ライフサイエンスコーパス: HIV-1

1 HIV-1 capsid core disassembly (uncoating) must occur bef

2 HIV-1 envelope (Env) trimers, stabilized in a prefusion-

3 HIV-1 latency is a major barrier to cure.

4 HIV-1 reservoirs in the central nervous system (CNS) are

5 HIV-1 salvage therapy can safely omit NRTIs without comp

6 HIV-1 transactivator of transcription (Tat) protein has

7 HIV-1 Vpr is necessary for maximal HIV infection and spr

8 HIV-1-specific CD4 and CD8 T-cell responses have remaine

9 The human immunodeficiency virus type 1 (HIV-1) accessory protein Vpr enhances viral replication

10 counter human immunodeficiency virus type 1 (HIV-1) after sexual contact.

11 The human immunodeficiency virus type 1 (HIV-1) capsid (CA) protein forms a conical lattice aroun

12 sion of human immunodeficiency virus type 1 (HIV-1) continues to cause new pediatric cases of infecti

13 d-kill" human immunodeficiency virus type 1 (HIV-1) cure strategy involves latency reversal followed

14 to the human immunodeficiency virus type 1 (HIV-1) every year, but not all acquire the virus, sugges

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

16 Human immunodeficiency virus type 1 (HIV-1) infection persists despite years of antiretrovira

17 role in human immunodeficiency virus type 1 (HIV-1) infection.

18 del for human immunodeficiency virus type 1 (HIV-1) vaccines, therapeutics, and cure strategies.

19 sion of human immunodeficiency virus type 1 (HIV-1) via breastfeeding is responsible for nearly half

20 against human immunodeficiency virus type 1 (HIV-1), but their assembly remains poorly understood.

21 tein of human immunodeficiency virus type 1 (HIV-1).

22 ow that human immunodeficiency virus type-1 (HIV-1) with HBV-associated amino acid substitutions Y115

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

24 subverted by human immunodeficiency virus 1 (HIV-1) to increase viral gene expression.

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

26 14 cases with sequences that shared 98-100% HIV-1 nucleotide identity.

27 mes in paired CSF and plasma samples from 12 HIV-1-positive participants in the CNS HIV Antiretrovira

28 e analyzed peripheral blood samples from 400 HIV-1(+) adults on ART from several diverse cohorts, rep

29 ood levels of 35 inflammatory markers in 406 HIV-1-negative individuals.

30 (N = 163) and previously published (N = 495) HIV-1 polymerase sequences collected during 2005-2019.

31 e presence of plasma bnAbs in a cohort of 51 HIV-1 clade-C infected infants and identify viral factor

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

33 rials and other protocols aimed at achieving HIV-1 remission.

34 plasma samples from blood donors with acute HIV-1 infection and one viral culture supernatant were s

35 To determine how CpG dinucleotides affect HIV-1 replication, we increased their abundance in multi

36 ed i.m. with plasmid DNA encoding a model Ag HIV-1 Env gp140 and selected chemokines/cytokine and boo

37 their in vitro neutralizing activity against HIV-1 Env pseudotyped viruses.

38 f1), which showed antiviral activity against HIV-1(HXB2), with a half maximal inhibitory concentratio

39 CD4-based decoy approaches against HIV-1 are attractive options for long-term viral control

40 ndidate for pre-exposure prophylaxis against HIV-1.

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

42 These studies illustrate that although HIV-1 RNA serves two functions, as a translation templat

43 lestone in the optimization of NBD-11021, an HIV-1 gp120 antagonist, by developing a new and novel an

44 3%) participants in the DTG + FTC arm had an HIV-1 RNA viral load of <50 copies/ml compared to 86/94

45 In an HIV-1 latency model using autologous CD8(+) T cell clone

46 is a major target for the development of an HIV-1 vaccine.

47 necessary for the rational development of an HIV-1 vaccine.

48 We investigated whether an HIV-1 vaccine platform designed to increase the number o

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

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

51 at some conjugates act as dNTP analogues and HIV-1 reverse transcriptase (RT) catalytically incorpora

52 itro deamination and DNA binding assays, and HIV-1 restriction assays identify R24, located in the NT

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

54 ecific recovery of human IgG, IFN-gamma, and HIV-1 RNA indicate the diagnostic utility of plasma obta

55 receptors, mGlu5 receptors, FFA1/GPR40, and HIV-1 RT.

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

57 romoter activity of diverse HIV-subtypes and HIV-1 replication in primary T cells.

