ライフサイエンスコーパス: HIV-2

1 unodeficiency virus types 1 and 2 (HIV-1 and HIV-2).

2 against human immunodeficiency virus type 2 (HIV-2).

3 ntiates the early response against HIV-1 and HIV-2.

4 d with specific antibodies against HIV-1 and HIV-2.

5 t of 1 ng mL(-1) (6.7 pM) for both HIV-1 and HIV-2.

6 doses (TCID50s) for HIV-1 and 87 TCID50s for HIV-2.

7 te to differential pathogenesis of HIV-1 and HIV-2.

8 ion pathway is the only pathway available to HIV-2.

9 ve against retroviruses, including HIV-1 and HIV-2.

10 The others restrict HIV-1 and FIV but not HIV-2.

11 ion of all HIV-1 groups (M, N, O, and P) and HIV-2.

12 protease inhibitors (PI) are active against HIV-2.

13 differential PI susceptibility in HIV-1 and HIV-2.

14 against 5 novel primary HIV-2 envelopes and HIV-2 7312A, whereas ROD A and 3 primary envelopes were

15 utralized heterologous primary virus strains HIV-2(7312A) and HIV-2(ST).

16 llular gp160 domain was substituted into the HIV-2(7312A) proviral backbone showed potent neutralizat

17 h HIV-2 against three primary HIV-2 strains: HIV-2(7312A), HIV-2(ST), and HIV-2(UC1).

18 1 restriction factor that is targeted by the HIV-2 accessory protein Vpx in myeloid lineage cells.

19 ses in 64 subjects chronically infected with HIV-2 against three primary HIV-2 strains: HIV-2(7312A),

20 HIV-2 also suppresses HLA-C expression through distinct

21 to 30% of persons infected with HIV type 2 (HIV-2); among persons infected with both types, the natu

22 can be inactivated by viral protein Vpx from HIV-2 and certain SIV.

23 In the same cells, the Vpx protein of HIV-2 and most SIVs counteracts SAMHD1.

24 doms and were regularly tested for HIV-1 and HIV-2 and other sexually transmitted infections.

25 Many lineages of lentiviruses, including HIV-2 and other simian immunodeficiency viruses, encode

26 In other lentiviruses, including HIV-2 and related simian immunodeficiency viruses (SIVs)

27 In contrast, HIV-2 and related simian immunodeficiency viruses (SIVsm

28 its HIV-1 infection and, to a lesser extent, HIV-2 and simian immunodeficiency virus (SIV) because of

29 HIV-2 and simian immunodeficiency virus (SIV) counteract

30 rse panel of neutralization-resistant HIV-1, HIV-2 and simian immunodeficiency virus isolates, includ

31 primate lentiviral family, including HIV-1, HIV-2 and SIV(cpz).

32 nondegradative lentiviral countermeasures of HIV-2 and SIVmac, respectively.

33 A3G degradation by Vif variants derived from HIV-2 and SIVmac, which both originated from SIV of soot

34 of SAMHD1 in MDM Concordantly, infection by HIV-2 and SIVsm encoding the SAMHD1 antagonist Vpx was i

35 Interestingly, HIV-2 and SIVsm viruses are able to counteract SAMHD1 by

36 Lentiviruses such as HIV-2 and some simian immunodeficiency viruses (SIVs) co

37 HIV-2 and some simian immunodeficiency viruses express v

38 To overcome SAMHD1, HIV-2 and some SIVs encode either of two lineages of the

39 therin with the accessory protein Vpu, while HIV-2 and the filovirus Ebola use their envelope (Env) g

40 We also observed that HIV-2 and the simian immunodeficiency virus SIVmac inter

41 Human immunodeficiency virus type 2 (HIV-2) and a simian immunodeficiency virus from rhesus m

42 spectra among HIV types (i.e., HIV-1 versus HIV-2) and among HIV groups (i.e., HIV-1 groups M-P and

43 stricts human immunodeficiency virus type 2 (HIV-2) and feline immunodeficiency virus (FIV) but not H

44 Human immunodeficiency virus type 2 (HIV-2) and some simian immunodeficiency viruses (SIVs) e

45 s replication of lentiviruses such as HIV-1, HIV-2, and simian immunodeficiency virus in macrophages

46 cted with a panel of globally diverse HIV-1, HIV-2, and SIV isolates in vitro.

