ライフサイエンスコーパス: primary infection

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

2 age and nasal mucosa compared with after the primary infection.

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

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

5 had lower shedding rates than children with primary infection.

6 ifelong latent infection in humans following primary infection.

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

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

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

10 on that lasts for at least a few months post primary infection.

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

12 tion factor of KSHV lytic replication during primary infection.

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

14 virus can reactivate and cause zoster after primary infection.

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

16 o suffered life-threatening influenza during primary infection.

17 zed in a database of 304 pregnant women with primary infection.

18 l effectors of KSHV lytic replication during primary infection.

19 decline during the first 18 months following primary infection.

20 irus infection, cells critical for resolving primary infection.

21 erefore the KSHV replication program, during primary infection.

22 to retain the incoming viral genomes during primary infection.

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

24 urrence of severe infectious diseases during primary infection.

25 nges experienced by virus populations during primary infection.

26 involvement of lytic DNA replication during primary infection.

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

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

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

30 umoral immune response following symptomatic primary infection.

31 ears of observation, 66 subjects experienced primary infection.

32 king NSs to examine host responses following primary infection.

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

34 ection were stronger than those derived from primary infection.

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

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

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

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

39 long latency in neural ganglia after initial primary infection.

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

41 oxicity of critical host tissue bystander to primary infection.

42 uently when humoral immunity wanes following primary infection.

43 secondary viral challenge >1 month after the primary infection.

44 cell infiltration were largely comparable to primary infection.

45 ore the T-cell phase of the host response in primary infection.

46 tion distinct from those intended to prevent primary infection.

47 ed with early immune viral control following primary infection.

48 ysis of the barcodes of these animals during primary infection.

49 EBV-associated malignancies and symptomatic primary infection.

50 d is exacerbated by delayed clearance of the primary infection.

51 d in a database of 304 pregnant women with a primary infection.

52 uator [BTLA]) also decreased latency but not primary infection.

53 sponse may improve viral control compared to primary infection.

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

55 nematode Strongyloides venezuelensis during primary infection.

56 extracellular traps in helminth damage after primary infections.

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

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

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

60 ey can interact as secondary infections with primary infections.

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

62 At the time of primary infection, 5 of 12 (42%) urine samples had multi

63 and clinical diagnoses, including 3 men with primary infections, 8 with secondary syphilis, 9 with ea

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

65 During primary infections, accumulation of M protein in infecte

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

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

68 The duration of initial infection, fate of primary infection, all-cause mortality and mortality sec

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

70 Preventing primary infections among the elderly is the most effecti

71 ship between the gestational age at maternal primary infection an the outcome of congenital CMV is ba

72 L10 in 288 patients with measles virus (MeV) primary infection and 16 patients with reinfection (vacc

73 models assumed CMV vaccination would prevent primary infection and 2 models also assumed prevention o

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

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

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

77 We collected data on women with a primary infection and an infected child aged at least 1

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

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

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

81 accine is urgently needed to protect against primary infection and enhance existing immunity in HCMV-

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

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

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

85 ith multiple CMV genotypes was common during primary infection and further diversification occurred o

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

87 Successful primary infection and persistent coexistence with host i

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

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

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

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

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

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

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

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

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

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

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

99 is associated with an increased risk of CMV primary-infection and a prolonged course of viral replic

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

101 ted in all 15 subjects within 3 months after primary infection, and the majority had different CMV ge

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

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

104 Primary infection antisera did not neutralize all viruse

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

106 nza vaccine effectiveness (VE), we find that primary infection appears to reduce the risk of medicall

107 Primary infections are frequently asymptomatic and best

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

109 infant vaccination increased average age at primary infection as a result of decreased secondary tra

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

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

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

113 e of the spike, not receptor binding, is the primary infection barrier for these two group 2c CoVs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 immunity restricts viral replication in the primary infection compartment.

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

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

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

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

136 PEC or E. faecalis was equal or greater than primary infection despite that a protective adaptive res

137 nital herpes infection in mice, we show that primary infection does not establish plasma cells in the

138 % of infected infants born of mothers with a primary infection during pregnancy.

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

140 We found that primary infection elicited oligoclonal expansions of T(H

141 h of some immune components in controlling a primary infection, even in the absence of serological da

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

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

144 nd step, we estimate to what extent avoiding primary infections for specific age groups would prevent

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

146 Typically, primary infection generates a robust neutralizing antibo

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

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

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

150 vors who were hospitalised for longer during primary infection had an increased risk of death, could

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

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

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

154 After primary infection, HHV-6B persists as a chronic, latent

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

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

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

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

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

160 Thus, primary infection in adolescence can manifest as infecti

161 VL decreased following primary infection in all fluids.

162 While primary infection in childhood is usually asymptomatic,

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

164 ry mediator (HVEM) decreases latency but not primary infection in ocularly infected mice.

