ライフサイエンスコーパス: natural infection

1 (DLAV) vaccine resemble those observed after natural infection.

2 alizing antibody response is directed during natural infection.

3 tute a safe vaccination strategy that mimics natural infection.

4 ssumption that the vaccine acts similarly to natural infection.

5 al Env and Vif proteins as they occur during natural infection.

6 ors has not been addressed in the context of natural infection.

7 ibody levels comparable to those achieved in natural infection.

8 T cell response is not stimulated following natural infection.

9 4- to 256-fold greater than those seen after natural infection.

10 1E4 may be useful for preventing C. burnetii natural infection.

11 do not recapitulate the protective effect of natural infection.

12 rong population bottlenecks occurring during natural infection.

13 t Abs provide effective protection against a natural infection.

14 nalysis indicates to be commonly elicited by natural infection.

15 ings that recapitulate those observed during natural infection.

16 distinct epitopes that exceeded responses to natural infection.

17 response to live attenuated DENV vaccine or natural infection.

18 f 7 distinct clades of viruses isolated from natural infection.

19 vidity antibodies after both vaccination and natural infection.

20 th hexon and fiber following vaccination and natural infection.

21 FXR may not greatly modulate viremia during natural infection.

22 but likely need to be more immunogenic than natural infection.

23 f a liquid virus suspension does not reflect natural infection.

24 ic CD4i epitope structures that exist during natural infection.

25 previously CMV-seropositive women by way of natural infection.

26 se in cell cultures, mouse liver, and during natural infection.

27 ttachment while recapitulating the events of natural infection.

28 lymphoid organs is likely required during a natural infection.

29 imic the excellent protection observed after natural infection.

30 of broadly reactive gp41 MPER antibodies in natural infection.

31 ounter tetherin during the typical course of natural infection.

32 ites to subvert host immune responses during natural infection.

33 M. catarrhalis LOS epitopes developed during natural infection.

34 ssociated with slower disease progression in natural infection.

35 the timing and magnitude that they occur in natural infection.

36 the presence of diverse iron sources during natural infection.

37 ic countries, with limited contribution from natural infection.

38 n may modulate viremia to some extent during natural infection.

39 hat gaps in protective immunity occur during natural infection.

40 ls and could dampen the immune response to a natural infection.

41 describes in vivo importance of NKG2D during natural infection.

42 the antibody and defective particles during natural infection.

43 eactive responses comparable to that of H7N9 natural infection.

44 ntibodies may prime an individual for ADE on natural infection.

45 se risk reduction on the basis of studies of natural infection.

46 roduce lower antibody levels than those with natural infection.

47 (HIGS) process as a defense mechanism during natural infection.

48 prior vaccination were also unresponsive to natural infection.

49 silence target genes in Phytophthora during natural infection.

50 itopes on the dimerized form of LukAB during natural infection.

51 challenge strain to the response induced by natural infection.

52 antigens as those recognized as dominant in natural infection.

53 ated whether vIL-10 could be detected during natural infection.

54 on breadth and potency that have occurred in natural infection.

55 target of neutralizing antibodies induced by natural infection.

56 mmunity could potentially be boosted through natural infections.

57 n sulphate (HS); this virus is attenuated in natural infections.

58 e kinetics of both virus and antibody during natural infections.

59 replication, and its presence is variable in natural infections.

60 em that most animal viruses must face during natural infections.

61 reen monkeys and after human vaccination and natural infections.

62 ory defective viral genomes generated during natural infections.

63 ce antibody responses that can be boosted by natural infections.

64 ine of defense that viruses must face during natural infections.

65 heir activities have rarely been analyzed in natural infections.

66 their defective interfering particles during natural infections.

67 stent infection among 14 stallions following natural infections.

68 em that most animal viruses encounter during natural infections.

69 pes shows interferon sensitivity observed in natural infections.

70 l bioterrorist weapons or could re-emerge as natural infections.

71 nse that all animal viruses must face during natural infections.

72 g the importance of this hidden niche during natural infections.

73 elicited an antibody response in humans with natural infections.

74 environment these pathogens encounter during natural infections.

75 n individual clone density during persistent natural infections.

76 with ISG induction and IFN resistance during natural infections.