47 HIV-1, HIV-2, and SIV Nefs counteract human, ape, monkey, and m

48 HIV-1 and HIV-2 are derived from two distinct primate viruses and

49 lying reasons for intrinsic PI resistance in HIV-2 are not known.

50 ed immunosorbent assay (ELISA) for HIV-1 and HIV-2 are precise but time-consuming and require sophist

51 HIV-1 and HIV-2 are two human pathogens that induce AIDS, and eluc

52 HIV-1 and HIV-2 arose via distinct zoonotic transmission events of

53 onal relevance not only to HIV-1 but also to HIV-2 as well.

54 rences between biomarker levels in HIV-1 and HIV-2 at equal time points prior to death.An 'immune act

55 HIV-2, but not HIV-1, inhibited IFN-alpha production in

56 of the enzyme that differ between HIV-1 and HIV-2 by constructing HIV-2 clones encoding the correspo

57 We show that, like the HIV-2 CA, the CA of HIV-1 is a strong determinant of Lv2

58 Infection with HIV-2 can ultimately lead to AIDS, although disease prog

59 Interestingly, recombinant HIV-2 carrying a mutant D67N/K70R/M73K RT showed 10-fold

60 s of pDC differentiation driven by HIV-1 and HIV-2 cause the observed differences in pathogenicity be

61 Using HIV-2 chimeras of susceptible and nonsusceptible viruses

62 opism phenotypic assays were performed on 53 HIV-2 clinical isolates using GFP expressing human osteo

63 We found that the HIV-2 clone containing all four changes (PRDelta4) was a

64 ffer between HIV-1 and HIV-2 by constructing HIV-2 clones encoding the corresponding HIV-1 amino acid

65 n HIV-2 controllers from the French ANRS CO5 HIV-2 cohort.

66 ta reveal the potential T-cell correlates of HIV-2 control and the detailed phenotype of virus-specif

67 HIV-2 controllers display a robust capacity to support l

68 ells and their capacity for viral control in HIV-2 controllers from the French ANRS CO5 HIV-2 cohort.

69 r knowledge, we show for the first time that HIV-2 controllers possess CD8(+) T cells that show an un

70 n phenotype and robust effector potential in HIV-2 controllers.

71 Understanding how HIV-1 and HIV-2 differentially influence the immune function may h

72 Gag processing was altered in the HIV-2 dimerization mutants, resulting in the accumulatio

73 of potent immune functions, thus preventing HIV-2 disease progression.

74 iated with HIV-1 disease showed no effect in HIV-2 disease.

75 nt of a real-time assay for the detection of HIV-2 DNA and RNA using reverse transcription-loop-media

76 Although HIV-2 does not encode a vpu gene, the ability to antagon

77 HIV-2 does not encode a vpu gene.

78 ase, and integrase and an automated tool for HIV-2 drug resistance analyses freely available on the I

79 exhibited higher transition frequencies than HIV-2, due mostly to single G-to-A mutations and (to a l

80 roTide 9b was found active against HIV-1 and HIV-2 (EC50 = 0.5-1.5 muM), indicating that the lack of

81 Lentiviruses such as HIV-1 and HIV-2 encode accessory proteins whose function is to ove

82 highlighted by the fact that viruses such as HIV-2 encode an accessory protein that is packaged in th

83 bserved previously, the Vpu-like activity in HIV-2 Env can be controlled by single-residue changes in

84 ilability of 15 human MAbs targeting diverse HIV-2 Env epitopes can facilitate comparative studies of

85 Instead, the HIV-2 Env glycoprotein was found to antagonize BST-2 in

86 nti-tetherin factors including HIV-1 Vpu and HIV-2 Env have been shown to decrease the cell surface p

87 Our data suggest that targeting BST-2 by HIV-2 Env is a dynamic process that can be regulated by

88 These findings indicate that HIV-2 Env is highly immunogenic in natural infection, th

89 HIV-2 Env is thus highly immunogenic in vivo and elicits

90 We found that half of the 34 tested primary HIV-2 Env isolates obtained from 7 different patients en

91 In contrast, the HIV-2 Env required only the ectodomain of the protein an

92 Our data show that as with Vpu, binding of HIV-2 Env to BST-2 is important but not sufficient for a

93 only elicited, and that unlike HIV-1, native HIV-2 Env trimers expose multiple broadly cross-reactive

94 e release of vpu-negative HIV-1 virions when HIV-2 Env was provided in trans.

