ライフサイエンスコーパス: HIV-1

1 HIV-1 and its surface envelope glycoproteins (Env), gp12

2 HIV-1 drug resistance to older thymidine analogue nucleo

3 HIV-1 entry into host cells starts with interactions bet

4 HIV-1 establishes chronic infection and stimulates vigor

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

6 HIV-1 infection from cell-to-cell may provide an efficie

7 HIV-1 integrates its viral genome into the host cell, le

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

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

10 HIV-1 reverse transcriptase (RT) possesses both DNA poly

11 HIV-1 transcription was quantified by measuring plasma H

12 HIV-1-induced PS redistribution depends on Ca(2+) signal

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

14 Human immunodeficiency virus type 1 (HIV-1) entry into cells is mediated by the viral envelop

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

16 of high human immunodeficiency virus type 1 (HIV-1) infection and tuberculosis coprevalence.

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

18 Human immunodeficiency virus type 1 (HIV-1) is the result of cross-species transmission of si

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

20 HIV type 1 (HIV-1) RNA was measured in paired SP and blood plasma (B

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

22 gens in human immunodeficiency virus type 1 (HIV-1) vaccine development programs.

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

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

25 The human immunodeficiency virus type 1 (HIV-1)/simian immunodeficiency virus (SIV) envelope spik

26 populations in longitudinal samples from 10 HIV-1-infected children who initiated ART when viral div

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

28 milar results were also obtained with tier 2 HIV-1 viruses using a human anti-gp41 nnAb, 246D.

29 al repertoire of 29 CTL responses against 23 HIV-1 epitopes longitudinally in nine chronically infect

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

31 adly neutralizing antibodies (bNAbs) against HIV-1 could overcome these shortcomings.

32 ty elicited by vaccination, not just against HIV-1.

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

34 The mechanism that allows HIV-1 to achieve such high efficiency of genome packagin

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

36 eted, with the ultimate goal of achieving an HIV-1 cure.

37 VRC01 is an HIV-1 CD4 binding site broadly neutralizing antibody (bn

38 Cabotegravir (GSK1265744) is an HIV-1 integrase strand transfer inhibitor with potent an

39 y, we examined the basis of resistance of an HIV-1 B/C recombinant Env (LT5.J4b12C) to non-neutralizi

40 the major barrier for the development of an HIV-1 cure.

41 ly promotes Env-mediated membrane fusion and HIV-1 infection.

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

43 with acute genotype 1 or 4 HCV infection and HIV-1 coinfection is similar to historic rates with inte

44 ependent cellular cytotoxicity responses and HIV-1-neutralizing antibodies.

45 , the (S)-FPMPA amidate prodrug, exerts anti-HIV-1 activity in TZM-bl and peripheral blood mononuclea

46 Highly potent and broadly neutralizing anti-HIV-1 antibodies (bNAbs) have been used to prevent and t

47 e in the in vivo protective activity of anti-HIV-1 antibodies.

48 n significantly enhance or decrease the anti-HIV-1 efficacy of nucleotide analogue reverse transcript

49 mechanism(s) by which viral proteins such as HIV-1 Transactivator of Transcription (Tat) protein can

50 .4mut-stabilized trimers may have utility as HIV-1 immunogens or in other antigen-specific contexts,

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

52 te to the immune-mediated control of clade B HIV-1 infection, yet there remains a relative paucity of

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

54 uggests that large A3G oligomers could block HIV-1 reverse transcriptase-mediated DNA synthesis, ther

55 , they exhibit a diminished ability to block HIV-1 cell-to-cell transmission.

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

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

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

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

60 MMP activity in TB differs by HIV-1 status and compartment, and releases matrix degrad

61 nce that are critical for its recognition by HIV-1 RT remain unclear.

62 st" RNA nuclear export dynamics regulated by HIV-1's Rev response element and the viral Rev protein;

63 V/AIDS vaccine candidates expressing clade C HIV-1 antigens, with one of them lacking the vaccinia vi

64 ukin diftitox in humanized mice with chronic HIV-1 infection.

65 inst several laboratory-adapted and clinical HIV-1 isolates.

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

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

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

69 CRF01_AE HIV-1 strains have an unusual Phe 43 cavity-filling His

70 eplication upon infection with Vpr-deficient HIV-1.

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

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

73 Interestingly, we find that LTR-driven HIV-1 gene expression is also enhanced by LY6E, suggesti

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

75 ents antiretroviral therapy from eliminating HIV-1 infection.