165 mitation of the cytopathological response to primary infection in the eye.IMPORTANCE HSV-1-induced ey

166 % of cases had sequelae following a maternal primary infection in the first and second or the third t

167 risk of cCMV and related sequelae following primary infection in the first trimester in subsequent p

168 30% of infected neonates following maternal primary infection in the first trimester suffer long-ter

169 interval [CI] 23.72-42.09) after a maternal primary infection in the first trimester, 0 (95% CI 0-6.

170 Following a maternal primary infection in the first trimester, up to 30% of i

171 sis, including epithelial cells, the site of primary infection in the host.

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

173 derstanding of how the virus initiates acute primary infection in vivo in diverse human cell types.

174 risk of cCMV and related sequelae following primary infections in the first trimester in subsequent

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

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

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

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

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

180 Although primary infection is generally asymptomatic in immunocom

181 y protective antibody response to DENV after primary infection is serotype specific.

182 Primary infection is thought to occur in the respiratory

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

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

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

186 However, RM treated with anti-IL-15 during primary infection manifested accelerated reactivation of

187 Characterizing primary infection may elucidate risk factors for maligna

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

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

190 protective immunity against SARS-CoV-2 after primary infection might not be likely.

191 During primary infection, murine cytomegalovirus (MCMV) spreads

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

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

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

195 ears old; for highest transmission pathogens primary infection occurred within the first year.

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

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

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

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

200 Primary infection of legumes by rhizobia involves the co

201 After primary infection of the cornea, the virus enters latenc

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

203 Primary infection of the vaginal epithelium with C. muri

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

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

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

207 host cells targeted by each bacterium at the primary infection or intoxication sites.

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

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

210 pic herpesvirus (EEHV) infection result from primary infection or reactivation of latent virus is a l

211 Whether lethal EEHV infections are due to primary infection or reactivation of latent virus remain

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

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

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

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

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

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

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

219 icating that the events were associated with primary infection rather than reactivation of latent vir

220 Individuals may experience primary infection, reactivation of latent infection, or

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

222 In primary infection, reduced frequencies of SIV-specific e

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

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

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

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

227 early HIV infection were recruited from the Primary Infection Resource Consortium.

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

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 ion of lesion spread of erythema area at the primary infection site at 48 to 72 hours (+/-2 hours), i

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

233 that facilitates its dissemination from the primary infection site.

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

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

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

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

238 During primary infection, the cultured ELISPOT response was mai

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

240 Following primary infection, the virus establishes latent infectio

241 3(+) CCR5(+) CD4(+) T (Th1) cells during the primary infection, thereby compromising the cellular imm

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

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

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

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

246 dividuals via cell-to-cell transmission, and primary infection typically occurs across juxtaposed muc

247 These cell lines, along with primary infection using genetically engineered viral par

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

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

250 After primary infection, VZV becomes latent in ganglionic neur

251 as intense: for most pathogens the window of primary infection was <3 years old; for highest transmis

252 accurate determination of the timing of the primary infection was based upon serial measurements of

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 defined by first positive anti-HCV

256 Primary infection was diagnosed based on seroconversion

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

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

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

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

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

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

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

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

265 piratory syndrome coronavirus 2 (SARS-CoV-2) primary infections, which indicates substantial transmis

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

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

268 Imprinting, or primary infection with a subtype, has modest to no effec

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

270 strikes otherwise healthy individuals during primary infection with common liver-tropic viruses.

271 30 to that of subjects following symptomatic primary infection with DENV1.

272 f type-specific neutralizing antibodies post-primary infection with different DENV1 genotypes in Asia

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

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

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

278 Primary infection with human cytomegalovirus (HCMV) is g

279 e obesity was established, all mice received primary infection with influenza X-31.

280 despite the increasing number of reports of primary infection with M tuberculosis or reactivation of

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

282 Primary infection with one DENV usually leads to acute i

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

284 In hamsters that received a primary infection with RSV, a booster infection with RSV

285 In African green monkeys that received a primary infection with RSV, a booster infection with RSV

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

287 Despite enhanced antimicrobial immunity upon primary infection with the DeltalipA mutant, we found th

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

289 sustaining adaptive immune responses during primary infection with the immune pathways that are pre-

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

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

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

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

294 uman varicella-zoster virus (VZV), developed primary infection with viremia and rash, which resolved

295 Primary infection with VZV causes chicken pox.

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

297 to identify several markers that can detect primary infections with as low as ten parasites and as e

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

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

300 , one with chronic infection, the other with primary infection, with a rhesusized, IL-15-neutralizing