ライフサイエンスコーパス: primary infection

1 sually abbreviated and less intense than the primary infection).

2 y limits lytic replication (as occurs during primary infection).

3 decline during the first 18 months following primary infection.

4 irus infection, cells critical for resolving primary infection.

5 erefore the KSHV replication program, during primary infection.

6 to retain the incoming viral genomes during primary infection.

7 nscription of a number of viral genes during primary infection.

8 urrence of severe infectious diseases during primary infection.

9 nges experienced by virus populations during primary infection.

10 involvement of lytic DNA replication during primary infection.

11 nematode Strongyloides venezuelensis during primary infection.

12 on the EBV genome during the early stages of primary infection.

13 extent of cross-reactivity observed after a primary infection.

14 virus (VZV) typically causes chickenpox upon primary infection.

15 BALB/c mice resulted in smaller lesions upon primary infection.

16 ears of observation, 66 subjects experienced primary infection.

17 in HIV-infected patients may initiate during primary infection.

18 king NSs to examine host responses following primary infection.

19 on levels were detected as early as 6 h post-primary infection.

20 ection were stronger than those derived from primary infection.

21 dition to their role in illness triggered by primary infection.

22 irus growth, despite a higher sensitivity to primary infection.

23 lymph node and lung parenchyma relative to a primary infection.

24 cy in cells of the myeloid lineage following primary infection.

25 long latency in neural ganglia after initial primary infection.

26 were each critical to host defense during a primary infection.

27 oxicity of critical host tissue bystander to primary infection.

28 lation likely to encounter HCMV early during primary infection.

29 prolonged RNA presence is characteristic of primary infection.

30 n CMV establishes lifelong persistence after primary infection.

31 infected 6 months following recovery from a primary infection.

32 transport of RRV particles to nuclei during primary infection.

33 te less severe clinical manifestations after primary infection.

34 reach levels observed in mice with a healed primary infection.

35 full spectrum of CDI similar to that of the primary infection.

36 erpesviridae is latent infection following a primary infection.

37 p65)-specific CD8(+) effector T cells during primary infection.

38 ting CD8(+) effector responses to CMV during primary infection.

39 irus and the cellular immune response during primary infection.

40 ut may also contribute to the control of the primary infection.

41 intranasally to neonatal mice at the time of primary infection.

42 from 18 HIV-1 controllers identified during primary infection.

43 year (long-term veterans [LTV]; n = 7) after primary infection.

44 sponse may improve viral control compared to primary infection.

45 had lower shedding rates than children with primary infection.

46 ifelong latent infection in humans following primary infection.

47 of ORF50/RTA-activated Vero cells undergoing primary infection.

48 and HHV-6 were shed at high rates following primary infection.

49 istence of memory CD8 T cells at the site of primary infection.

50 but similar peak viral loads compared to the primary infection.

51 of human cytomegalovirus (HCMV) following a primary infection.

52 tion factor of KSHV lytic replication during primary infection.

53 +) compared with CD8(+) T cells during acute primary infection.

54 virus can reactivate and cause zoster after primary infection.

55 r role in viral transport to the skin during primary infection.

56 o suffered life-threatening influenza during primary infection.

57 l effectors of KSHV lytic replication during primary infection.

58 sophils to S. venezuelensis egg clearance in primary infections.

59 atients can lead to chronic infection, as in primary infections.

60 y greater than those seen in mild illness or primary infections.

61 nt role in S. venezuelensis egg clearance in primary infections.

62 After primary infection, 7 LTRs lacked immune control with rel

63 timate that undiagnosed men, the majority in primary infection, accounted for 82% of new infections.

64 A gradient of sensitivity to primary infection across the eight cell lines was observ

65 The incidence decreased by 70% following a primary infection (adjusted hazard ratio = 0.30, 95% con

66 ive at the time of transplant and at risk of primary infection (aIRR = 1.95); and within the first 1.

67 e of cytokine and chemokine responses during primary infection also correlated positively with both a

68 dicated transmission in 2 cases of IUGR with primary infection and 3 asymptomatic recurrent infection

69 r subunit, Il17rb, were upregulated during a primary infection and a secondary challenge infection wi

70 the lytic cycle of replication after de novo primary infection and after spontaneous, tetradecanoyl p

71 dritic cells, the RIG-I agonist blocked both primary infection and antibody-dependent enhancement of

72 rozoites consist of tachysporozoites causing primary infection and bradysporozoites leading to relaps

73 d effector function in CD8(+) T cells during primary infection and differentiating the capacity of hi

74 thus permitting study of immune response to primary infection and disease.