95 44A inhibited the downregulation of BST-2 by HIV-2 Env, and it inhibited the release of vpu-negative

96 We propose that HIV-1 Vpu, and probably HIV-2 Env, traps BST-2 in an endosomal compartment follo

97 the downregulation of BST-2 by either Vpu or HIV-2 Env.

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

99 The HIV-1 and HIV-2 envelope glycoproteins, the sole targets of neutra

100 ,000 to 1:1,000,000) against 5 novel primary HIV-2 envelopes and HIV-2 7312A, whereas ROD A and 3 pri

101 rmed using IgG purified from patient plasma, HIV-2 Envs cloned by single-genome amplification, viruse

102 HIV-2 exhibits intrinsic resistance to most FDA-approved

103 HIV-2 favored plasmacytoid dendritic cell (pDC) differen

104 384 samples from 71 patients included in the HIV-2 French cohort ANRS CO5 and followed for a median o

105 Despite this, HIV-1 and HIV-2 Gag polyproteins can coassemble into the same part

106 so observed that the coassembly of HIV-1 and HIV-2 Gag proteins is not required for the heterologous

107 tners occurs prior to encapsidation and that HIV-2 Gag proteins primarily package one dimeric RNA rat

108 HIV-2 Gag-specific CD8(+) T cells are at an earlier stag

109 Our data support the presence of HIV-2 Gag-specific CD8(+) T cells that display an early

110 However, in virions, HIV-2 genome dimerization does not depend on the DIS.

111 nvestigated further the relationship between HIV-2 genome dimerization, particle maturation, and infe

112 equence at the 5'-untranslated region of the HIV-2 genome.

113 V4, and CD4bs MAbs for binding to monomeric HIV-2 gp120 at titers that correlated significantly with

114 of HIV-2, we solved a 3.0-A structure of an HIV-2 gp120 bound to the host receptor CD4, which reveal

115 All 15 MAbs bound specifically to HIV-2 gp120 monomers and neutralized heterologous primar

116 Antigenic peptides from HIV-1 gp41 or HIV-2 gp36 were covalently attached to a SU-8 substrate

117 among HIV groups (i.e., HIV-1 groups M-P and HIV-2 groups A-H) and HIV-1 Group M subtypes (i.e., subt

118 Human immunodeficiency virus type 2 (HIV-2) has been reported to have a distinct RNA packagin

119 Similar to HIV-2, HIV-1 Env can rescue sensitive CAs from restricti

120 ing and neutralization properties of 15 anti-HIV-2 human monoclonal antibodies (MAbs), 14 of which we

121 ignificant trend: controls <HIV-2-LV <HIV-1 <HIV-2-HV (P < .01 for all cell types).

122 V-2-infected subjects with high viral loads (HIV-2-HV), and 10 with HIV-1 infection.

123 he rapid and accurate detection of HIV-1 and HIV-2 in both simple and complex solutions, including hu

124 ary human peripheral blood cells to HIV-1 or HIV-2 in vitro.

125 HIV-2 induced a gene expression profile distinct from HI

126 amount of virus were comparable in HIV-1 and HIV-2 infected subjects.

127 HIV-1 and HIV-2 infected wild-type CEM/0 and HIV-2 infected thymidine kinase deficient CEM cells.

128 diastereomers were tested against HIV-1 and HIV-2 infected wild-type CEM/0 and HIV-2 infected thymid

129 One participant was HIV-2 infected, yielding positive results on both RDTs.

130 While a significant proportion of HIV-2-infected individuals are asymptomatic and maintain

131 ous NAb responses from a community cohort of HIV-2-infected individuals with a broad range of disease

132 resence of broad and potent NAb responses in HIV-2-infected individuals, these are not the primary fo

133 mutations (TAMs)) are rare in the virus from HIV-2-infected individuals.