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

59 sts for the generation of highly active anti-HIV-1 antibodies with the potential to engineer PTMs.

60 The selection of anti-HIV-1 bNAbs for clinical development was primarily guide

61 the magnitude and functionality of the anti-HIV-1 antibody response, we will have the foundation nec

62 approach to design new targeted peptides as HIV-1 fusion inhibitors and lead us to define a retro-en

63 the replication of orthoretroviruses such as HIV-1 and are proven therapeutic targets.

64 ted primary CD4(+) T cells, thus attenuating HIV-1-induced upregulation of Tim-3.

65 tasets that were subsamples of the available HIV-1 genomes from 1978 to 2014, showing the inherent ph

66 We investigated the interface between HIV-1 RT and a broad-spectrum UCAA-family aptamer.

67 arize current knowledge of the links between HIV-1 infection and immunometabolism, and we discuss the

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

69 ants and imaging revealed that CLIP170 bound HIV-1 cores in a manner distinct from currently known ca

70 ar protein that is incorporated into budding HIV-1 particles and reduces HIV-1 infectivity by inhibit

71 ssion as well as viral infection, notably by HIV-1.

72 proteolytic cleavage of precursor p66/p66 by HIV-1 protease, suggesting that it stabilizes the produc

73 ubule-containing TNT that are long and carry HIV-1 cargo.

74 terferes with capsid binding to the cellular HIV-1 cofactors Nup153 and CPSF6 that mediate viral nucl

75 fied sex-specific differences during chronic HIV-1 infection, but little is known about sex differenc

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

77 Moreover, SECH clears HIV-1 in blood samples from HIV-1-infected patients.

78 recent study has revealed that Dbr1 cleaves HIV-1 gRNA lariats that form early after viral entry.

79 and independent t-tests were used to compare HIV-1-infected individuals within or outside an identifi

80 ed effector memory T (T(EM)) cells contained HIV-1 DNA that was genetically identical to viral sequen

81 roviral therapy suppresses but does not cure HIV-1 infection due to the existence of a long-lived res

82 s an important milestone for efforts to cure HIV-1 infection.

83 nd that, on average, half of the cytoplasmic HIV-1 RNAs are being actively translated at a given time

84 ages, while depletion of cyclin L2 decreased HIV-1 replication.

85 B sensitivity and cofactor binding defective HIV-1 capsid mutants P90A (defective for cyclophilin A a

86 tream of the gag gene start codon of diverse HIV-1 strains by using next-generation sequencing (NGS)

87 We observed that diverse HIV-1 strains exhibit a range of sensitivities to such t

88 to better understand the mechanisms driving HIV-1 pathogenesis and to identify new targets for thera

89 During HIV-1 entry into target cells, binding of the virus to h

90 ells is associated with viral control during HIV-1 infection, but little is known about CD8 cross-rea

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

92 fferences between men and women during early HIV-1 infection by contributing to both viral control an

93 ays a key role in shaping responses to early HIV-1 infection that influence the chronic phase of dise

94 To elucidate responses to early HIV-1 replication, we studied blood pDCs in 29 HIV-infec

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

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

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

98 Enhanced HIV-1 replication correlated with higher percentages of

99 ART interruption is associated with enhanced HIV-1-specific T cell responses.

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

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

102 face human BST-2 expression, and facilitated HIV-1 virion release in the presence of human BST-2.

103 out seven thousand molecules inhibiting five HIV-1 proteins were used to develop regression and class

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

105 odels to inform cure-directed approaches for HIV-1-infected children.

106 en the subdomains of SERINC5 as critical for HIV-1-restriction activity.

107 any patients, currently there is no cure for HIV-1, presumably due to the presence of reservoirs of t

108 site analyses reveal a strong preference for HIV-1 to integrate into speckle-associated genomic domai

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

110 lly, we tested how polygenic risk scores for HIV-1 acquisition influence blood levels of 35 inflammat

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

112 nital tract, a dynamic anatomical target for HIV-1 infection throughout all disease stages.

113 Chemical depletion of cholesterol from HIV-1 particles inactivates their infectivity.

114 ver, SECH clears HIV-1 in blood samples from HIV-1-infected patients.

115 labeled fluorescent reporter red/green (R/G)-HIV-1 was used to identify and enrich restricted and act

116 on, DC continues to experience a generalized HIV-1 epidemic.

117 tal features of human bNAbs, thereby guiding HIV-1 immunogen design.