75 T cell response is required for clearance of primary infection and enhances memory protection.

76 -producing CD8 T cells are induced following primary infection and enriched in elite controllers, sug

77 la-zoster virus (VZV) causes chickenpox upon primary infection and establishes latency in ganglia.

78 phaherpesvirus that causes chickenpox during primary infection and establishes latency in sensory gan

79 ila caviae) were characterized both during a primary infection and following a challenge infection.

80 with higher peripheral blood viral loads in primary infection and greater changes in viral diversity

81 ic regions may develop HHV-8 reactivation or primary infection and manifest with Kaposi's sarcoma or

82 munity and target cell depletion in limiting primary infection and modulating pathology.

83 tralizing antibody responses correlated with primary infection and protection from reinfection in the

84 SAR is induced upon primary infection and protects distal tissues from secon

85 regulators of HCMV replication, both during primary infection and reactivation from viral latency.

86 there are effective vaccines to prevent VZV primary infection and reactivation in immunocompetent ad

87 de burden of the Group A Streptococcus (GAS) primary infection and sequelae is considerable, although

88 rved when the interval between initiation of primary infection and subsequent challenge was <1 week.

89 HV activates the MSK1/2-CREB1 pathway during primary infection and that it depends on this pathway fo

90 ma(+)IL-10(+) T cells following clearance of primary infection and their subsequent influence on the

91 Here, using primary infection and treatment interruption data from m

92 le between wild-type and DeltaDC mice during primary infection and upon rechallenge of memory mice.

93 ibutes to anti-VACV immunity, following both primary infection and vaccination.

94 us that causes varicella (chickenpox) during primary infection and zoster (shingles) upon reactivatio

95 alphaherpesvirus that causes varicella upon primary infection and zoster upon reactivation from late

96 s-8 (HHV8)/Kaposi sarcoma herpesvirus (KSHV) primary infection and/or reactivations are associated wi

97 eins can suppress KSHV replication following primary infection and/or viral reactivation.

98 ural immunity to the virus is induced during primary infections and that this immunity can be cross p

99 TCD8 impairment, reduced viral titers during primary infection, and enhanced protection of immunized

100 n metapneumovirus (HMPV) several weeks after primary infection, and found that HMPV replicated to hig

101 Understanding the kinetics of primary infection, and its effect on the establishment o

102 wo HIV-1 strains--of 50% to 100% of those of primary infection, and our normal-risk HIV-positive coho

103 al growth and their prolonged survival after primary infection, and upon secondary challenge, compare

104 econdary immune responses, with only 6 clear primary infections, and all 4 dengue virus serotypes wer

105 rinfection, on average 8.5 months from their primary infection; and 27 patients remained infected wit

106 Primary infection antisera did not neutralize all viruse

107 wing HI patterns that would be expected from primary infection antisera, while 11 sera had lower, mor

108 fic CD8(+) effector responses at the time of primary infection are important predictors of immune con

109 Primary infections are frequently asymptomatic and best

110 E that are important for antigenicity during primary infection, are unknown.

111 Compared to mice undergoing primary infection as adults, neonatally sensitized mice

112 d mode (cell-free versus cell-associated) of primary infection as well as the modulation of dendritic

113 cally important for the efficient control of primary infections as well for the development of 'train

114 l for controlling viral dissemination during primary infection, as indicated by the marked increase o

115 ormal children whose mothers had a confirmed primary infection at </= 20 weeks' gestation.

116 er was detected over their calving season of primary infection, Bluetongue was detected more rapidly

117 egrin) was low in all tissues sampled during primary infection but increased in the airways after vir

118 Serious disease can be seen during primary infection but is more frequent following second

119 lations; it is not cleared by the host after primary infection but persists for life.

120 HCMV is never cleared after primary infection but persists in the host for life.

121 NTES) were elicited in the urethra following primary infection, but only CCL5 showed increased levels

122 Both are generated after primary infections, but their clonal origins have been u

123 with MF59 adjuvant reduced the incidence of primary infection by 50%.

124 s were detected during the calving season of primary infection by Bluetongue in 28% (n = 23) of the u

125 ry and sufficient to establish resistance to primary infection by F. graminearum and highlight a nove

126 not mutation of the Bradi5g03300 gene alters primary infection by F. graminearum, highlighting the in

127 III IFNs is required for protection against primary infection by influenza virus in humans.

128 We showed that HIV-specific CD8 T cells in primary infection can be distinguished by their metaboli

129 prolonged oral CMV shedding observed during primary infection can be explained by slow viral expansi

130 ir observed frequency to that of established primary infections, characterized by persistent high-lev

131 terized, antiretroviral therapy (ART)-naive, primary infection cohort of men who have sex with men.