134 ere, we cloned multiple Env sequences from 7 HIV-2-infected patients and found that about half were a

135 the virus causing AIDS, and the majority of HIV-2-infected patients exhibit long-term nonprogression

136 HIV-2-infected patients experiencing virological failure

137 herapy in heavily antiretroviral-experienced HIV-2-infected patients with virus harboring resistance

138 ce from HIV type 1 and from the follow-up of HIV-2-infected patients, a panel of European experts vot

139 In this cohort of HIV-2-infected patients, sCD14 represents a better predi

140 twice daily) in antiretroviral-experienced, HIV-2-infected patients.

141 subjects with low viral loads (HIV-2-LV), 7 HIV-2-infected subjects with high viral loads (HIV-2-HV)

142 a, West Africa: 10 HIV-negative controls, 10 HIV-2-infected subjects with low viral loads (HIV-2-LV),

143 Thirteen HIV-2-infected-patients, with a median duration of 15 ye

144 te of monocyte and mDC activation throughout HIV-2 infection (characterized by CD14(bright)CD16(+) ex

145 ease progression is inhibited by concomitant HIV-2 infection and that dual infection is associated wi

146 ated significantly with poor prognosis after HIV-2 infection and that HLA-B*0801 is associated with s

147 how an unusually strong capacity to suppress HIV-2 infection in autologous CD4(+) T cells ex vivo, an

148 Compared with HIV-1, HIV-2 infection is characterized by a larger proportion

149 pproximately 20 years), according to whether HIV-2 infection occurred first, the time to the developm

150 in participants with dual infection in whom HIV-2 infection preceded HIV-1 infection.

151 Participants with dual infection with HIV-2 infection preceding HIV-1 infection had the longes

152 th either HIV-1 infection alone or HIV-1 and HIV-2 infection) in a cohort with a long follow-up durat

153 munity allows for immune-mediated control of HIV-2 infection, similar to that observed in the minorit

154 (NAATs) for the detection or confirmation of HIV-2 infection.

155 e selection and escape from host immunity in HIV-2 infection.

156 rediction of R5- and/or X4-tropic viruses in HIV-2 infection.

157 of replication, and this feature extends to HIV-2 infection.

158 Human immunodeficiency virus type 2 (HIV-2) infection is characterized by a slower progressio

159 ols for disease monitoring in both HIV-1 and HIV-2 infections, whereas sUPAR performed less well.

160 was approved by the FDA to detect HIV-1 and HIV-2 infections.

161 patients approaching death in both HIV-1 and HIV-2 infections.

162 rst direct comparison of levels in HIV-1 and HIV-2 infections.

163 tently found to be reduced by both HIV-1 and HIV-2 infections.

164 an anti-viral cytokine which inhibits HIV-1, HIV-2, Influenza virus and herpes simplex virus infectio

165 HIV-2 is a naturally attenuated form of HIV, and HIV-2 p

166 HIV-2 is a nonpandemic form of the virus causing AIDS, a

167 ed from antibody binding and neutralization, HIV-2 is surprisingly vulnerable to broadly reactive NAb

168 rence in disease phenotype between HIV-1 and HIV-2 is that more efficient T cell-mediated immunity al

169 usly called I207V), a potent determinant for HIV-2, is a weak determinant of susceptibility for HIV-1

170 Thirty-four HIV-2 isolates were classified as R5, 7 as X4, and 12 as

171 romal antigen 2 (BST-2) is conserved in some HIV-2 isolates, where it is controlled by the Env glycop

172 onserved the Vpu-like activity is in primary HIV-2 isolates.

173 studies have shown that natural infection by HIV-2 leads to the elicitation of high titers of broadly

174 binding site for Vif proteins of the SIVsmm/HIV-2 lineage differs from that of HIV-1.