118 Eighteen cases (49%) had HIV-1 viral loads (VLs) >100,000 copies/mL and 47% had C

119 In the highly resistant group, 53% had HIV-1 RNA <200 copies/mL at week 96.

120 Proliferation of CD4+ T cells harboring HIV-1 proviruses is a major contributor to viral persist

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

122 In this study, we investigated how HIV-1 protein Nef secreted in extracellular vesicles (ex

123 However, HIV-1 persists in a latent reservoir in resting CD4(+) T

124 sis, and X-ray structural analysis of hybrid HIV-1 protease inhibitors (PIs) containing bis-tetrahydr

125 We propose to identify HIV-1-suppressing agents that can inhibit HIV-1 reactiva

126 with Env glycoprotein components.IMPORTANCE HIV-1 Env protein is a major target for the development

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

128 e the use of antiretroviral therapy (ART) in HIV-1 infected mothers approximately 5% of new HIV-1 inf

129 nly subneutralizing plasma concentrations in HIV-1-infected humanized mice but elicited CD4-binding s

130 mprehensive evaluation of deubiquitinases in HIV-1 latency and establishes that they may hold a criti

131 In three independent experiments in HIV-1-infected humanized mice and one pivotal experiment

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

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

134 Identification of key regulators in HIV-1 trans-infection between DC and CD4(+) T cells has

135 We analyzed rs111200466 in HIV-1 disease progression and showed a correlation with

136 e ESCRT complexes drive membrane scission in HIV-1 release, autophagosome closure, multivesicular bod

137 ive-control, randomized, open-label study in HIV-1-infected antiretroviral therapy-naive adults (CD4+

138 simultaneously enhance viral suppression in HIV-1-infected macrophages.

139 even 1-18 alone fully suppressed viremia in HIV-1-infected humanized mice without selecting for resi

140 s spikes with other viral proteins including HIV-1 envelope, Lassa virus glycoprotein complex, and in

141 es of many vertebrate RNA viruses, including HIV-1.

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

143 Knockdown or inhibition of DYRK1A increased HIV-1 replication in macrophages, while depletion of cyc

144 Tim-3 blockade increases HIV-1 replication, suggesting a potential negative role

145 ualize and track translation from individual HIV-1 RNA molecules in living cells.

146 ug resistance mutations (DRMs) on individual HIV-1 polymerase genomes in the cerebrospinal fluid (CSF

147 tify doses of RMD that were safe and induced HIV-1 expression.

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

149 to how pre-existing Mtb infection influences HIV-1 pathogenesis.

150 fy HIV-1-suppressing agents that can inhibit HIV-1 reactivation and reduce HIV-1-induced immune activ

151 correlated with SERINC5's ability to inhibit HIV-1 infectivity.

152 nscripts due to depletion of NAT10 inhibited HIV-1 replication by reducing viral RNA stability.

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

154 Interestingly, HIV-1 infection down-regulated miR-125b expression concu

155 1 infection, cognitive impairments, that is, HIV-1-associated neurocognitive disorders remain prevale

156 combination eliminated reactivated latently HIV-1-infected cells in an ex vivo quantitative viral ou

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

158 Least-squares mean HIV-1 RNA at 7 days after dose decreased from 1.67 log(1

159 83% of whom had undetectable (<20 copies/mL) HIV-1 viral load (VL).

160 e of low-level viremia that persists in most HIV-1-positive individuals on antiretroviral therapy (AR

161 Recently, numerous broadly neutralizing HIV-1 monoclonal antibodies (bNAbs) have been developed

162 it humoral responses capable of neutralizing HIV-1 strains closely matched in sequence to the immuniz

163 V-1 infected mothers approximately 5% of new HIV-1 infections still occur in breastfed infants annual

164 velopment of novel strategies to prevent new HIV-1 infections in infants.

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

166 by both phylogenetic and network analyses of HIV-1 pol sequences.

167 tabolic labeling and pulse-chase analysis of HIV-1 Gag proteins, we verified that chicken BST-2 block

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

169 ant gp120 proteins from four major clades of HIV-1 (A, B, C, and AE), produced either as research-gra

170 about CD8 cross-reactivity in the context of HIV-1 vaccination.

171 gonist against human BST-2 in the context of HIV-1.

172 Three individuals with natural control of HIV-1 infection (controllers) on ART, included because c

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

174 IV-1 genome in controlling the life cycle of HIV-1 indicates that this region significantly influence

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

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

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

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

179 argeted therapy to reduce trans-infection of HIV-1 in vivo.

