ライフサイエンスコーパス: bnAb

1 bnAbs against this region have some shared features and

2 bnAbs appear very late, and patients are typically not p

3 bnAbs are therefore expected to evolve only when the B c

4 uctured HCDR3s similar to those of the HIV-1 bnAb PG9.

5 imer probes for efficient isolation of HIV-1 bnAbs.

6 nctional requirement for indels within HIV-1 bnAbs.

7 Here, we report a second group 2 bnAb, CR8043, which was derived from a different germ-li

8 generate a strain expressing the entire 2F5 bnAb specificity, 2F5 V(H) x V(L) KI mice, and find an e

9 with an MPER peptide-liposome vaccine in 2F5 bnAb VHDJH and VLJL knock-in mice and rhesus macaques mo

10 article, we demonstrate that neither the 2F5 bnAb nor HIV MPER-KYNU cross-reactive Abs elicited by im

11 (MPER) (2F5) and outer domain glycan (2G12) bnAbs were also efficient in preventing infection of muc

12 A bnAb directed to the CD4-binding site of the HIV-1 envel

13 Here, we described a bnAb lineage targeting the Env V2 apex and the Ab-Env co

14 Here, we study the B cell response in a bnAb-producing individual and report cooperation between

15 n has demonstrated the ability to initiate a bnAb response in animal models, but recall and maturatio

16 Here, we present the development of a bnAb lineage targeting the high-mannose patch in an HIV-

17 f incomplete neutralization the ability of a bnAb to mediate sterilizing protection diminishes.

18 Here, we show that a bnAb with enhanced FcRn binding has increased gut mucosa

19 active with the HIV broadly neutralizing Ab (bnAb) 2F5.

20 Broadly neutralizing Abs (bnAbs) against HIV have been isolated from patients, pro

21 aim to initiate bnAb induction by activating bnAb germline precursor B cells.

22 N332 supersite on envelope but, unlike adult bnAbs targeting this site, lacks indels and has low SHM.

23 hat influence the evolution of high-affinity bnAbs remain elusive.

24 lly influence the evolution of high-affinity bnAbs.

25 virion-associated spikes present nearly all bnAb epitopes and are therefore promising vaccine antige

26 Although bnAbs may provide the greatest level of protection, thei

27 t advanced candidate exhibits structural and bnAb binding properties comparable to those of full-leng

28 Apex broadly neutralizing HIV antibodies (bnAbs) recognize glycans and protein surface close to th

29 on of three broadly neutralizing antibodies (bnAbs) against gp120-gp41 interface epitopes has expande

30 Broadly neutralizing antibodies (bnAbs) against HIV are believed to be a critical compone

31 neration of broadly neutralizing antibodies (bnAbs) against HIV in a large longitudinal cohort of HIV

32 Broadly neutralizing antibodies (bnAbs) against HIV-1 protect from infection and reduce v

33 elopment of broadly neutralizing antibodies (bnAbs) against HIV-1 usually requires prolonged infectio

34 on of human broadly neutralizing antibodies (bnAbs) against influenza virus provide valuable insights

35 rization of broadly neutralizing antibodies (bnAbs) against influenza viruses have raised hopes for t

36 Broadly neutralizing antibodies (bnAbs) against the N332 supersite of the HIV envelope (E

37 nduction of broadly neutralizing antibodies (bnAbs) against this diversity by vaccination likely requ

38 (p.i.) with broadly neutralizing antibodies (bnAbs) against tier 2 HIV-1.

39 a panel of broadly neutralizing antibodies (bnAbs) and nnAbs, including those associated with protec

40 iters by 16 broadly neutralizing antibodies (bnAbs) and sera from 30 subjects with chronic clade C in

41 target for broadly neutralizing antibodies (bnAbs) and the focus for design of an antibody-based HIV

42 rized HIV-1 broadly neutralizing antibodies (bnAbs) are polyreactive with additional specificities fo

43 -1-specific broadly neutralizing antibodies (bnAbs) at high titers that are present before exposure m

44 action with broadly neutralizing antibodies (bnAbs) at the molecular level and using this understandi

45 on of HIV-1 broadly neutralizing antibodies (bnAbs) by vaccines is a priority.

46 nduction of broadly neutralizing antibodies (bnAbs) capable of inhibiting infection with diverse vari

47 Such broadly neutralizing antibodies (bnAbs) could in the future become therapeutic agents.

48 HIV-1 broadly neutralizing antibodies (bnAbs) develop in a subset of infected adults and exhibi

49 r target of broadly neutralizing antibodies (bnAbs) developed during infection in some individuals.