175 nodeficiency virus of sooty mangabey (SIVsm)-HIV-2 lineage, SAMHD1 is counteracted by the virion-pack

176 ue, sooty mangabey, and HIV-2 (SIVsmm/SIVmac/HIV-2) lineage packaged into virions target SAMHD1 for p

177 ratios (P=.013), and frequency of detectable HIV 2-long terminal repeat circular DNA (P=.013) were si

178 -HIV-1 (high), SIVsm-SIVmac (low), and SIVsm-HIV-2 (low).

179 n groups with a significant trend: controls <HIV-2-LV <HIV-1 <HIV-2-HV (P < .01 for all cell types).

180 IV-2-infected subjects with low viral loads (HIV-2-LV), 7 HIV-2-infected subjects with high viral loa

181 e resistant to neutralization (by plasma and HIV-2 monoclonal antibodies).

182 HIV-2 MPER antibodies did not contribute to neutralizati

183 -1 Nefs are more active against SERINC5 than HIV-2 Nefs, and chimpanzee SIV (SIVcpz) Nefs are more po

184 HIV-2 non-progressors have low rates of T-cell turnover

185 SIV and HIV-2 overcome this restriction via the accessory protei

186 ransmission events that led to the HIV-1 and HIV-2 pandemics and evolution of host-virus interactions

187 These studies revealed that >90% of the HIV-2 particles contained viral RNAs and that RNAs deriv

188 A better understanding of HIV-2 pathogenesis should open new therapeutic avenues t

189 In comparing the Env sequences from one HIV-2 patient, we found that similar to the ROD10/ROD14

190 HIV-2 patients are mostly treated with a combination of

191 of the connection and RNase H domains of the HIV-2 patients did not reveal any of the mutations that

192 2 is a naturally attenuated form of HIV, and HIV-2 patients display a slow-progressing disease.

193 se, connection, and RNase H domains of RT in HIV-2 patients failing NRTI-containing therapies.

194 Interestingly, most HIV-2 patients harbored a mixed population of viruses co

195 Importantly, most HIV-2 patients harbored a mixed population of viruses co

196 sCD14) may predict disease progression among HIV-2 patients.

197 f IRIS in a West African cohort of HIV-1 and HIV-2 patients.

198 We established a strong association between HIV-2 phenotypic tropism and V3-loop sequences, allowing

199 idering human immunodeficiency virus type 2 (HIV-2) phenotypic data and experience from HIV type 1 an

200 oviding a structural rationale for intrinsic HIV-2 PI resistance and resolving long-standing question

201 g cleft of protease are the primary cause of HIV-2 PI resistance.

202 e monocyte and mDC imbalances in HIV type 2 (HIV-2)-positive patients, who typically feature reduced

203 Importantly, HIV-2-positive patients also featured overexpression of

204 PRs examined have this ability; however, the HIV-2 PR does not interact with RNA and does not exhibit

205 d minimal immune activation; high viral load HIV-2 progressors had high values, similar to or exceedi

206 he combination of four amino acid changes in HIV-2 protease confer a pattern of PI susceptibility com

207 rule set for interpretation of mutations in HIV-2 protease, reverse transcriptase, and integrase and

208 llographic structures of wild-type HIV-1 and HIV-2 proteases complexed with amprenavir and darunavir

209 ing crystallographic structures of HIV-1 and HIV-2 proteases complexed with amprenavir and darunavir.

210 al for retroviral replication, and HIV-1 and HIV-2 proteases share a great deal of structural similar

211 s resistance are unclear; although HIV-1 and HIV-2 proteases share just 38 to 49% sequence identity,

212 dually infected cell lines that contain two HIV-2 proviruses, one with a wild-type gag/gag-pol and t

213 HIV antigen-antibody combination, HIV-1 and HIV-2 rapid antibody test, and quantitative anti-gp120 I

214 h can replicate despite mutation of the DIS, HIV-2 replication depends critically on genome dimerizat

215 from the viral promoter to inhibit HIV-1 and HIV-2 replication in acutely and chronically infected ce

216 In HIV-2, resistance to zidovudine (3'-azido-3'-deoxythymid

217 Mutation V111I in the HIV-2 reverse transcriptase enzyme was identified in pat

218 Plasma HIV-2 RNA (pVL) was assessed at time of dolutegravir ini

219 We found that when HIV-1 and HIV-2 RNA are present in viral particles at similar rati

220 emely low frequency, implying that HIV-1 and HIV-2 RNA can be copackaged into the same particle.