77 Following natural infection, 10 to 70% of infected stallions can b

78 adults born before 1950, presumed primed by natural infection (51%; -8% to 77%) versus those born 19

79 adults born before 1950, presumed primed by natural infection (51%; -8-77%) versus those born 1950 o

80 s, mimicking the preferences observed during natural infection (A16 and B14).

81 rotein, potentially expressed in vivo during natural infection, acting both as a nuclease with its am

82 in principle, the longer-nested sgmRNAs in a natural infection, all of which contain potential intern

83 s surprisingly high genomic diversity during natural infection although little is known about the lim

84 have been proposed as serological markers of natural infections among vaccinated populations.

85 ak illustrates that monkeypox is an emerging natural infection and a potential biological weapon.

86 o independent model systems, one that mimics natural infection and a second model with temporary tran

87 From observational studies of natural infection and challenge studies in volunteers, b

88 rate Abs to regions that are not targeted in natural infection and could provide additional protectio

89 is, and their implications for understanding natural infection and current and future vaccines.

90 The core set of viral genes expressed in natural infection and differentially regulated depending

91 our understanding of protection generated by natural infection and for the design of vaccines, which

92 pes simplex virus (HSV) glycoproteins during natural infection and how these antibodies affect virus

93 tails of antibodies derived from vaccines or natural infection and how they interact with their cogna

94 equired to initiate adaptive responses after natural infection and oral vaccination.

95 tions for understanding immunity elicited by natural infection and strategies to develop live attenua

96 590 that accumulated in two patients during natural infection and that lowers viral loads but increa

97 t most of the Env surface can be targeted in natural infection and that the neutralizing epitopes are

98 osed to HBV using a model system that mimics natural infection and the expression of host DNA methylt

99 by the rare nature of these responses during natural infection and the lack of longitudinal sampling

100 e speculate that PilA1 is immunogenic during natural infection and undergoes antigenic variation to e

101 Natural infection and vaccination also induced serum-neu

102 Here, I review the differences between natural infection and vaccination in terms of the antibo

103 cific for influenza virus are generated from natural infection and vaccination, persist long-term, an

104 es of lipid-specific T cell responses during natural infection and vaccination.

105 itro to H1 and H3 following exposure through natural infection and vaccination.

106 ponses that correlate with protection during natural infection and vaccination.

107 HIV remains a daunting goal, data from both natural infection and vaccine-induced immune responses s

108 arget of the antibodies that are elicited by natural infection and vaccines that are being developed

109 We show that T cell reactivity following natural infection and Zostavax vaccination dominantly ta

110 is process for systems experiencing complex, natural infections and environmental challenges are unkn

111 shaping outcomes of experimental as well as natural infections and explore the mechanisms by which D

112 spleen-dependent antigens are immunogenic in natural infections and that antibodies to HYP1 are assoc

113 SAMHD1 antagonism is actively maintained in natural infections and that this function must be advant

114 Natural infections and vaccination with a pathogen typic

115 ne subjects, with important implications for natural infections and vaccine development.

116 ection, if they have a high baseline risk of natural infection, and if during the trial they receive

117 ntation of the investigated HIV-1 epitope in natural infection, and the consequences for viral contro

118 FeLV subgroup A (FeLV-A) is transmitted in natural infections, and FeLV subgroups B, C, and T can e

119 evolution, beyond those already observed in natural infections, and may help predict its future dire

120 In natural infection, antibodies interact with HIV-1 primar

121 We speculate that during natural infection, antibodies target similar short antig

122 s in human serum, and their association with natural infection, are limited.

123 which contribute to the control of HIV-1 in natural infections, are currently being considered in bo

124 xamine gametocyte dynamics in controlled and natural infections as well as the impact of different an

125 ng the ligands for RIG-I under conditions of natural infection, as many previous studies have been ba

126 These findings suggest that, in response to natural infection at a peripheral mucosal site such as t

127 We hypothesize that over the course of natural infection, B cells are programmed to develop bro

128 However, during a natural infection, B7.1 is not functional, likely relate

129 Understanding of the mechanisms of natural infection-based immunity and advances in adjuvan

130 epitopes that are not typically targeted in natural infection but may lead to control when included

131 tive epitopes that are not often targeted in natural infection but that may be potentially useful in

132 ent neutralizing antibodies that emerge from natural infection, but these specificities are generally

133 Over 8 y, we studied natural infection by a rapidly evolving single-strand DN

134 Recent studies have shown that natural infection by HIV-2 leads to the elicitation of h

135 nt study was to investigate the effects of a natural infection by L. wallacei on the hemipteran insec