76 roduction by cells infected with CG-enriched HIV-1.

77 nsidered the primary obstacle to eradicating HIV-1 from patients, and multiple strategies are being i

78 In presence of cells expressing HIV-1 envelope glycoproteins (Envs), these BiKEs activat

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

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

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

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

83 in primary CD4(+) T cells, target cells for HIV-1.

84 xposure of specific epitopes is critical for HIV-1 vaccine development.

85 A major goal for HIV-1 vaccine development is an ability to elicit strong

86 ts reveal an important role of PI(4,5)P2 for HIV-1 morphogenesis beyond Gag recruitment to the PM and

87 g-induced conformational change required for HIV-1 entry into host cells.

88 one of the major mucosal invasion sites for HIV-1.

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

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

91 ietin protein, a V3 polypeptide derived from HIV-1 gp120, or a simple 9-fluorenylmethyl chloroformate

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

93 ntioxidant capacity in exosomes derived from HIV-1-infected and uninfected macrophages.

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 be therapeutically targeted for a functional HIV-1 cure.

97 Intact, near-full-genome HIV-1 DNA sequences that were derived from such clonally

98 hly active antiretroviral treatment (HAART), HIV-1 is still not curable due to the persistence of the

99 3 (96.9%) of 65 in the bictegravir group had HIV-1 RNA loads of less than 50 copies per mL compared w

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

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

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

103 g HIV-1 clade C-specific products.IMPORTANCE HIV-1 group M includes nine clades and many recombinants

104 In HIV-1, substitution of large residues such as histidine

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

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

107 tudies have traced the emergence of bNAbs in HIV-1 infection, inspiring novel approaches to recapitul

108 Median of the maximum declines in HIV-1 RNA were similar for the 40-120 mg once-daily dose

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

110 udies have implicated a role for exosomes in HIV-1 pathogenesis, their mechanisms are not well define

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

114 LY6E, suggesting additional roles of LY6E in HIV-1 replication.

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

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

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

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

119 We evaluated the fraction of variation in HIV-1 set point viral load attributable to viral or huma

120 Aspartic proteinases, which include HIV-1 proteinase, function with two aspartate carboxy gr

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

122 In cell lines, including HIV-1 latency models, increased HIV-1 production was obs

123 n (LINC) complex, may interact with incoming HIV-1 replication complexes and affect key steps of infe

124 s, including HIV-1 latency models, increased HIV-1 production was observed, along with changes in cel

125 e found that the host protein Naf1 inhibited HIV-1 LTR-driven transcription of HIV genes and contribu

126 e-mediated DNA synthesis, thereby inhibiting HIV-1 replication.

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

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

129 -week results from a study comparing initial HIV-1 treatment with bictegravir-a novel INSTI with a hi

130 This study provides new insights into HIV-1's capacity to escape aptamer-mediated inhibition,

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

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

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

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

135 y permissive for the establishment of latent HIV-1 infection.

136 effectively eliminate the reactivated latent HIV-1-infected T cells.

137 recruitment paradoxically reactivates latent HIV-1 transcription.

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

139 The latent HIV-1 reservoir represents the major barrier for the dev

140 y reactivation agents to reduce their latent HIV-1 reservoirs indicated that their HIV-1-specific imm

141 In our attempt to optimize the lead HIV-1 entry antagonist, NBD-11021, we present in this st

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

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

144 RT as the genetic locus for aptamer-mediated HIV-1 inhibition.

145 may provide the basis for a B cell-mediated HIV-1 vaccine.

146 f intravirion fluid phase markers to monitor HIV-1 uncoating at the individual particle level.

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

148 a recombinant, trimeric mimic of the native HIV-1 viral spike (BG505 SOSIP.664) compared to the corr

149 In nature, HIV-1 Envs must balance the requirements to maintain the

150 ained neuronal injury is that the neurotoxic HIV-1 regulatory protein trans-activator of transcriptio

151 V-1 autoantibody response able to neutralize HIV-1.

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

153 n and to determine the immunogenicity in new HIV-1 Env trimer vaccine designs.

