom 234 had perinatal HIV infection, and reported age at sexual debut and hist

192 a key initial mechanism associated with poor HIV control.

193 The potent HIV-1 capsid inhibitor GS-6207 is an investigational pri

194 aking ART and persons taking PrEP to prevent HIV infection are donating blood.

195 or preexposure prophylaxis (PrEP) to prevent HIV-1 transmission.

196 tion and post-intervention surveys, previous HIV diagnosis increased from 47.4% (41.3-53.4) to 76.2%

197 rties of transmitted/founder (TF) or primary HIV-1 isolates, such as CCR5 tropism, tier 2 neutralizat

198 ommunities were randomly assigned to receive HIV prevention and treatment interventions, including en

199 MMC is a key component of programs to reduce HIV incidence.

200 nsmission networks of the five most relevant HIV-1 types (B and circulating recombinant forms [CRFs]

201 (from under 100 to over 1000 newly reported HIV cases among PWID) and in the extent to which combine

202 The HLA-B*57:01-restricted, HIV epitope-specific CD8 T-cell responses showed benefic

203 or anal cancer screening in HIV+ and at-risk HIV-negative women.

204 d enhances the ELL2-SEC formation for robust HIV-1 transactivation.

205 representative experimental systems to study HIV-CNS pathology.

206 aining integrase inhibitors rapidly suppress HIV viral load in non-pregnant adults, few published dat

207 Second, filgotinib suppresses HIV-1-driven aberrant cancer-related gene expression at

208 We sorted all participants of the Swiss HIV Cohort Study (SHCS) with at least 1 documented MTB t

209 re more susceptible to severe infection than HIV-unexposed, uninfected (HUU) children, with altered i

210 Interestingly, our data indicate that HIV-1 MA binds cooperatively to the PM with a dissociati

211 Clinical observation suggests that HIV progress more rapid in females than males.

212 The HIV Prevention Trials Network (HPTN) 067/Alternative Dos

213 The HIV-1 envelope protein (Env) is the target of neutralizi

214 be released in order for it to activate the HIV-1 LTR promoter and facilitate HIV-1 viral replicatio

215 Additionally, viral factors such as the HIV-1 accessory protein Nef can antagonize this antivira

216 Patients attending the HIV outpatient clinic of Pathophysiology Department at <

217 that although some common motifs between the HIV-1 Vif and MVV Vif are involved in recruiting Cul5, d

218 to reach national targets of the ending the HIV epidemic initiative by 2030.

219 addressing the opioid crisis and Ending the HIV Epidemic.

220 and measurable impact on the quality of the HIV-specific T cell immune responses and transcriptional

221 ross the in vitro BBB model and suppress the HIV-1 in macrophage cells.

222 iption by reducing RNAPII recruitment to the HIV-1 genome.

223 ha (TNF-alpha), CCL3, CCL4, and CCL20, their HIV-1 reactivation capacity was almost completely blocke

224 o overcome social and structural barriers to HIV care will be required to reach national targets of t

225 We compared plasma antibody binding to HIV antigens between 51 nontransmitting mother-infant pa

226 ome countries, HIV-negative children born to HIV-positive mothers (HIV exposed, uninfected [HEU]) are

227 uences the susceptibility of CD4+ T cells to HIV-1 replication.

228 reduce the risk of reactivation of TB due to HIV to inform treatment strategies in patients with M. t

229 and their molecular drivers, and apply it to HIV infection.

230 hospital and its association with linkage to HIV care, frequency of outpatient care visits, retention

231 migratory patterns and their relationship to HIV among 38 communities in Rakai, Uganda with HIV preva

232 e and robust classification of resistance to HIV protease inhibitors.

233 nderstanding the earliest immune response to HIV-1 and suggest that changes in blood pDC frequency an

234 naling in the context of immune responses to HIV-1 infection.

235 associated with increased susceptibility to HIV infection.

236 The primary endpoint was total HIV DNA isolated from peripheral blood CD4(+) T-cells at

237 al contraceptives may increase genital tract HIV viral load (gVL) and sexual transmission risk to mal

238 and mortality during antiretroviral-treated HIV disease.

239 strategies in patients with M. tuberculosis/HIV coinfection.

240 mouse mammary tumor virus (MMTV) and C-type HIV-1, which assemble in the cytoplasm and at the plasma

241 race/ethnicity, and those with uncontrolled HIV experienced higher rates and worse hospitalization o

242 However, the molecular events underlying HIV neuropathogenesis remain elusive, mainly due to lack

243 6-0.85]; p=0.0001 vs 2-5 years), and unknown HIV status of the mother (aOR 0.81 [0.68-0.98], p=0.027

244 men who were HIV-uninfected (n = 314) versus HIV-infected (n = 42).