136 Using a model mimicking natural infection by Plasmodium yoelii, we delineated ea

137 Natural infection by Toxoplasma gondii occurs via oral i

138 ection, is important to our understanding of natural infections by the virus, in which late gene expr

139 ion, we show that the immunosignaturing of a natural infection can be used to discriminate a protecti

140 (bnAbs) to HIV envelope (Env) develop during natural infection can help guide the rational design of

141 we present data showing that antibodies from natural infections can recognize a recombinant form of t

142 ARF-encoded HIV epitopes are induced during natural infection, can contribute to viral control in vi

143 We conclude that natural infections caused by strains expressing L3,7 LPS

144 During natural infections Chlamydia trachomatis urogenital sero

145 d replication; however, during the course of natural infection, compensatory mutations restore the ab

146 the first time identifies RIG-I PAMPs under natural infection conditions and implies that full-lengt

147 t immunity against MSP1(33) after cumulative natural infections consists of low-magnitude and difficu

148 adaptation to variation in A3H activity in a natural infection context, we determined the A3H haploty

149 ascertain whether antibodies produced during natural infection could recognize the mimetics, we scree

150 lia burgdorferi during a unique point in its natural infection cycle, which alternates between ticks

151 s varied effects on different aspects of the natural infection cycle.

152 ons, QS mutants are frequently isolated from natural infections, demonstrating that the function of Q

153 is important viral protein in the context of natural infection due to the lack of a highly specific a

154 levels of cross-protection are attained via natural infection during an early (herald) wave of infec

155 ecies were also susceptible to BSE either by natural infection (e.g., felids, caprids) or in experime

156 to show that circulating HTLV-1(+) clones in natural infection each contain a single integrated provi

157 ferent HPV types for niche occupation during natural infection, elimination of 1 type may lead to an

158 exposure to the influenza hemagglutinin via natural infection enhances broad protection through expa

159 Natural infections expose the immune system to escalatin

160 5-haploinsufficient mice prone to B-ALL upon natural infection exposure.

161 10(-)) are gradually acquired in response to natural infection, exposure to P. falciparum also result

162 mmune response mismatched to that induced by natural infection, fails to prevent colonization or tran

163 nt role of CD4 T cells in vaccine design and natural infection, few studies have characterized HIV-sp

164 ive influenza virus to mimic the response to natural infection following vaccination, using previousl

165 in parasite biology, exemplified by malaria: natural infection has a defined, potently immunosubversi

166 This suggests that prior natural infection has a profound effect on shaping the a

167 t a full accounting of the immunogens during natural infections has not been achieved.

168 D8(+) T cells, in response to vaccination or natural infection, has been associated with improved pro

169 n these humanized mice, a key feature of the natural infection, has not been assessed fully.

170 The effects of SpA during natural infection, however, have not been addressed.

171 tively low risk of serious disease following natural infection, if they have a high baseline risk of

172 ree modes of immunization were compared: (i) natural infection; (ii) intramuscular administration of

173 ting HIV-specific CD4(+) T cell responses in natural infections.IMPORTANCE Increasing evidence sugges

174 them did not elicit T cell responses during natural infection in a Japanese cohort, they included th

175 ly cross-neutralizing antibodies elicited in natural infection in an elite neutralizer infected with

176 transcriptome analysis of P. aeruginosa in a natural infection in CF patients, and the results indica

177 B. anthracis causes natural infection in humans and animals and has been a t

178 which are involved in protective immunity to natural infection in humans.

179 s live attenuated vaccine acts like a silent natural infection in priming or boosting host immunity.

180 DENV2Delta30 are largely similar to those to natural infection in terms of specificity, highlighting

181 We infer that modified susceptibility due to natural infection in the previous influenza season is th

182 RDC and viruses that are encountered during natural infection in the respiratory tract.

183 tial mechanism by which bNAbs develop during natural infection in which an epitope target is acquired

184 n norovirus immunity, particularly following natural infection in young children during the first 2 y

185 NAbs elicited by vaccination in macaques and natural infections in humans illustrate commonalities be

186 However, no data exist on natural infections in humans, and these antibodies do no

187 cination and prototypic V3 NAbs derived from natural infections in humans, highlighting the convergen

188 udies of experimental infections in mice and natural infections in humans, to elucidate the biologica

189 o associate with more occurrence of OBI than natural infections in unvaccinated subjects.

