ライフサイエンスコーパス: natural infection

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

2 challenge strain to the response induced by natural infection.

3 ings that recapitulate those observed during natural infection.

4 response to live attenuated DENV vaccine or natural infection.

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

6 vidity antibodies after both vaccination and natural infection.

7 th hexon and fiber following vaccination and natural infection.

8 FXR may not greatly modulate viremia during natural infection.

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

10 ic CD4i epitope structures that exist during natural infection.

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

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

13 ttachment while recapitulating the events of natural infection.

14 lymphoid organs is likely required during a natural infection.

15 imic the excellent protection observed after natural infection.

16 of broadly reactive gp41 MPER antibodies in natural infection.

17 ounter tetherin during the typical course of natural infection.

18 ites to subvert host immune responses during natural infection.

19 M. catarrhalis LOS epitopes developed during natural infection.

20 antigens as those recognized as dominant in natural infection.

21 ssociated with slower disease progression in natural infection.

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

23 the presence of diverse iron sources during natural infection.

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

25 hat gaps in protective immunity occur during natural infection.

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

27 describes in vivo importance of NKG2D during natural infection.

28 -elicited immune responses can be boosted by natural infection.

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

30 considerably lower than those observed after natural infection.

31 ve led to enhanced immunopathology following natural infection.

32 tavirus antigenemia is a common event during natural infection.

33 ells and induce host immune responses during natural infection.

34 pB heterogeneity occurs over the course of a natural infection.

35 eparation experienced enhanced illness after natural infection.

36 ies are generated against all seven during a natural infection.

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

38 equivalent to titers found clinically after natural infection.

39 while human titers are commonly acquired via natural infection.

40 One child in each group showed evidence of natural infection.

41 by the quasispecies invariably present in a natural infection.

42 HBeAg may serve an immunoregulatory role in natural infection.

43 n attempt to understand the role of HBeAg in natural infection.

44 V also replicates in extrahepatic tissues in natural infection.

45 target of neutralizing antibodies induced by natural infection.

46 tibodies and memory cells before their first natural infection.

47 the host immune response, as it is during a natural infection.

48 pression occurring in human tissues during a natural infection.

49 se enhanced disease in naive hosts following natural infection.

50 g antibodies are evoked during the course of natural infection.

51 HLA-restricted cytotoxic T cells (CTL) after natural infection.

52 nd were higher than usually achieved through natural infection.

53 y CD8+ cytotoxic T lymphocytes induced after natural infection.

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

55 alizing antibody response is directed during natural infection.

56 tute a safe vaccination strategy that mimics natural infection.

57 ssumption that the vaccine acts similarly to natural infection.

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

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

60 ibody levels comparable to those achieved in natural infection.

61 T cell response is not stimulated following natural infection.

62 4- to 256-fold greater than those seen after natural infection.

63 1E4 may be useful for preventing C. burnetii natural infection.

64 do not recapitulate the protective effect of natural infection.

65 rong population bottlenecks occurring during natural infection.

66 t Abs provide effective protection against a natural infection.

67 nalysis indicates to be commonly elicited by natural infection.

68 ory defective viral genomes generated during natural infections.

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

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

71 heir activities have rarely been analyzed in natural infections.

72 their defective interfering particles during natural infections.

73 with ISG induction and IFN resistance during natural infections.

74 stent infection among 14 stallions following natural infections.

75 em that most animal viruses encounter during natural infections.

76 pes shows interferon sensitivity observed in natural infections.

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

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

79 elicited an antibody response in humans with natural infections.

80 environment these pathogens encounter during natural infections.

81 peripheral memory T cell populations during natural infections.

82 equently within the capsid (core) protein in natural infections.

83 mmunity could potentially be boosted through natural infections.

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

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

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

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

88 reen monkeys and after human vaccination and natural infections.

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

90 nses were measured following experimental or natural infection after rotavirus was isolated from stoo

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

92 -lymphocyte (CTL) responses in the course of natural infection allowed us to address HIV-1C-specific

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

94 ned was used to determine the probability of natural infection among vaccinated dogs residing in area

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

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

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

98 ent humoral immune responses elicited during natural infection and after gp120 vaccination and help t

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

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

101 fection in several animal models and because natural infection and current vaccines do not appear to

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

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

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

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

106 l antibody responses to rTbps as a result of natural infection and represents a baseline over which a

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

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

109 the early, primary target of dengue virus in natural infection and the vigor of CMI is modulated by t

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

111 Natural infection and vaccination also induced serum-neu

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

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

114 description of two risk profiles related to natural infection and vaccination.