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

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

182 nderstanding of the regulatory mechanisms of HIV-1 replication, we adapted a recently described syste

183 We used an infant rhesus macaque model of HIV-1 infection via breastfeeding to identify key sites

184 estigated in primary and cell line models of HIV-1 latency and reactivation.

185 role for host genetics in the moderation of HIV-1 acquisition.

186 The presence of HIV-1 in the brain often leads to HIV associated neuroco

187 lly reconstitute the sequential processes of HIV-1 assembly and maturation from purified components.I

188 h protection from and delayed progression of HIV-1 infection provides a rationale to leverage ADCC-me

189 The proportion of HIV-1 infections due to recombinants was highest in Sout

190 much smaller reduction in the proportion of HIV-1-infected cells within LNs per year on therapy that

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

192 e potential of exposing hidden reservoirs of HIV-1 to elimination by the immune system.

193 A total of 209 partial pol gene sequences of HIV-1 CRF55_01B were sampled during 2007-2015 from 7 pro

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

195 reconstituted and imaged the early stages of HIV-1 replication in a cell-free system.

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

197 spatio-temporal staging of critical steps of HIV-1 infection and provide an experimental system to se

198 controllers (EC) represent a small subset of HIV-1-infected people that spontaneously control viral r

199 antiretroviral therapy for the treatment of HIV-1 infection, cognitive impairments, that is, HIV-1-a

200 e a potential candidate for the treatment of HIV-1-associated brain inflammation.

201 When we examined the effect of CVF on HIV-1 transmigration through endocervical epithelium, we

202 ved function of Nef has a positive effect on HIV-1 replication, allowing for more efficient replicati

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

204 ntrolling infections by influenza, Ebola, or HIV-1 in animal models.

205 ification (SGA) was used to generate partial HIV-1 polymerase genomes in paired CSF and plasma sample

206 Pharmacological HIV-1 reactivation to reverse latent infection has been

207 proportion of participants who had a plasma HIV-1 RNA concentration of less than 50 copies per mL at

208 e, and efavirenz group had achieved a plasma HIV-1 RNA concentration of less than 50 copies per mL.

209 tive phase with an ATLAS-2M screening plasma HIV-1 RNA less than 50 copies per mL.

210 inicians for nonsuppressible viremia (plasma HIV-1 RNA above 40 copies/mL) despite reported adherence

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

212 yndrome, is distinct from the more prevalent HIV-1 in several features including its evolutionary his

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

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

215 tic stochasticity across subsets of the real HIV-1 diversity.

216 at can inhibit HIV-1 reactivation and reduce HIV-1-induced immune activation.

217 ted into budding HIV-1 particles and reduces HIV-1 infectivity by inhibiting virus-cell fusion.

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

219 health, including influenza virus, reovirus, HIV-1, human metapneumovirus, and vesicular stomatitis v

220 At week 48, a virologic response (HIV-1 RNA level, <40 copies per milliliter) had occurred

221 membrane protein SERINC5 potently restricts HIV-1 infectivity and sensitizes the virus to antibody-m

222 ne deacetylase inhibitor reported to reverse HIV-1 latency.

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

224 Here we have use genetics to separate HIV-1 nuclear import cofactor dependence from MxB sensit

225 proteome for each participant and sequenced HIV-1 outgrowth viruses from resting CD4+ T cells.

226 ime points after viral rebound, we sequenced HIV-1 env (C2-V3), gag (p24), and pol (reverse transcrip

227 Several HIV-1 and SIV vaccine candidates have shown partial prot

228 Since HIV-1 fusion inhibitor peptides need to be embedded in t

229 ration sequencing of near-full-length single HIV-1 genomes and corresponding chromosomal integration

230 racted by retroviral proteins, specifically, HIV-1 Nef, MLV glycoGag, and EIAV S2.

231 RT, included because controllers have strong HIV-1-specific CTL responses, had a smaller proportion o

232 We studied HIV-1 reactivation in the female genital tract, a dynami

233 In summary, HIV-1 and MMTV share common features such as membrane bi

234 nscription, but not splicing nor supernatant HIV-1 RNA.