190 Both vaccination and natural infection induce the formation of antibodies to

191 Natural infection-induced humoral immunity to matrix pro

192 A better understanding of how natural infection induces broad and long-lived immune re

193 The findings indicate that natural infection induces only low titers of SR antibodi

194 Natural infection induces partial immunity to Chlamydia

195 ction assumed that vaccination, similarly to natural infection, induces transient, heterologous prote

196 ty to human cytomegalovirus (HCMV) following natural infection is compromised by the presence of immu

197 , we established that anti-AM IgG induced in natural infection is highly heterogeneous in its binding

198 Understanding these NA responses during natural infection is key to exploiting these properties

199 The primary humoral immune response to natural infection is neutralizing antibodies (Abs).

200 icrobial diversity means that immunity after natural infection is often ineffective for prevention of

201 mmunodeficiency virus (HIV-1) replication in natural infection is widely recognized.

202 However, the relevance of these vectors to natural infections is questionable, as they have not bee

203 is unclear, although as IgG2a is induced by natural infection, it is assumed this isotype is importa

204 irus (HIV) antibody response produced during natural infection, leading to responses that can vary in

205 Natural infection leads to partial but incomplete protec

206 GMTs remained above natural infection levels across all age groups up to 64

207 l, and seroconversion is often delayed after natural infection, limiting the use of serology.

208 ifc Abs induced by vaccination (U.S.) and by natural infection (Mali) have comparable biological acti

209 suggest that achieving herd immunity through natural infection may be difficult.

210 t Ags that are only weakly recognized during natural infection may circumvent this evasion strategy a

211 ly neutralizing anti-HIV-1 antibodies during natural infection may help guide the development of immu

212 vitro and in vivo They impact the outcome of natural infections, may help drive virus-host coevolutio

213 ulin M or immunoglobulin G antibodies during natural infection, mice immunized with a recombinant ver

214 giform encephalopathy affecting cervids, and natural infection occurs through oral and nasal mucosal

215 Natural infection occurs via the oral route, and as a co

216 or an FHV-based replicon and facilitates the natural infection of C. elegans by Orsay virus but is no

217 hus, this study demonstrates that, following natural infection of cows with M. bovis, as the stage of

218 During natural infection of female animals, C. burnetii shows t

219 ere detected in canines, we found widespread natural infection of horses by a novel pegivirus.

220 Since natural infection of humans often occurs by the oral rou

221 Although natural infection of humans with an avian H3N8 influenza

222 Although natural infection of humans with an avian H3N8 influenza

223 he molecular complexity of swine IAVs during natural infection of pigs in which novel strains of IAVs

224 cell lines that may not necessarily reflect natural infection of susceptible T cells.

225 icked changes seen in viruses recovered from natural infections of alternative hosts, suggesting that

226 analyzed viral population structures during natural infections of animals with canine parvovirus (CP

227 information that we can obtain from studying natural infections of humans and other animals.

228 Although natural infections of humans with EIV have not been repo

229 as a result, there are few reports detecting natural infections of this organism.

230 tics of the immune response that result from natural infection or autoimmunity.

231 g on whether subjects were exposed to Ad5 by natural infection or by vaccination.

232 compromise the buildup of herd immunity from natural infection or deployment of current vaccines.

233 unity to LASV of distinct lineages following natural infection or immunization.

234 al event in protective immunity generated by natural infection or man-made vaccines.

235 nt virus will translate into protection from natural infection or serve solely as a fail-safe mechani

236 Although natural infection or standard vaccination may not induce

237 lthough rarely elicited during the course of natural infection or upon conventional vaccination, the

238 features of the immune response elicited by natural infection or vaccination are still uncertain.

239 , depending on whether they were elicited by natural infection or vaccination in HIV vaccine trial su

240 ate protection against reinfection following natural infection or vaccination, but HA and NA protein

241 g in escape from prior immunity generated by natural infection or vaccination.

242 o insufficient exposure to PV type 1 through natural infection or vaccination.

243 DENV4 targeted by human antibodies following natural infection or vaccination.IMPORTANCE The four ser

244 ted with Shingrix vaccination, as opposed to natural infection or Zostavax vaccination.