50 Broadly neutralizing antibodies (bnAbs) directed to the V2 apex of the HIV envelope (Env)

51 nv) elicits broadly neutralizing antibodies (bnAbs) during natural infection relatively frequently, a

52 Broadly neutralizing antibodies (bnAbs) elicited in HIV-1(+) elite neutralizers typically

53 review how broadly neutralizing antibodies (bnAbs) exploit these evolutionary constraints to protect

54 with HIV-1 broadly neutralizing antibodies (bnAbs) generally requiring years to develop.

55 it broadly reactive neutralizing antibodies (bnAbs) has been a major obstacle to HIV-1 vaccine develo

56 HIV broadly neutralizing antibodies (bnAbs) have been shown to occasionally display unusual v

57 volution of broadly neutralizing antibodies (bnAbs) in infection and to recreate those events by vacc

58 elopment of broadly neutralizing antibodies (bnAbs) in rhesus macaques, commonly used to assess vacci

59 very of HIV broadly neutralizing antibodies (bnAbs) in some HIV-infected individuals.

60 tion of HIV-1 broad neutralizing antibodies (bnAbs) is a goal of HIV-1 vaccine development but has re

61 nduction of broadly neutralizing antibodies (bnAbs) is a major HIV vaccine goal.

62 nduction of broadly neutralizing antibodies (bnAbs) is a primary goal of HIV vaccine development.

63 citation of broadly neutralizing antibodies (bnAbs) is a primary HIV vaccine goal.

64 citation of broadly neutralizing antibodies (bnAbs) is likely to be a key component of a successful v

65 infection, broadly neutralizing antibodies (bnAbs) must be active at the portals of viral entry in t

66 nd broadly reactive neutralizing antibodies (bnAbs) or vaccines that induce "conventional antibodies,

67 IV-specific broadly neutralizing antibodies (bnAbs) protect rhesus macaques from HIV acquisition.

68 Most broadly neutralizing antibodies (bnAbs) recognize these native trimers.

69 rity of the broadly neutralizing antibodies (bnAbs) targeting HIV-1 have been isolated from non-subty

70 on of human broadly neutralizing antibodies (bnAbs) targeting the hemagglutinin (HA) stem revitalized

71 Broadly neutralizing antibodies (bnAbs) targeting the trimer apex of HIV envelope are fav

72 of inducing broadly neutralizing antibodies (bnAbs) that bind to the viral envelope glycoprotein (Env

73 ver, potent broadly neutralizing antibodies (bnAbs) that target this shield have been isolated.

74 on of HIV-1 broadly neutralizing antibodies (bnAbs) to date has only been observed in the setting of

75 Broadly neutralizing antibodies (bnAbs) to HIV delineate vaccine targets and are prophyla

76 tanding how broadly neutralizing antibodies (bnAbs) to HIV envelope (Env) develop during natural infe

77 ely require broadly neutralizing antibodies (bnAbs) with maximum breadth and potency to ensure therap

78 tion of HIV broadly neutralizing antibodies (bnAbs) with remarkable potency, breadth and epitope dive

79 target for broadly neutralizing antibodies (bnAbs), but to date, no vaccination regimen has elicited

80 solated two broadly neutralizing antibodies (bnAbs), CH01 and VRC-CH31, from two clonal lineages of m

81 target for broadly neutralizing antibodies (bnAbs), Env is a focus for rational vaccine design.

82 cts develop broadly neutralizing antibodies (bnAbs), such as the potent VRC01-class bnAbs, that neutr

83 licit/boost broadly neutralizing antibodies (bnAbs), thereby limiting their efficacy.

84 generating broadly neutralizing antibodies (bnAbs).

85 t to elicit broadly neutralizing antibodies (bnAbs).

86 ognition by broadly neutralizing antibodies (bnAbs).

87 by multiple broadly neutralizing antibodies (bnAbs).

88 or anti-HIV broadly neutralizing antibodies (bnAbs).

89 potent and broadly neutralizing antibodies (bnAbs).

90 or inducing broadly neutralizing antibodies (bnAbs).

91 n (Env) for broadly neutralizing antibodies (bnAbs).

92 ents evolve broadly neutralizing antibodies (bnAbs).