132 g (UDS) to estimate the frequency of DI in a primary infection cohort of predominantly men who have s

133 cation of multiple HHVs is common in our HIV primary infection cohort.

134 and viral load were higher in children with primary infection compared to children with chronic infe

135 ng analysis of mucosal host responses in the primary infection compartment during acute SIV infection

136 immunity restricts viral replication in the primary infection compartment.

137 e pulmonary CD8(+) predominance during acute primary infection, compartmental equalization occurred i

138 However, Abs generated by primary infections confer serotype-specific protection,

139 NA and its capsid play multiple roles during primary infections, consistent with ribosome-mediated ge

140 infection with B. melitensis Our analysis of primary infection demonstrated that the effectors implic

141 light exposure that plants receive after the primary infection determines the extent to which MeSA is

142 % of infected infants born of mothers with a primary infection during pregnancy.

143 as were orally shedding GbbLCV-1, suggesting primary infection during this stage of life, similar to

144 Following primary infection, EBV remains latent in the memory B-ce

145 cross-reactive antibodies generated during a primary infection facilitate entry into Fc receptor bear

146 e cross-reactive antibodies induced during a primary infection facilitate virus entry into Fc recepto

147 nd duration of treatment were highest during primary infection, followed by reinfection then reactiva

148 datory for the successful establishment of a primary infection following viral entry as well as for e

149 d dendritic cells using PBMC obtained during primary infection from relapsers and observed impaired m

150 stic mathematical model, we found that while primary infection generates an adaptive immune memory re

151 could explain why the lesion associated with primary infection (Ghon focus) is anatomically separated

152 Beta-amyloid was elevated in the primary infection group (P = .0005) and correlated with

153 als with higher NAb titers immediately after primary infection had delayed symptomatic infections com

154 Children who experienced primary infections had broad, serotype-cross-neutralizin

155 Thus, some patients with asymptomatic primary infections have very high circulating viral load

156 It is generally accepted that, following primary infection, human cytomegalovirus (HCMV) establis

157 After primary infection, human cytomegalovirus (HCMV) persists

158 Following primary infection, human herpesvirus 6 (HHV-6) establish

159 he mode of inoculation, (ii) the dynamics of primary infection, (iii) consequent immune responses, an

160 for gammadelta T cell activation during the primary infection, IL-1 signaling was dispensable for ac

161 unterpart of HPIV1) to noninvasively measure primary infection, immune responses, and protection from

162 smitted from the donor organ, giving rise to primary infection in a CMV negative recipient or reinfec

163 Thus, primary infection in adolescence can manifest as infecti

164 VL decreased following primary infection in all fluids.

165 ed general acceptance that JC virus causes a primary infection in childhood and enters a latent state

166 While primary infection in childhood is usually asymptomatic,

167 1 in the central nervous system (CNS) during primary infection in childhood, in at least some patient

168 est burden of serious disease occurring upon primary infection in infants and children.

169 reduction in the Th2 immune response during primary infection in neonates prevents Th2-mediated pulm

170 a serological constellation consistent with primary infection in pregnancy and their children was pe

171 In the case of HSV-1, primary infection in the human begins in the epidermis o

172 tion but do not prove that AIEC is causing a primary infection in the Peyer's patches that is necessa

173 Immune responses after primary infection included serum IgA, IgG, ASC, and IFN-

174 V-seronegative participants, 9 developed EBV primary infections, including 2 with infectious mononucl

175 trated that expression of alpha-toxin during primary infection increases the severity of recurrent di

176 Three to 6 months after primary infection, individuals who would later become su

177 acquired by the oral route in children, and primary infection is associated with abundant mucosal re

178 Although primary infection is generally asymptomatic in immunocom

179 Primary infection is thought to occur in the respiratory

180 innate immunity during the establishment of primary infection, latency, and reactivation by varicell

181 show that an absence of IL-10 at the time of primary infection leads to enhanced local virus-specific

182 Primary infection leads to reduced nucleosomal density n

183 While primary infection leads to the typically self-limiting c

184 , and virus titers in the eyes and TG during primary infection, level of viral gB DNA in TG on day 28

185 In primary infection, loss of DC number and function occurs

186 Characterizing primary infection may elucidate risk factors for maligna

187 e P. vivax vaccine with low efficacy against primary infection may substantially reduce transmission