245 m people previously exposed to primary DENV4 natural infections or a monovalent DENV4 vaccine were an

246 In most natural infections or after recovery, small numbers of L

247 Antibodies induced by natural infection persisted at constant high titer for a

248 ry modes of a model retroviral Ag, including natural infection, preferentially expanded initially rar

249 s accessory proteins whose importance in the natural infection process is currently unclear.

250 Children with untreated natural infection progress rapidly to disease, especiall

251 As natural infection progresses, the immune response streng

252 HPV antibodies acquired through natural infection provide modest protection against subs

253 ilar in magnitude and breadth to those after natural infection, recognized the same antigen hierarchy

254 Prior vaccination with Vi vaccines, or natural infection, reduces onward transmission of S. Typ

255 18 antibody levels remained stable and above natural infection-related antibody levels for up to 12 y

256 oadly neutralizing antibodies (bnAbs) during natural infection relatively frequently, and consequentl

257 anism of autophagy targeting and its role in natural infection remain unclear.

258 m signaling between bacteria and host during natural infection remains poorly understood.

259 The functional role of DI-like RNAs in natural infections remains to be established.

260 specificities targeted by vaccination versus natural infection, revealing that, unlike prME-VRP and l

261 t the merits of studies that can incorporate natural infection routes and emphasize that accurate mea

262 Because hydathodes are natural infection routes for several pathogens, we inves

263 of the innate immune response to C. burnetii natural infection, SCID mice were exposed to aerosolized

264 individuals achieving control of HIV during natural infection seem unique in their dominant targetin

265 ralizing antibody activity in vaccination or natural infection settings.

266 he viral proteins targeted by T cells during natural infection should be useful in designing vaccines

267 ably, preexisting immunity to Ad5 fiber from natural infection significantly reduced the CD4 and CD8

268 chosen to screen sera from vaccine trials or natural-infection studies for neutralization responses.

269 he first spatiotemporal analysis of HBx in a natural infection system and also suggest that HBV trans

270 formed a spatiotemporal analysis of HBx in a natural infection system.

271 say detects a subset of antibodies following natural infection that are specifically linked to immuni

272 cate that HIV-2 Env is highly immunogenic in natural infection, that high-titer broadly neutralizing

273 vely with IFN-alpha/beta or IFN-gamma during natural infections to inhibit virus replication, and mig

274 We have shown that during natural infection, virus-neutralizing antibodies are pri

275 Natural infection was associated with a significant incr

276 sting that the level of NAbs elicited during natural infection was not sufficient to block infection.

277 ) can provide protection against C. burnetii natural infection, we examined if passive transfer of 1E

278 ure of broad NAb responses that arise during natural infection, we screened patients for sera able to

279 stic factors to restrict reassortment during natural infection, we sought to determine its efficiency

280 examine whether this is due to a paucity of natural infections, we used noninvasive methods to scree

281 Neutralizing antibodies elicited by natural infection were directed largely to the Ad5 fiber

282 against cryptic epitopes not targeted during natural infection were induced by vaccinating mice with

283 ognized following rDEN2Delta30 infection and natural infection were largely overlapping for both the

284 mucosal localization for immune response in natural infection, which is clinically interesting, espe

285 d by specific TCR clonotypes selected during natural infection, which provides a functional explanati

286 nduce responses similar to those that follow natural infection will be limited.

287 pathogens and subsequent host survival after natural infection with a variety of microorganisms.

288 ty against reinfection and memory induced by natural infection with B. pertussis.

289 Natural infection with Bordetella pertussis is thought t

290 ricted CD4(+) T-cell epitopes resulting from natural infection with dengue virus in a hyperepidemic s

291 Immune responses to natural infection with influenza virus in humans are rel

292 protection against infectious diseases after natural infection with pathogens or immunization, thereb

293 hepatic damage caused by parasite ova during natural infection with Schistosoma mansoni, but the role

294 Natural infection with simian retrovirus (SRV) has long

295 be confounded by unrecorded revaccination or natural infection with wild yellow fever virus during a

296 nd the humoral immune response elicited upon natural infections with coronaviruses, we structurally c

297 Natural infections with Plasmodium falciparum are often

298 eractions, over a period of 13 months during natural infections with two Theileria spp., pathogenic (

299 of PRC7-reactive PrP(Sc) in experimental and natural infections with various mouse-adapted scrapie st

300 ses were so far observed only in response to natural infection within a subset of individuals.