ライフサイエンスコーパス: HIV-2

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

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

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

4 insights into the replication mechanisms of HIV-2.

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

6 narily conserved in various SIV isolates and HIV-2.

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

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

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

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

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

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

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

14 enetic diversity for the second type of HIV, HIV-2.

15 V-1, but no data are currently available for HIV-2.

16 ori sequence knowledge, which is lacking for HIV-2.

17 18 guanosines located in 9 sites within the HIV-2 5' UTR and performed substitution analyses.

18 ate the importance of specific guanosines in HIV-2 5'UTR in mediating genome packaging.

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

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

21 HIV-2, a human pathogen that causes acquired immunodefic

22 s complicated by the limited availability of HIV-2-active antiretroviral drugs and inadequate access

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

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

25 HIV)-infected NHPs, and humans infected with HIV-2, an SIV-related virus.

26 HIV prevalence was 3.3% for HIV-1, 0.8% for HIV-2 and 0.9% for HIV-1/2.

27 d inhibitor with exceptional potency against HIV-2 and all major HIV-1 types, including viral variant

28 ating the applicability of this technique to HIV-2 and allowing us to generate a dynamic picture of g

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

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

31 Together, these findings indicate that HIV-2 and HIV-1 support similar levels of CD4 T cell dep

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

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

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

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

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

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

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

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

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

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

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

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

44 HIV-2 and some simian immunodeficiency viruses express v

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

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

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

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

49 A significant decline in HIV-1, HIV-2, and HIV-1/2 prevalence was observed over time.

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

51 human immunodeficiency virus type 1 (HIV-1), HIV-2, and simian immunodeficiency virus isolate it has

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

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

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

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

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

57 2 TSMs will improve approaches to predicting HIV-2 ARV susceptibility and treating HIV-2-infected per

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

59 A better understanding of HIV-2 biology is relevant to the HIV vaccine field becau

60 applied RNA-Seq to total RNA extracted from HIV-2 blood plasma samples, demonstrating the applicabil

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

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

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

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

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

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

67 Using HIV-2 chimeras of susceptible and nonsusceptible viruses

68 Our results confirm the potency of INSTI on HIV-2 clinical isolates with wild-type integrase.

69 assessed the phenotypic susceptibility of 12 HIV-2 clinical isolates, obtained from 2 antiretroviral-

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

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

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

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

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

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

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

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

78 However, in tonsil cell cultures, HIV-2, HIV-2 DeltaVpx, and HIV-1 induced indistinguishable leve

79 In contrast to our hypothesis, HIV-2, HIV-2 DeltaVpx, and HIV-1 induced similar levels of byst

80 tures (HLACs) infected with wild-type HIV-2, HIV-2 DeltaVpx, or HIV-1.

81 HIV-1 and HIV-2 differ in their antiretroviral (ARV) susceptibilit

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

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

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

85 us (SIV) and human immunodeficiency virus 2 (HIV-2) display unique ability to infect nondividing targ

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

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

88 HIV-2 does not encode a vpu gene.

89 d the ARV association of previously reported HIV-2 DRMs and identified novel TSMs.

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

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

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

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

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

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

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

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

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

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

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

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

102 ,000 to 1:1,000,000) against 5 novel primary HIV-2 envelopes and HIV-2 7312A, whereas ROD A and 3 pri

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

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

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

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

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

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

109 sought to define cis-acting elements in the HIV-2 genome that are important for the encapsidation of

110 The landscapes of persisting SIV, SHIV, and HIV-2 genomes are also dominated by defective sequences.

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

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

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

114 Mutation prevalences were determined by HIV-2 group and ARV status.

115 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

116 at successfully emerged in humans (HIV-1 and HIV-2) had to evolve novel anti-tetherin strategies.

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

118 However, in tonsil cell cultures, HIV-2, HIV-2 DeltaVpx, and HIV-1 induced indistinguishab

119 In contrast to our hypothesis, HIV-2, HIV-2 DeltaVpx, and HIV-1 induced similar levels

120 ate cultures (HLACs) infected with wild-type HIV-2, HIV-2 DeltaVpx, or HIV-1.

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

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

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

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

125 The treatment of HIV-2 in resource-limited settings (RLS) is complicated

126 f genetic diversity over the whole genome of HIV-2 in the context of low-bias sequencing.

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

128 ompounds are highly active against HIV-1 and HIV-2 in wild-type CEM/O cells and more importantly in t

129 rus type 1 (HIV-1) is delayed by HIV type 2 (HIV-2) in individuals with dual HIV-1/HIV-2 infection.

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

131 Additionally, the milder clinical course of HIV-2-induced disease is apparently not explained by a d

132 ral genomes compared to ART-treated HIV-1 or HIV-2 infected humans.