93 ross-reactive broadly neutralizing antibody (bnAb) and not by nonneutralizing antibodies.

94 ucture of the broadly neutralizing antibody (bnAb) AP33, bound to a peptide corresponding to hepatiti

95 s involved in broadly neutralizing antibody (bnAb) development holds great promise for improving the

96 f anti-CD4-BS broadly neutralizing antibody (bnAb) epitopes on recombinant Env, Env immunization has

97 an generate a broadly neutralizing antibody (bnAb) response against the enormous sequence diversity o

98 binding site broadly neutralizing antibody (bnAb) that is active against a broad range of HIV-1 prim

99 obstacle to a broadly neutralizing antibody (bnAb)-based HIV vaccine is the activation of appropriate

100 y, we solved the atomic structure of an apex bnAb, PGT145, in complex with Env.

101 of immunization strategies to induce V2 apex bnAb responses.

102 serve as an immunogen to initiate a V2-apex bnAb response.

103 The evolution of apex bnAbs from one donor (CAP256) has been studied in detail

104 H01, PGT145, and CAP256.VRC26.09) of V2 apex bnAbs and showed that all recognized a core epitope of b

105 afforded by analyses of recombinant Ig-based bnAb structures, it became apparent that key functional

106 y better coordinate the relationship between bnAb epitope structure and therapeutic expectations.

107 nt of CD4-binding site (CD4bs), HCDR3-binder bnAbs via sequential HIV-1 Env vaccination.

108 ifferent angle of approach to the antigen by bnAb AP33 and slight variation in its beta-hairpin confo

109 ere screened on the basis of high binding by bnAbs and low binding by nonneutralizing antibodies.

110 Elicitation of and recognition by bnAbs are hindered by the arrangement of spikes on virio

111 ) in complex with a CD4 binding site (CD4bs) bnAb, PGV04, at 5.8 angstrom resolution.

112 Thus, stepwise immunization initiates CD4bs-bnAb responses, but immune tolerance mechanisms restrict

113 The infant cross-clade bnAb targets the N332 supersite on envelope but, unlike

114 We tested the ability of the VRC01-class bnAb germline-targeting immunogen eOD-GT8 60mer (60-subu

115 eered an immunogen that binds to VRC01-class bnAb precursors and immunized knock-in mice expressing g

116 Because many VRC01-class bnAb SHMs are not required for broad neutralization, hig

117 VRC01-class bnAbs are important vaccine leads because their precurso

118 bodies showed characteristics of VRC01-class bnAbs, including a short CDRL3 (light-chain complementar

119 Mature VRC01-class bnAbs, including VRC-PG04, accumulate very high SHM leve

120 dies (bnAbs), such as the potent VRC01-class bnAbs, that neutralize diverse HIV-1 strains.

121 jectory that leads toward mature VRC01-class bnAbs.

122 immunogen (eOD-GT8) for diverse VRC01-class bnAbs.

123 breadth and antiviral efficacy by combining bnAbs for therapeutic indications.

124 IV envelope (Env) trimer are the most common bnAbs induced during infection, making them promising le

125 In contrast, bnAb 35O22 binding to a partially overlapping quaternary

126 ely tolerated by a panel of glycan-dependent bnAbs targeting these regions, indicating a degree of pl

127 nity reagent to isolate quaternary-dependent bnAbs from the peripheral blood mononuclear cells of a c

128 wever, some HIV-infected individuals develop bnAbs after approximately 2-4 years of infection, enabli

129 tibodies to Env revealed that four different bnAb families targeted the (324)GDIR(327) peptide stretc

130 report an haemagglutinin (HA) stem-directed bnAb, 3I14, isolated from human memory B cells, that uti

131 eration between two B cell lineages to drive bnAb development.

132 nogens/regimens for effectiveness in driving bnAb responses.

133 d diversity at key V2 epitope residues drove bnAb maturation toward breadth, mirroring the Env evolut

134 for the design of HA stem mimics that elicit bnAbs against influenza A group 1 viruses.

135 trategies for designing immunogens to elicit bnAbs have not been identified.

136 ept for an HIV-1 vaccine that aims to elicit bnAbs of multiple specificities.

137 fferent immunogens may be required to elicit bnAbs that have the optimal characteristics of the two b

138 to date, no vaccination regimen has elicited bnAbs against this region.