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

155 or functions of antibodies elicited by novel HIV-1 immunogens engineered to improve exposure of speci

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

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

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

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

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

161 The prefusion-closed conformation of HIV-1 Env has been identified as one such preferred conf

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

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

164 f RV144 identified an inverse correlation of HIV-1 infection risk with antibodies (Abs) to the V1V2 r

165 The life cycle of HIV-1 has been studied extensively, yet important steps

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

167 nterfaces associated with the development of HIV-1 resistance to PIs, we traced viral evolution under

168 Our study confirms that the diversity of HIV-1 CRF01_AE originated in Central Africa in the mid-1

169 The entry of HIV-1 into target cells is mediated by the viral envelop

170 The envelope glycoproteins (Envs) of HIV-1 continuously evolve in the host by random mutation

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

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

173 ight the importance of multiscale imaging of HIV-1-infected tissues and are adaptable to other animal

174 eing considered for passive immunotherapy of HIV-1 infection.

175 Heat inactivation of HIV-1 blocks nuclear localization of LysRS, but treatmen

176 ystem that permits synchronized induction of HIV-1 assembly leading to induced production of infectio

177 Infection of HIV-1 was rescued in IFN-alpha-treated myeloid cells via

178 nfection with cell-free virus, inhibition of HIV-1 transmission from infected to uninfected CD4(+) T

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

180 ipate in DC-SIGN mediated internalization of HIV-1 in DCs.

181 ptibilities of different primary isolates of HIV-1 to the inhibition of viral infectivity by IFITMs.

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

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

184 genes and contributed to the maintenance of HIV-1 latency.

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

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

187 The mean percentage of HIV-1 Gag-specific CD8+ T cells expressing interferon ga

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

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

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

191 nAb) that is active against a broad range of HIV-1 primary isolates in vitro and protects against sim

192 1 with SAMHD1 controls the metabolic rate of HIV-1 replication by tuning the availability of building

193 ease during the development of resistance of HIV-1 to PIs.

194 in Env can enhance the global sensitivity of HIV-1 to neutralization by antibodies.

195 C8 to alter the SRSF10-dependent splicing of HIV-1 transcripts, with minor effects on cellular splici

196 POBEC3G (A3G) antagonizes the early steps of HIV-1 infection through the combined effects of inhibiti

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

198 Studies of HIV-1 latency have focused on regulation of viral gene e

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

200 Despite the efficient suppression of HIV-1 replication that can be achieved with combined ant

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

202 was shown to increase the susceptibility of HIV-1-infected cells to ADCC despite the activity of Vpu

203 antibody events that occur from the time of HIV-1 transmission to development of bnAbs.

204 TANCE Recombinant trimeric proteins based on HIV-1 env genes are being developed for future vaccine t

205 the impact of cytoreductive chemotherapy on HIV-1 reservoir dynamics, persistence, and immune respon

206 the influence of endogenous retroviruses on HIV-1 replication.IMPORTANCE Endogenous retroviruses inh

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

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

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

210 very early Fiebig stage I (detectable plasma HIV-1 RNA, antibody negative) followed by 4-drug ART int

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

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

213 In 6 of 15 participants, plasma HIV-1 RNA increased from <20 copies/mL to >1500 copies/m

214 ts (including those with undetectable plasma HIV-1 RNA), co-regulates the glucocorticoid receptor and

215 s the proportion of participants with plasma HIV-1 RNA of less than 50 copies per mL at week 48 (asse

216 s the proportion of participants with plasma HIV-1 RNA of less than 50 copies per mL at week 48 (US F

217 immune response combinations best predicting HIV-1 infection.

218 1.IMPORTANCE An effective vaccine to prevent HIV-1 infection does not yet exist.

219 portance of antibody responses in preventing HIV-1 infection.

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

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

222 for chemokine receptor binding in promoting HIV-1 entry.

223 eripheral tolerance permits a cross-reactive HIV-1 autoantibody response able to neutralize HIV-1.

224 recombinant poxvirus (ALVAC) and recombinant HIV-1 gp120 subtype B/subtype E (B/E) proteins demonstra

225 Each rod contained recombinant HIV-1 CN54gp140 protein (167mug)+/-R848 (167mug) adjuvan

226 However, envelope-defective recombinant HIV-1 did not infect the renal epithelial cell lines.

227 ns, of which A3D, A3F, A3G, and A3H restrict HIV-1.

228 y of the protein and its ability to restrict HIV-1, and correlates with increased propensity to form

229 ognizing the identical HLA-B*2705-restricted HIV-1 epitope KK10 (KRWIILGLNK).

230 These results imply that SERINC5 restricts HIV-1 fusion at a step prior to small pore formation by

231 lecular mechanism by which SERINC5 restricts HIV-1 particle infectivity is still unclear.