245 reased risk of human immunodeficiency virus (HIV) acquisition, but whether they alter TFV-DP or 3TC-T

246 le living with human immunodeficiency virus (HIV) and is associated with reduced systemic inflammatio

247 The human immunodeficiency virus (HIV) epidemic in India is concentrated among 3.1 million

248 oing spread of human immunodeficiency virus (HIV) has driven novel interventions, such as antiretrovi

249 re at risk for human immunodeficiency virus (HIV) infection and unintended pregnancies.

250 ral markers of human immunodeficiency virus (HIV) infection that increase before viral rebound during

251 utbreak of new human immunodeficiency virus (HIV) infections among persons who inject drugs (PWID).

252 ransmission of human immunodeficiency virus (HIV) is uncertain.

253 transcript of Human Immunodeficiency Virus (HIV) perturb translation elongation.

254 y and nondaily human immunodeficiency virus (HIV) preexposure prophylaxis (PrEP) regimens among high-

255 ssociated with human immunodeficiency virus (HIV) type 1.

256 6 months when human immunodeficiency virus (HIV) viral loads exceed 1,000 copies/mL.

257 , particularly human immunodeficiency virus (HIV), malaria and tuberculosis.

258 a prospective human immunodeficiency virus (HIV)-negative UK cohort of 333 tuberculosis contacts.

259 bnAbs) against human immunodeficiency virus (HIV).

260 le living with human immunodeficiency virus (HIV)/AIDS.

261 IC patients had human immunodefiency virus (HIV)/AIDS, cancer, stem cell or organ transplantation, n

262 the mother (aOR 0.81 [0.68-0.98], p=0.027 vs HIV-positive status).

263 ) were HBsAg-positive, and 22/100 (22%) were HIV infected.

264 e factors in pregnant African women who were HIV-uninfected (n = 314) versus HIV-infected (n = 42).

265 Participants (aged 18-65 years), who were HIV-uninfected and at low-risk for HIV, were randomly as

266 121 women aged 30-65 years, 586 of whom were HIV-negative and 535 HIV-positive.

267 ughout the programme coverage area, at which HIV testing by certified testing service counsellors was

268 PHIVs were on stable ART with HIV-1 RNA <400 copies/mL.

269 PHIV were on ART, with HIV-1 RNA levels <=400 copies/mL.

270 The SMR for COVID-19 death associated with HIV was 2.39 (95%CI 1.96-2.86); population attributable

271 nts were included, 667 (64%) coinfected with HIV.

272 X-ray structures in complex with HIV-1 RT/dsDNA showed binding of the conjugates at the p

273 rvational study evaluated 6 individuals with HIV (n = 4 with viral suppression using antiretroviral [

274 t drugs identified as recently infected with HIV (n = 23) were analyzed for clustering of their viral

275 nized mice and rhesus macaques infected with HIV and SIV, respectively.

276 en and adolescents perinatally infected with HIV with low LS BMD, 48 weeks of alendronate was well-to

277 f 1353) were on ART; 1166 people living with HIV (88% of 1321 with available viral load) were virally

278 vention communities, 1228 people living with HIV (91% of 1353) were on ART; 1166 people living with H

279 Children living with HIV (CLHIV) receiving antiretroviral treatment (ART) in

280 f these, there were 246 children living with HIV (HIV+) who were initiated on ART before 3 years of a

281 fficacy of IPT in pregnant women living with HIV (PWLHIV) are mixed.

282 Of 436 and 435 people living with HIV aged 18-49 years who participated in pre-interventio

283 ess the holistic needs of people living with HIV beyond viral suppression.

284 , ART use among diagnosed people living with HIV increased from 68.0% (60.9-75.2) to 93.1% (90.2-96.0

285 od supplements provided to women living with HIV significantly increased weight and CD4+ T cells, and

286 udy end the proportion of people living with HIV who were diagnosed was significantly higher in inter

287 ow reinfection rate among people living with HIV, suggesting that microelimination is feasible.

288 Among men with HIV, the prevalence of the 7 HR-HPV types in the 9v vacc

289 Among participants with HIV infection, 36/108 (33%) had incidental findings comp

290 follow-up in preexisting DM in patients with HIV-1 infection.

291 People with HIV (PWH) may have numerous risk factors for acquiring C

292 People with HIV should receive ongoing HIV prevention counselling an

293 s the increased cancer burden in people with HIV, the increasing evidence for the safety and efficacy

294 rated, and durable treatment for people with HIV, with no emergent resistance.

295 e and achieve desired outcomes, persons with HIV must be consistently engaged in care and able to acc

296 inical, and behavioral factors for PWID with HIV diagnosed during 2017 and 2018.

297 gely from diagnosis of TB amongst those with HIV who are not yet in HIV care, and who would thus be i

298 V among 38 communities in Rakai, Uganda with HIV prevalence ranging from 9 to 43%.

299 n scores for PLWH compared to people without HIV when using a conventional measure of cognitive funct

300 antiretroviral therapy; and 57 women without HIV from the same geographic location with comparable ch