139 The immunogen elicited bnAbs that neutralized highly divergent group 1 (H1 and

140 nAb development, the challenges of eliciting bnAbs via immunizations, and the putative central roles

141 e review the progress to date in elucidating bnAb B cell lineages in HIV-1 infection, discuss new res

142 mbled into variable region exons that encode bnAb precursors), have been engineered to evaluate novel

143 scape mutants that resulted in both enhanced bnAb lineage envelope binding and escape mutant neutrali

144 frustration maximizes the chance of evolving bnAbs.

145 specificities approaching those of existing bnAbs.

146 ely need to incorporate strategies to expand bnAb precursor pools.

147 se IgH and IgL loci has been used to express bnAbs in mice.

148 imers suitable for use as antigenic bait for bnAb isolation, structural studies, and use as potential

149 We discuss implications of our findings for bnAb affinity maturation mechanisms.

150 C01 class, appears to be a major problem for bnAb induction.

151 large compound VHDJH indel was required for bnAb activity.

152 or predictor of both potency and breadth for bnAbs at clinically relevant concentrations, and may bet

153 eractions, and the CD4bs epitope cluster for bnAbs, which covers a more extensive area and defines a

154 omplete neutralization is not imperative for bnAbs to prevent infection but that with increasing leve

155 ns and 13 SHIVSF162P3N-infected macaques for bnAbs and found that, similar to HIV-1-infected humans,

156 e and demonstrate that this would select for bnAbs.

157 Here, we review insights gained from bnAb KI studies regarding the regulation and induction o

158 may suggest a more direct path to generating bnAbs.

159 GDIR-glycan bnAbs, in contrast, bound both (324)GDIR(327) peptide re

160 w exceptions, CD4-binding site and V3-glycan bnAbs exhibit slopes >1, indicative of higher expected t

161 oximal external region (MPER) and gp120-gp41 bnAbs exhibit less favourable slopes <1.

162 n vivo, to further facilitate vaccine-guided bnAb induction studies.

163 zing antibodies (non-nAbs), which may hinder bnAb induction.

164 known about the immunological process of HIV bnAb development, the challenges of eliciting bnAbs via

165 ial immunization can guide maturation of HIV bnAb responses.

166 t for many of the recently isolated anti-HIV bnAbs and is therefore under constant pressure from the

167 ration of carbohydrate epitopes for anti-HIV bnAbs.

168 ll be a critical parameter to monitor if HIV bnAbs are to be induced by vaccination.

169 iking amount of somatic hypermutation in HIV bnAbs led to the hypothesis that T follicular helper (Tf

170 Increasingly, HIV bnAbs are being identified that bind to the N-linked gly

171 germline targeting for other classes of HIV bnAbs and for Abs to other pathogens.

172 The generation of HIV bnAbs may be one of the greatest feats of the human immu

173 Therefore, the development of HIV bnAbs might depend on Tfh cells.

174 s, and it is thought that elicitation of HIV bnAbs will be an important component of an effective vac

175 ntrol new infections, and elicitation of HIV bnAbs will likely be an important component of an effect

176 of Tfh cells and GC in the generation of HIV bnAbs.

177 Only one human bnAb (CR8020) specifically recognizing group 2 influenza

178 s to use mice expressing precursors of human bnAbs as vaccination models.

179 d pharmacokinetics similar to those of human bnAbs, and conferred complete immunity against a mixture

180 und a wide range of HAs, competed with human bnAbs for HA stem binding, neutralized H5N1 viruses, and

181 ound that, similar to HIV-1-infected humans, bnAbs in SHIV-infected macaques are also rare, but their

182 of the GC and Tfh-cell processes involved in bnAb generation, including the difficulty of quantifying

183 Increasingly, bnAbs that bind to the cluster of high-mannose glycans o

184 distant variants is shown to robustly induce bnAbs that focus on conserved elements of the target epi

185 However no vaccine was able so far to induce bnAbs demanding their expensive biotechnological product

186 ns as key components of strategies to induce bnAbs to HIV-1.

187 t suggests sequential immunization to induce bnAbs, in which the germline-targeting prime is followed

188 ng them maximize the probability of inducing bnAbs.

189 The identification of this infant bnAb illustrates that HIV-1-specific neutralization brea

190 ermline-targeting immunogens aim to initiate bnAb induction by activating bnAb germline precursor B c

191 The newly isolated bnAbs, named "PGDM1400-1412," show a wide range of neutr

192 However, methods of isolating bnAbs against this site have been limited by the quatern

193 engage the germline-reverted forms of known bnAbs that target the CD4-BS.