221 eterodimerization, indicating that HIV-1 and HIV-2 RNA can heterodimerize prior to packaging using th

222 To determine the frequency of HIV-1 and HIV-2 RNA copackaging and to dissect the mechanisms that

223 proteins are capable of mediating HIV-1 and HIV-2 RNA copackaging.

224 ed event, drop in CD4 <350 cells/microL, and HIV-2 RNA detection.

225 are consistent with interdependence between HIV-2 RNA dimerization and the correct proteolytic cleav

226 anisms of HIV-2 RNA packaging, we visualized HIV-2 RNA in individual particles by using fluorescent p

227 The biomarkers were correlated with HIV-2 RNA in unadjusted analyses only.

228 omatic, 34% were treated; 30% had detectable HIV-2 RNA load, and median CD4 cell count was 415/microL

229 gether, these results revealed mechanisms of HIV-2 RNA packaging that are, contrary to previous studi

230 To further characterize the mechanisms of HIV-2 RNA packaging, we visualized HIV-2 RNA in individu

231 at trans packaging is the major mechanism of HIV-2 RNA packaging.

232 tion of human immunodeficiency virus type 2 (HIV-2) RNA occurs by interaction of a self-complementary

233 ced human immunodeficiency virus (HIV)-1 and HIV-2 RNAs from the nucleus to the cytoplasm during the

234 e viral particles encapsidate both HIV-1 and HIV-2 RNAs.

235 The 3D models for the HIV-2 RRE and folding intermediates are also presented,

236 mmunication, the secondary structures of the HIV-2 RRE and two RNA folding precursors have been ident

237 Our analysis collectively suggests that the HIV-2 RRE undergoes two conformational transitions befor

238 sion-based resistance mechanism against AZT, HIV-2 RT can use only the exclusion mechanism.

239 e to the nucleoside analog zidovudine (AZT), HIV-2 RT does not appear to use this pathway.

240 s but negatively affects the fidelity of the HIV-2 RT enzyme.

241 All of our attempts to make HIV-2 RT excision competent did not produce an AZT-resis

242 These data suggest that HIV-2 RT exhibits higher fidelity during viral replicati

243 ibed data that suggested that wild-type (WT) HIV-2 RT has a much lower ability to excise AZT monophos

244 demonstrate that mutant M41L/D67N/K70R/S215Y HIV-2 RT lacks ATP-dependent excision activity, and reco

245 T and suggested that this is the reason that HIV-2 RT more readily adopts an exclusion pathway agains

246 Our work highlights critical HIV-2 RT residues impeding the development of excision-m

247 cision activity when TAMs are present in the HIV-2 RT.

248 Mutant HIV-2 RTs were tested for their ability to unblock and e

249 The related viruses HIV-1 and HIV-2 share many of the same resistance pathways to nucl

250 , found in all primate lentiviruses, and its HIV-2/simian immunodeficiency virus (SIV) SIVsm paralogu

251 HIV-1 Vpr and HIV-2/simian immunodeficiency virus (SIV) Vpr and Vpx en

252 HIV-2/SIV (simian immunodeficiency virus) viral protein

253 Both HIV-1 Vpr and HIV-2/SIV Vpr tap CRL4 to initiate G2 cell cycle arrest.

254 e determined CUL4 requirements for HIV-1 and HIV-2/SIV Vpr-mediated G2 cell cycle arrest, HIV-1 Vpr-m

255 HIV-2/SIV Vpx secures CRL4 to degrade the antiviral prot

256 t to degradation by diverse Vifs from HIV-1, HIV-2, SIVagm, and chimpanzee SIV (SIVcpz), suggesting a

257 AMHD1 C terminus contains a docking site for HIV-2/SIVmac Vpx and is known to have evolved under posi

258 ted by the Vpx accessory virulence factor of HIV-2/SIVsm viruses, which targets SAMHD1 for proteasome

259 virus of rhesus macaque, sooty mangabey, and HIV-2 (SIVsmm/SIVmac/HIV-2) lineage packaged into virion

260 ith the strong conservation of A-K-N in most HIV-2/SIVsmm isolates and the analogous residues in HIV-

261 rved tryptophan at position 375 (Trp 375) in HIV-2/SIVsmm.