235 hed nonhuman primate model of ART-suppressed HIV-1 infection, we tested strategies to overcome these

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

237 s intrinsic membrane protein that suppresses HIV-1 infectivity when incorporated into budding virions

238 In this study we employ as a model system HIV-1 TAR RNA and its interaction with the ligand argini

239 We highlight the importance of the TF HIV-1 phenotype and the role of different DC subsets in

240 Here, we demonstrate that HIV-1 Vpu downregulates Tim-3 from the surface of infect

241 tion by wild-type capsid, demonstrating that HIV-1 can use distinct nuclear import pathways during in

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

243 or at least 30 years, it has been known that HIV-1 Vpr, a protein carried in the virion, is important

244 We recently reported that HIV-1 Vif is also able to degrade the PPP2R5 family of r

245 We showed that HIV-1 infection is exacerbated in macrophages exposed to

246 The HIV-1 capsid is the key determinant of MxB sensitivity a

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

248 The HIV-1 secreted protein HIV Tat has been found to synergi

249 The HIV-1 virulence factor Nef promotes high-titer viral rep

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

251 early 100-fold depending on the bNAb and the HIV-1 clade.

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

253 mulations, revealed that the residues at the HIV-1 MA C terminus help stabilize protein-protein inter

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

255 es control key replication events during the HIV-1 life cycle.

256 o this failure and report a key role for the HIV-1 protein NEF in preventing B-cell maturation into a

257 ggesting that cholesterol depletion from the HIV-1 envelope membrane reduces virus entry.

258 Overall, the position of CpGs in the HIV-1 genome determines the magnitude and mechanism thro

259 entified all reactive T cell epitopes in the HIV-1 proteome for each participant and sequenced HIV-1

260 for passive translocation of dNTPs into the HIV-1 capsid.

261 RINC5 protein alters the conformation of the HIV-1 Env proteins and that this action is correlated wi

262 the regulatory elements at the 5' end of the HIV-1 genome in controlling the life cycle of HIV-1 indi

263 n eOD-GT8, an engineered outer domain of the HIV-1 glycoprotein-120, on DNA origami nanoparticles to

264 A comparison of the membrane topology of the HIV-1 MA, using the surface-mapping method and molecular

265 nverts the conformational equilibrium of the HIV-1 transactivation response element (TAR) RNA, such t

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

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

268 iverse viral subtypes that contribute to the HIV-1 pandemic.

269 ng simulation has been carried out using the HIV-1 protease as receptor, thus paving the way to study

270 lize protein-protein interactions within the HIV-1 MA lattice at the plasma membrane.

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

272 nteractions, in this work for the first time HIV-1 LTR model featuring repressed, intermediate, and a

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

274 eplication while potentially contributing to HIV-1 pathogenesis by triggering T cell activation and c

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

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

277 urface mapping, indicated that, similarly to HIV-1, MMTV uses a myristic switch to anchor the MA to t

278 rts, representing a robust sample of treated HIV-1 infection in the United States.

279 The trimeric HIV-1 Envelope protein (Env) mediates viral-host cell fu

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

281 as to understand the biology of unintegrated HIV-1 DNA and reveal the mechanisms involved in its tran

282 reatment of adults with previously untreated HIV-1 infection.

283 replication of Human Immunodeficiency Virus (HIV-1) in many patients, currently there is no cure for

284 The primary endpoint at week 48 was HIV-1 RNA >=50 copies per mL (Snapshot, intention-to-tre

285 ks was non-inferior to dosing every 4 weeks (HIV-1 RNA >=50 copies per mL; 2% vs 1%) with an adjusted

286 nt, particularly in Sub-Saharan Africa where HIV-1 subtype C predominates.

287 ion and exhaustion were performed along with HIV-1 RNA and deoxyribonucleic acid quantification and m

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

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

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

291 and women (aged 18-60 years, inclusive) with HIV-1 infection who were ART naive.

292 inhibition is mediated by interference with HIV-1 Env and can impact a variety of viral clades.

293 therapy, 30 to 50% of the people living with HIV-1 suffer from mild to moderate neurocognitive disord

294 More than 36 million people are living with HIV-1 worldwide, and despite antiretroviral therapy, 30

295 of a prospective cohort of outpatients with HIV-1 attending a reference HIV unit from January 2005 o

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

297 depleted in the blood and gut of people with HIV-1, even with effective antiretroviral therapy.

298 egy for virologically suppressed people with HIV-1.

299 amous-cell carcinoma (IASCC) in persons with HIV-1, we performed a single-center, retrospective analy

300 allenges of wild-type (WT), Y181C, and Y181V HIV-1 were performed in mice left untreated or after RPV