194 capable of identifying impediments limiting bnAb induction and ranking vaccine strategies for their

195 immunologic tolerance mechanisms in limiting bnAb development.

196 allowed immune tolerance mechanisms limiting bnAb production to be elucidated and strategies to overc

197 increase thermal stability while maintaining bnAb antigenicity.

198 operly display epitopes for all of the major bnAb classes, including quaternary-dependent, trimer-ape

199 ction in HIV-1-infected individuals who make bnAbs is a key strategy for immunogen design.

200 (designed to bind progressively more mature bnAb precursors) to initiate affinity maturation.

201 ced precursor V(D)J rearrangements of mature bnAbs or unrearranged germline V, D, J segments (that ca

202 ing with monomeric gp120 indicated that most bnAbs bind to the envelope trimer rather than the gp120

203 This enhanced FcRn-binding mutant bnAb, denoted VRC01-LS, displayed increased transcytosis

204 Here we describe the isolation of new bnAbs targeting this region.

205 This study evaluates the novel bnAb N6-LS alone or in combination with the bnAb PGT121,

206 regimens targeted at sustained activation of bnAb lineages to achieve the required SHM and indel even

207 wnselection after hierarchical clustering of bnAb neutralization titers.

208 ht into immunologic mechanisms of control of bnAb development.

209 elected panels to represent the diversity of bnAb neutralization profiles and Env neutralization sens

210 ure of the Env trimer influences exposure of bnAb epitopes.

211 understanding the immunologic mechanisms of bnAb induction, and address issues relevant to the use o

212 From these studies has come a picture of bnAb development that has led to new insights in host-pa

213 ore explore the functional sequence space of bnAb C05, which targets the receptor-binding site (RBS)

214 Determining the steps of bnAb induction in HIV-1-infected individuals who make bn

215 incomplete neutralization for the ability of bnAbs to mediate protective effects in vivo, however, is

216 ys epitopes recognized by a diverse array of bnAbs.

217 ll repertoire, suggesting that this class of bnAbs is a favorable target for rationally designed prev

218 unogens that can induce different classes of bnAbs against this region.

219 We identify two classes of bnAbs that differ in their recognition of the high-manno

220 ese cells correlated with the development of bnAbs against HIV in a large cohort of HIV(+) individual

221 A recent study reports the development of bnAbs in an elite controller that, along with the help o

222 sheds light on the timing and development of bnAbs in SHIV-infected macaques in comparison to HIV-1-i

223 time of HIV-1 transmission to development of bnAbs.

224 ages cooperated to induce the development of bnAbs.

225 al tissues, while the protective efficacy of bnAbs targeting V1-V2 glycans (PG9 and PG16) was more va

226 ising immunogens aimed at the elicitation of bnAbs.

227 Under such circumstances the evolution of bnAbs is much more consistent.

228 by vaccination may speed up the evolution of bnAbs.

229 distances may best promote the evolution of bnAbs.

230 that entropically disfavor the evolution of bnAbs.

231 rtoire markedly facilitates the evolution of bnAbs.

232 nipulate the production and/or expression of bnAbs in vivo, to further facilitate vaccine-guided bnAb

233 ame apparent that key functional features of bnAbs often are problematic for their elicitation in mic

234 pt has emerged that one path to induction of bnAbs is to define the viral and immunologic events that

235 es regarding the regulation and induction of bnAbs, and discuss new Ig KI methodologies to manipulate

236 rate a strategy to transition from panels of bnAbs to vaccine candidates.

237 or binding of Env to unmutated precursors of bnAbs, including those of the VRC01 class, appears to be

238 rotection strategies, we assessed a range of bnAbs and nnAbs for their potential to block ex vivo cha

239 lope trimer probes for efficient recovery of bnAbs.

240 Mapping the epitope specificities of bnAbs provides useful information for vaccine design.

241 s, consistent with the glycan specificity of bnAbs that target this region.

242 allenging partially due to unusual traits of bnAbs, including high somatic hypermutation (SHM) freque

243 In particular, bnAbs from IAVI donor 36 (PGT125 to PGT131) have been sh

244 d animals and was linked to declining plasma bnAb levels over time.

245 oportion of HIV-infected individuals, potent bnAb responses do develop, and isolation of the correspo

246 entification of favorable donors with potent bnAb sera and by development of improved methods for hum

247 quest for an HIV vaccine that induces potent bnAbs.