262 We performed a detailed study of HIV-2-specific cellular responses in a unique community

263 This potentially protective HIV-2-specific response is surprisingly narrow.

264 t three primary HIV-2 strains: HIV-2(7312A), HIV-2(ST), and HIV-2(UC1).

265 ogous primary virus strains HIV-2(7312A) and HIV-2(ST).

266 opes potently neutralized the majority of 32 HIV-2 strains bearing Envs from 13 subjects.

267 of a panel of naturally occurring HIV-1 and HIV-2 strains behaved like prototype strains and were co

268 We identified HIV-1 and HIV-2 strains that are unaffected by SUN2, suggesting th

269 samples tested against a larger panel of 17 HIV-2 strains where the extracellular gp160 domain was s

270 wo strains are progenitors for all HIV-1 and HIV-2 strains, respectively).

271 SAMHD1 proteins and Vpx proteins from SIV or HIV-2 strains.

272 utralizing antibodies (NAbs) against primary HIV-2 strains.

273 ly infected with HIV-2 against three primary HIV-2 strains: HIV-2(7312A), HIV-2(ST), and HIV-2(UC1).

274 At least 2095 samples from 137 HIV-1 and 198 HIV-2 subjects with starting CD4% of >/= 28 and median f

275 little is known about the susceptibility of HIV-2 to antibody neutralization.

276 des new insights into mechanisms employed by HIV-2 to counteract innate immune defenses against viral

277 rogression despite the recognized ability of HIV-2 to establish viral reservoirs and overcome host re

278 7I, and M76L increased the susceptibility of HIV-2 to multiple PI, but no single change conferred cla

279 formation exists regarding the resistance of HIV-2 to NRTIs.

280 does not strongly affect the sensitivity of HIV-2 to nucleoside analogues but increases the fitness

281 The ability of HIV-2 to reduce HO-1 expression suggests that this is a

282 egrated proviral DNA, and concomitant HIV-1, HIV-2 transcription in co-infected cells.

283 dy was to identify genotypic determinants of HIV-2 tropism located in the gp105 V3 loop.

284 HIV-2 tropism phenotypic assays were performed on 53 HIV

285 predict human immunodeficiency virus type 2 (HIV-2) tropism, as established in HIV-1.

286 d a third heterologous primary virus strain, HIV-2(UC1).

287 HIV-2 strains: HIV-2(7312A), HIV-2(ST), and HIV-2(UC1).

288 IV-1 uses the accessory protein Vpu, whereas HIV-2 uses its envelope glycoprotein (Env).

289 an monoclonal antibodies (MAbs) specific for HIV-2 V3 (6.10F), V4 (1.7A), CD4 binding site (CD4bs; 6.

290 analysis of the N-terminal 62 amino acids of HIV-2 Vif (Vif2) and analyzed A3G/A3F chimeras that reta

291 the determinants of the interaction between HIV-2 Vif (Vif2) with human A3 proteins and compared the

292 HIV-2 viral control was significantly associated with a

293 zing antibody (NAb) responses in controlling HIV-2 viremia and disease progression.

294 In contrast, we find that HIV-2 Vpr is unable to efficiently program HLTF or UNG2

295 In this study, we demonstrate that HIV-2 Vpx interacts with IRF5, and Vpx inhibits IRF5-med

296 yeloid cells and is countered by the SIV(SM)/HIV-2 Vpx protein.

297 st, HIV-1 Vpr-mediated UNG2 degradation, and HIV-2 Vpx-mediated SAMHD1 degradation.

298 autologous NAb titer and greater control of HIV-2 was found.

299 n understanding the reduced pathogenicity of HIV-2, we solved a 3.0-A structure of an HIV-2 gp120 bou

300 The divergent interactions of HIV-1 and HIV-2 with DNA repair enzymes and SAMHD1 imply that thes