188 ies suggest that ART, initiated early during primary infection, may induce post-treatment control (PT

189 During primary infection, murine cytomegalovirus (MCMV) spreads

190 ained lower, but between 2 and 3 years after primary infection, NAb levels strengthened and reached t

191 Upon primary infection, naive T cells that recognize their co

192 Primary infection occurred in 18 (81.8%) cases.

193 EBV primary infection occurred in 27 of 43 (63%) seronegativ

194 When the primary infection occurred late in the day and as a resu

195 In Africa, EBV primary infection occurs during early childhood, but lit

196 Primary infection of a host with a fluorescent protein-t

197 immunodominant CD8(+) T cell antigen during primary infection of C57BL/6 mice with Yersinia pseudotu

198 mited during between-host transmission, with primary infection of hosts representing a major constrai

199 g in an increase in lytic replication during primary infection of human peripheral blood mononuclear

200 causative polyomavirus (TSPyV) occur during primary infection of the immunosuppressed host.

201 s in the kidney, resulting in a disseminated primary infection of the recipient.

202 Primary infection of the vaginal epithelium with C. muri

203 ve donor/seronegative recipient) developed a primary infection, one of whom developed a lethal nonmal

204 were investigated in the second month after primary infection onset in 44 pregnant women (15 transmi

205 duals develop clinical disease either during primary infection or during reactivation from latency or

206 atically with HCV NS2 to -4A chimera RNA for primary infection or intravenously injected with chimera

207 ch, mortality in late sepsis from persistent primary infection or opportunistic new infection often e

208 ocesses can cause recurrence: relapse of the primary infection or re-infection with an exogenous stra

209 Following a severe primary infection or trauma, the risk of developing pneu

210 RNA level was lower during reinfection than primary infection (P = .011).

211 del to evaluate the protective efficacies of primary infection, P particles, and virus-like particles

212 e hypothesis that ART initiated early during primary infection permits PTC by limiting the size of th

213 f the parental R144A strain, indicating that primary infection primes effector CD8(+) T cells indepen

214 r early antiviral immunity at local sites of primary infection prior to the initiation of circulating

215 trasubtype DI was frequent and comparable to primary infection rates among MSM in San Diego; however,

216 ne surveillance and Epstein-Barr virus (EBV) primary infection/reactivation are key factors in the pa

217 ls generated by low-avidity stimulation in a primary infection recognize a cross-reactive epitope wit

218 MAb 131-2G administration 1 day prior to primary infection reduced the pulmonary inflammatory res

219 nhibitor of the toxin receptor ADAM10 during primary infection reduces reinfection abscess severity.

220 matically compared for their permissivity to primary infection, replication, and spread of seven huma

221 ell priming during tumor development or many primary infections requires cross-presentation by XCR1(+

222 from 195 HIV-infected men from the San Diego Primary Infection Resource Consortium and 67 seminal sam

223 in lung and spleen tissues at 6-12 wk after primary infection (resting memory).

224 In vivo lymphocyte depletion during primary infection resulted in a brief elevation of virem

225 In contrast, CD4 depletion during primary infection resulted in the failure to establish a

226 tabolic state of HIV-specific CD8 T cells in primary infection resulting from hyperproliferation and

227 infection of the CNS is an early event after primary infection, resulting in neurological complicatio

228 During primary infection, SARS-CoV replicated in the AGM lung f

229 rinfection identified from the 76 women with primary infection screened at two time points (rate of s

230 gs suggests that early HIV diagnoses by this primary infection screening program probably contributed

231 colistin dose, polymicrobial infection, and primary infection site, excess 14-day mortality was asso

232 t all time points tested, up to 30 days post-primary infection, suggesting a delay in the generation

233 leic acid and serology testing to screen for primary infection targeting local high-risk individuals.

234 During primary infection, tegument protein-specific B cells exp

235 sterilizing immunity is induced following a primary infection that prevents a secondary infection.

236 In pregnant women with primary infection, the cultured ELISPOT assay detected a

237 During primary infection, the cultured ELISPOT response was mai

238 Allowing low infectiousness during primary infection, the likelihood of elimination becomes

239 During primary infection, the number of HIV-1 particles in plas

240 Following primary infection, the virus establishes latent infectio

241 After the primary infection, the virus remains latent in sensory g

242 on is more commonly associated with DHF than primary infections, the acquired immune response to deng

243 3(+) CCR5(+) CD4(+) T (Th1) cells during the primary infection, thereby compromising the cellular imm

244 es and lymphocyte recruitment to the site of primary infection, thereby controlling invading pathogen

245 wed that eosinophils protect the parasite in primary infection, these new data show that eosinophils

246 important role in immune evasion during KSHV primary infection, through inhibition of the host cytoso

247 tion as well as to treat pregnant women with primary infection, thus decreasing the fetal and neonata

248 boosting must be more easily triggered than primary infection to account for age-incidence data.