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

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

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

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

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

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

139 ection and are preferential viral targets in HIV-2-infected individuals.

140 -targeted ADCC were frequently identified in HIV-2-infected individuals.

141 viral stocks and patient plasma samples from HIV-2-infected individuals.

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

143 thod for blood plasma samples collected from HIV-2-infected individuals.IMPORTANCE An accurate pictur

144 nfants did not receive treatment, and 67% of HIV-2-infected mothers and 77% of their infants received

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

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

147 HIV-2-infected patients experiencing virological failure

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

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

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

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

152 th the ex vivo study of circulating Tfh from HIV-2-infected patients.

153 icting HIV-2 ARV susceptibility and treating HIV-2-infected persons.

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

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

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

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

158 We reveal that Tfh support productive HIV-2 infection and are preferential viral targets in HI

159 d, for the first time, Tfh susceptibility to HIV-2 infection by combining in vitro infection of tonsi

160 xperience long-term viral control, and prior HIV-2 infection has been associated with slower HIV-1 di

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

162 studies of antiretroviral therapy (ART) for HIV-2 infection in Senegal and subjected them to genotyp

163 HIV-2 infection is associated with milder disease and lo

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

165 The milder disease course observed with HIV-2 infection likely stems from factors other than abo

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

167 We hypothesized that HIV-2 infection produces lower levels of pyroptosis due

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

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

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

171 ype 2 (HIV-2) in individuals with dual HIV-1/HIV-2 infection.

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

173 Human immunodeficiency virus type 2 (HIV-2) infection results in a milder course of disease a

174 of HIV-1 cross-reactive ADCC activity during HIV-2 infections depended on the HIV-1 Env origin and wa

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

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

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

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

179 a 5-amino-acid insertion at codon 231 of the HIV-2 integrase (231INS)-in 6 patients at the virologica

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

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

182 -based genotypic drug resistance testing for HIV-2 is feasible and can be deployed in RLS with limite

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

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

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

186 a lower IC50 than the other INSTIs on those HIV-2 isolates bearing major, resistance-associated muta

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

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

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

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

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

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

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

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

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

196 nt cellular cytotoxicity (ADCC) in HIV-1 and HIV-2 monoinfection or dual infection.

197 HIV-2 MPER antibodies did not contribute to neutralizati

198 -1 Nefs are more active against SERINC5 than HIV-2 Nefs, and chimpanzee SIV (SIVcpz) Nefs are more po

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

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

201 Like other retroviruses, HIV-2 packages two copies of full-length viral RNA durin

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

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

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

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

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

207 2 is a naturally attenuated form of HIV, and HIV-2 patients display a slow-progressing disease.

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

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

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

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

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

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

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

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

216 We analyzed published HIV-2 pol sequences to identify HIV-2 treatment-selected

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

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

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

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

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

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

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

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

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

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

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

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

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

230 the TriPPPro-NTP prodrugs against HIV-1 and HIV-2 replication in cultures of infected wild-type CD4(

231 o corresponding with inhibition of HIV-1 and HIV-2 replication.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

251 challenging task of nuclear translocation of HIV-2/SIV genome in nondividing target cells.

252 Viral protein X (Vpx) of HIV-2/SIV is known to be involved in the nuclear import

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 actor SAMHD1, and is conserved among diverse HIV-2/SIV Vpx.

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

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

259 e-DCs is further enhanced in the presence of HIV-2/SIVmac Vpx, indicating that Siglec-1 does not coun

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

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

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

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

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

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

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

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

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

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

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

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

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

275 7I, and M76L increased the susceptibility of HIV-2 to multiple PI, but no single change conferred cla

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

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

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

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

280 ed published HIV-2 pol sequences to identify HIV-2 treatment-selected mutations (TSMs).

281 Genotypic and phenotypic studies of HIV-2 TSMs will improve approaches to predicting HIV-2 A

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

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

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

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

286 HIV-2 viral control was significantly associated with a

287 ntiretroviral drugs and inadequate access to HIV-2 viral load and drug resistance testing.

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

289 ral-experienced patients with multiresistant HIV-2 viruses.

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

291 in 1 (SAMHD1) host restriction factor by the HIV-2 Vpx gene product, thereby diminishing abortive inf

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

293 also not reduced by forced encapsidation of HIV-2 Vpx into HIV-1 virions.

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

295 els of CD4 T cell depletion in vitro despite HIV-2 Vpx-mediated degradation of the SAMHD1 transcripti

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

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

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

299 suggest that preexisting antibodies against HIV-2, which mediate intertype ADCC, might contribute to

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