248 Some of the most potent bnAbs target a quaternary epitope at the apex of the sur

249 Here we predict bnAb potency at therapeutic levels by analysing dose-res

250 provide T cell help to B cells that produce bnAbs are crucial for optimal immunization strategies.

251 cine strategies for their ability to promote bnAb development.

252 One branch (prototype bnAb PGT128) has a 6-amino-acid insertion in CDRH2 that

253 The other branch (prototype bnAb PGT130) lacks the CDRH2 insertion.

254 ine (iGL) versions of three of the prototype bnAbs.

255 Two prototype bnAbs were derived from VH-germlines that were 99% ident

256 eting to prime specific and exceedingly rare bnAb-precursor B cells within a humanlike repertoire.

257 g immunogens must be capable of priming rare bnAb precursors in the physiological setting.

258 In this regard, bnAb KI models expressing deduced precursor V(D)J rearra

259 Although several bnAbs bind to the conserved stem domain of HA, focusing

260 breadth than any previously described single bnAb, showed pharmacokinetics similar to those of human

261 in nonhuman primates, in contrast to single bnAbs.

262 , reconstruction of a HIV-1 CD4-binding site bnAb clonal lineage revealed that a large compound VHDJH

263 Thus, as for the CD4 binding site, bnAb effectiveness relies on circumventing the defenses

264 The solid protection provided by specific bnAbs clearly demonstrates their superior potential over

265 CD4-binding site (CD4bs)-specific bnAbs, in particular VRC01, were consistent in blocking

266 mation of HA and binds conformation specific bnAbs with high affinity.

267 members of a family of oligomannose-specific bnAbs and their putative common germline precursor when

268 enic mimicry to elicit oligomannose-specific bnAbs to HIV-1.

269 but it diminishes binding to trimer-specific bnAbs while exposing non-neutralizing epitopes.

270 everted precursors of PGT121-class supersite bnAbs.

271 teins lack detectable affinity for supersite-bnAb germline precursors and are therefore unsuitable im

272 ore unsuitable immunogens to prime supersite-bnAb responses.

273 evolutionary rate change for HIV-1-targeting bnAb lineages.

274 nother donor who developed V2-apex targeting bnAbs.

275 ions, and/or autoreactivity, suggesting that bnAb generation is likely to be highly dependent on the

276 e of somatic hypermutation in broadening the bnAb response.

277 onses were not significantly enhanced in the bnAb-treated animals compared to control animals, arguin

278 bnAb N6-LS alone or in combination with the bnAb PGT121, in rhesus macaques that were chronically in

279 The bnAbs of the VRC01-class derive from the IGHV1-2 immunog

280 t allowed for complete neutralization by the bnAbs.

281 Combination of these bnAbs enhanced neutralization breadth considerably, sugg

282 ructures, which is a primary target of these bnAbs.

283 ne of the mimetics bound to a member of this bnAb family confirms the antigenic resemblance.

284 rions and the relatively difficult access to bnAb epitopes on spikes, including the proximity of vari

285 s, with no unique properties attributable to bnAb-producing individuals.

286 ibody generation, and how this is related to bnAb development, and considers the implications for HIV

287 ent of IC50/IC80 and specifically relates to bnAb epitope class.

288 mal models, but recall and maturation toward bnAb development has not been shown.

289 In the current study, we selected two bnAbs, PGT121 and 3BNC117, as they incompletely neutrali

290 ing complex glycosylation of Env affected V2 bnAb recognition, as previously described, but also nota

291 A number of Env-stabilizing mutations and V2 bnAb-enhancing mutations were identified in Env, but the

292 ions together increased neutralization by V2 bnAb and eliminated binding by V3 crown antibodies.

293 that when mutations outside V2 increased V2 bnAb recognition, they often also increased Env stabilit

294 e stability of mutant Envs and the MPN of V2 bnAb, PG9, as well as an inverse correlation between sta

295 relates to neutralization sensitivity to V2 bnAbs and V3 crown antibodies that engage subunit interf

296 In addition to the effect on plasma viremia, bnAb administration resulted in significantly reduced pr

297 al unmet challenges are to determine whether bnAb precursor naive B cells bind germline-targeting imm

298 While bnAbs are highly effective against cell-free virus, they

299 Comparison with bnAb HCV1 bound to the same epitope reveals a different

300 t Env trimers, alone and in interaction with bnAbs, are providing new insights that are fueling the d