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

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

117 s of the adaptive humoral immune response in natural infection and, potentially, as components of an

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

119 These findings have implications for both natural infections and vaccines.

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

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

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

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

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

125 epitopes that are highly immunogenic during natural infection are located at structurally analogous

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

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

128 HBV capsids are known to exist in natural infection as dimorphic T=3 or T=4 icosahedral pa

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

130 tent to which these proteins are targeted in natural infection, as well as precise CTL epitopes withi

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

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

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

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

135 he proteins whose expression is important in natural infection but are modified once M. avium subsp.

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

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

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

139 The lytic outcome of natural infection by Chlamydia trachomatis was exploited

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

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

142 Natural infection by Toxoplasma gondii occurs via oral i

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

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

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

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

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

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

149 During natural infections Chlamydia trachomatis urogenital sero

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

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

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

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

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

155 nd that the majority of variants observed in natural infections could not arise simply through mutati

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

157 erm persistence in ticks and completion of a natural infection cycle.

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

159 This observation that natural infection did not confer protection during the f

160 It is not clear why natural infections do not induce protection against the

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

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

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

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

165 Natural infections expose the immune system to escalatin

166 10(-)) are gradually acquired in response to natural infection, exposure to P. falciparum also result

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

184 ion of a broad repertoire of CD8+ CTLs after natural infection in vivo.

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

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

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 -gamma was by far a subdominant response) vs natural infection; in addition, there was fairly signifi

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

192 Natural infection-induced humoral immunity to matrix pro

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 stablished, the effect of these molecules in natural infection is not well understood.

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

199 nfection is common in humans, the biology of natural infection is poorly understood.

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

201 r bacterial responses to host signals during natural infections is poorly understood.

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

203 osed viral transcriptional template found in natural infection, is regulated either by subtle alterat

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

205 Natural infection leads to partial but incomplete protec

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

207 n of a very few arthroconidia, but following natural infection, long-lived immunity is the norm.

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

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

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

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

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

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

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

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

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

217 Although natural infection of humans with an avian H3N8 influenza

218 Although natural infection of humans with an avian H3N8 influenza

219 We show that, in a natural infection of MDBK cells, cpBVDV activates the ER

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

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

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

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

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

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

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

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

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

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

230 In patients, the outcome, whether it is a natural infection or results from an interferon-alpha-ba

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

232 Although natural infection or standard vaccination may not induce

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

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

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

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

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

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

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

240 ited a moderate degree of protection against natural infection (P < 0.01).

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

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

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

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

245 As natural infection progresses, the immune response streng

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

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

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

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

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

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

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

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

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

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

256 ralizing antibody activity in vaccination or natural infection settings.

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

258 onferring an unfavorable prognosis following natural infection, showed no such disadvantage for vacci

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

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

261 are neutralizing antibodies elicited during natural infection that are directed against gp120 epitop

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

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

264 Moreover, under conditions of natural infection, the CD4 T-cell response is not suffic

265 In fact, in most cases of natural infection, the host immune response leads to a c

266 Ag-specific T cells elicited by vaccines or natural infection to determine lineage and differentiati

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

268 an respiratory syncytial virus (RSV) is that natural infection typically does not confer solid immuni

269 ell function induced by HIV-1 immunogens and natural infection using polychromatic flow cytometry.

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

271 L-10 in establishing latency associated with natural infection was confirmed in IL-10-deficient mice

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

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

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

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

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

277 When responses in natural infection were compared with vaccine-induced res

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

279 Serum IgG antibodies following natural infection were directed predominantly at OMP G1a

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

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

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

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

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

285 the mucosal inductive site at the portal of natural infection with a replicating vaccine, followed b

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

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

288 Natural infection with Bordetella pertussis is thought t

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

290 ay, inducing the innate immune response upon natural infection with gram-negative bacteria.

291 A natural infection with Helicobacter pylori (H. pylori) i

292 Natural infection with HSV-2 is associated with a persis

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

294 out 46 species of mammals are known to carry natural infection with S. japonicum, only a few might be

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

296 Natural infection with simian retrovirus (SRV) has long

297 During natural infection with the agent of Lyme disease, Borrel

298 During natural infection with the agent of Lyme disease, Borrel

299 Natural infections with Plasmodium falciparum are often

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