249 man sensory and cranial nerve ganglia during primary infection (varicella), and the virus can reactiv

250 f the JCV life cycle including transmission, primary infection, viremia, and establishment of asympto

251 After primary infection, VZV becomes latent in ganglionic neur

252 1000 person-years) and that attributable to primary infection was 60.1 per 1000 person-years (95% CI

253 Although viral RNA during primary infection was cleared from blood plasma and urin

254 Oral CMV shedding by 14 infants with primary infection was comprehensively characterized usin

255 Primary infection was diagnosed based on seroconversion

256 The risk to deliver an infected baby after primary infection was increased in younger (OD = 7.9), p

257 The bacterial burden during primary infection was significantly enhanced and the ind

258 pe, associated with viral control during CMV primary infection, was predominantly found on the membra

259 t reservoir sizes in patients treated during primary infection, we also predict population-level VR t

260 nderstand the role of DNA replication during primary infection, we performed de novo PBMC infections

261 In the context of primary infection, we show that in cells with depleted l

262 Immune responses during primary infection were analyzed for association with vir

263 crete IL-2 on antigenic restimulation during primary infection were inversely correlated with the vir

264 IE1-specific CD8(+) effector T cells during primary infection were not associated with early relapsi

265 LLO118 T cells proliferate more strongly to primary infection, whereas surprisingly, LLO56 has a sup

266 er the superinfecting transmission resembles primary infection, which has not been established.

267 Re-infection of six animals 45 d after primary infection with a heterologous strain resulted in

268 e the source of host-protective IL-10 during primary infection with a number of different pathogens,

269 Fifteen subjects underwent a primary infection with C. jejuni CG8421; 14 (93.3%) expe

270 30 to that of subjects following symptomatic primary infection with DENV1.

271 erscored the association of HHV-6B and HHV-7 primary infection with febrile status epilepticus as wel

272 cal lesions consistent with PRLH, suggesting primary infection with GbbLCV-1 is associated with PRLH

273 ity occurred in the basopenic mice following primary infection with H. polygyrus bakeri, parasite rej

274 In the course of primary infection with herpes simplex virus 1 (HSV-1), c

275 In this review evidence is reviewed that primary infection with herpesviruses may have an atypica

276 Primary infection with HHV-6B occurs in nearly all child

277 Between 2000 and 2009, 37 men who had primary infection with HIV-1 subtype B, no indication fo

278 (+) T-cell decline in men who have untreated primary infection with HIV-1 subtype B.

279 eloped encephalitis in the course of natural primary infection with HSV-1.

280 Primary infection with human cytomegalovirus (HCMV) is g

281 Primary infection with influenza A virus (IAV) results i

282 hil-specific IL-4Ralpha(-/-) mice to control primary infection with L. donovani and to respond to che

283 e absence of an effective vaccine to prevent primary infection with Mycobacterium tuberculosis and tu

284 Primary infection with one DENV usually leads to acute i

285 eory, skewing of T-cell responses induced by primary infection with one serotype causes less effectiv

286 Primary infection with s-H1N1 influenza virus followed b

287 critical determinants of host resistance to primary infection with T. cruzi.

288 We also demonstrated that the primary infection with TC-PC177 failed to induce complet

289 acity to expand significantly in response to primary infection with the bacteria Listeria monocytogen

290 nstrating that the altered host responses to primary infection with the DeltatolC mutant led to alter

291 virus-specific immune response during acute primary infection with the lymphocytic choriomeningitis

292 have shown previously that when mice undergo primary infection with the parasitic nematode Trichinell

293 tigen for Yersinia pseudotuberculosis and if primary infection with this enteric pathogen elicits a C

294 dings demonstrate the clinical importance of primary infection with this rapidly expanding group of h

295 Primary infection with Toxoplasma gondii stimulates prod

296 Primary infection with varicella-zoster virus (VZV), a n

297 e expression that occurs within 4 days after primary infection with wild-type EBV, the ZV ZV' ZIIR tm

298 peptide at the peak of the response) during primary infection with Y. pseudotuberculosis, as shown b

299 kedly increased in the jejunal mucosa during primary infections with S. venezuelensis Studies in baso

300 Virus growth was generally concordant with primary infection, with a gradient in virus replication