232 NA elements derived from three retroviruses (HIV-1, murine leukemia virus, and Mason-Pfizer monkey vi

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

234 The pyridine-based multimerization selective HIV-1 integrase (IN) inhibitors (MINIs) are a distinct s

235 AC-C-KC vectors induced enhanced and similar HIV-1-specific CD4(+) and CD8(+) T cell responses, simil

236 Previous reports indicate that some HIV-1 gp120 envelope proteins bind to and signal through

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

238 Tregs suppress HIV-1 replication in T cells and contribute to HIV-1 res

239 ife cycle through integration but suppressed HIV-1 gene transcription, thus allowing the establishmen

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

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

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

243 on two different outbreaks from the Swedish HIV-1 epidemic.

244 rom different trials and study sites testing HIV-1 clade C-specific products.IMPORTANCE HIV-1 group M

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

246 ingly, we find that transmitted/founder (TF) HIV-1 viruses can resist a late block that is induced by

247 Previous studies demonstrated that HIV-1 envelope protein gp120 binds and signals through a

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

249 Our results indicate that HIV-1 Nef-mediated inhibition of cellular PQC is one pos

250 We show that HIV-1 NL4-3(IN T124N/V165I/T174I) confers marked (>2000-

251 It has been shown that HIV-1 utilizes rhesus CD4 less efficiently than human CD

252 The HIV-1 envelope (Env) glycoprotein binds to host cell rec

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

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

255 lysine residue at position 169 (K169) in the HIV-1 envelope (Env) V2 region.

256 ese cells allowed completion of steps in the HIV-1 life cycle through integration but suppressed HIV-

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

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

259 By sequencing a subgenomic fragment of the HIV-1 envelope from study participants in the DRC, we id

260 linear epitope in the gp120 C1 region of the HIV-1 envelope glycoprotein.

261 The extraordinary genetic diversity of the HIV-1 envelope spike [Env; trimeric (gp160)3, cleaved to

262 ll not curable due to the persistence of the HIV-1 reservoir during treatment.

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

264 he structures of the Fas death receptor, the HIV-1 gp41 fusion protein, the influenza proton channel,

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

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

267 latent HIV-1 reservoirs indicated that their HIV-1-specific immune responses were insufficient to eff

268 Despite antiretroviral therapy, HIV-1 persists in memory CD4(+) T cells, creating a barr

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

270 hown that broadly neutralizing antibodies to HIV-1 can prevent infection, suggesting that a vaccine t

271 Here, we applied a similar approach to HIV-1 Vif and A3H and successfully generated a Vif-A3H i

272 uninfected and sexually active consented to HIV-1 RNA testing twice a week and biological sampling a

273 V-1 replication in T cells and contribute to HIV-1 reservoir persistence.

274 a SMYD2-H4K20me1-L3MBTL1 axis contributes to HIV-1 latency and can be targeted with small-molecule SM

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

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

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

278 sal ganglia are preferentially vulnerable to HIV-1.

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

280 Studies treating HIV-1-infected individuals with latency reactivation age

281 The RV144 Thai trial HIV-1 vaccine of recombinant poxvirus (ALVAC) and recomb

282 , placebo-controlled, non-inferiority trial, HIV-1-infected adults were screened and enrolled at 119

283 mpartmentalized and active macrophage-tropic HIV-1 variants are present in the brain tissue of indivi

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

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

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

287 Here, we show that upon HIV-1 infection, a free pool of non-MSC-associated LysRS

288 However, recent data generated using HIV-1 as a model system strongly suggest that sites of m

289 zed heterologous primary isolates of various HIV-1 subtypes in a standardized in vitro neutralization

290 ioplex), 2 antibody-based rapid tests (Vikia-HIV-1/2 and Autotest-VIH), and 1 antigen/antibody rapid

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

292 ell, leading to persistent infection wherein HIV-1 can remain transcriptionally silent in latently in

293 A total of 306 participants (62% with HIV-1 coinfection, of whom 71% received antiretroviral t

294 Children coinfected with HIV-1 had higher levels of TNF-alpha and IL-1beta than H

295 , 2.1 million individuals were infected with HIV-1 in 2015 worldwide.

296 u-mice) that were persistently infected with HIV-1.

297 creening for host factors that interact with HIV-1 MA, we found that heme oxygenase (HO-2) specifical

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

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

300 Delta20 IFITM2 suppresses replication of X4 HIV-1 strains by inhibiting their entry.