ライフサイエンスコーパス: initial infection

1 device removal and reimplantation during the initial infection.

2 down-regulate flagella production following initial infection.

3 e later phase of infection, but early in the initial infection.

4 ntigens could be detected for days after the initial infection.

5 EhV-86 was seen as early as 2 days after the initial infection.

6 on of kidney tissue for up to 247 days after initial infection.

7 or vaginal flora, in the same manner as the initial infection.

8 ral immunity to prevent the establishment of initial infection.

9 ad rapidly through the environment following initial infection.

10 ment of the fungus in plant tissue following initial infection.

11 a different HPV type within 24 months of the initial infection.

12 , and DENV-3 occurred 325-621 days after the initial infection.

13 could help HIV enter cells and establish the initial infection.

14 er, and UV damage to the skin at the site of initial infection.

15 t persist chronically in those tissues after initial infection.

16 regardless of patient's age or intensity of initial infection.

17 in chimpanzees, died of AIDS 11 years after initial infection.

18 sal tissues are major sites of HIV entry and initial infection.

19 ias that occurred at a site distant from the initial infection.

20 ing is a major pathway for adaptation during initial infection.

21 eam to tissue sites distant from the site of initial infection.

22 t appear on leaves for months to years after initial infection.

23 differentiation in LNs draining the site of initial infection.

24 ancer, often many years to decades after the initial infection.

25 d-stage infections weeks to months after the initial infection.

26 superinfected this individual 15 weeks after initial infection.

27 than naive T (TN) cells do in response to an initial infection.

28 s is greatest in the several years following initial infection.

29 examined mice on day 35 of life, 28 d after initial infection.

30 es do not exhibit cellular preference during initial infection.

31 ls of viral protein as long as 37 days after initial infection.

32 pathy/tropical spastic paraparesis after the initial infection.

33 ride, a mediator of biofilm formation during initial infection.

34 Two children demonstrated evidence of an initial infection.

35 ricidal mechanisms that remain intact during initial infection.

36 infected persons, as well as to prevent the initial infections.

37 g sequential P. aeruginosa infections during initial infections.

38 use illness at a rate equal to that seen for initial infections.

39 he tissue that does not receive the primary (initial) infection.

40 he risk of reinfection within 6 months of an initial infection (12.9%) was high compared with risks i

41 women less than age 20 years at the time of initial infection, 6% were reinfected by 6 months, 11% b

42 estricted to tissues adjacent to the site of initial infection; A. brassicicola infection in systemic

43 Such a response failed to contain the initial infection and allowed the spirochetes to dissemi

44 Both initial infection and cell-to-cell spread by herpes simp

45 programmed death-1 (PD-1), from the time of initial infection and correlated these with HCV RNA leve

46 d interactions that determine the outcome of initial infection and highlight immune targets for thera

47 iology and structure and its relationship to initial infection and inflammation are poorly understood

48 ate groups of BALB/c mice were drug-cured of initial infection and later reinfected and treated with

49 n individuals for periods of years after the initial infection and led to gut communities marked by h

50 anti-OVA serum IgG and IgM titers after the initial infection and marked up-regulation of activation

51 A vaccine against HIV-1 virus would block initial infection and must target conserved residues.

52 ns activation shortened the interval between initial infection and onset of cell-cell fusion associat

53 he immune mechanisms that lead to control of initial infection and prevent reactivation of latent inf

54 icited in the mucosa, which is a key site of initial infection and subsequent HIV-1 replication in vi

55 virus requires transgene expression for both initial infection and subsequent retrograde transsynapti

56 sal immunity may be critical to control both initial infection and the massive early spread of virus.

57 ates of viral transmissibility, clearance of initial infection and waning immunity were derived in a

58 iagnosed at the same clinical setting as the initial infection, and 50% were diagnosed at the same ty

59 ralizing antibodies are generated late after initial infection, and the neutralizing antibody respons

60 Initial infections are cleared but chronic infection wit

61 ted IgA knockout (IgA(-/-)) mice cleared the initial infection as effectively as wild-type mice and p

62 lear targeting of the incoming virion during initial infection, as well as assembly of progeny virion

63 in vivo complement depletion facilitates the initial infection (assayed at the 2-day time point) by a

64 ernation in virus transmission to humans and initial infection at the molecular level.

65 However, factors of the initial infection attributed to the stimulation of mucin

66 In this work, we develop a model of initial infection, based on the well-known standard mode

67 e and duration of viremia (compared with the initial infection), broadened cellular immune responses,

68 plication and likely develops to contain the initial infection but allows bacterial dissemination to

69 tance to a fungal pathogen not by preventing initial infection but by limiting its spread through the

70 icates that vector activity is essential for initial infection but is not necessary for continued inf

71 HIV-1-P. gingivalis complexes 2 hr after the initial infection but not in cells exposed to HIV-1 alon

72 ty of Pgl+ hosts to support a phage burst on initial infection but subsequent cycles are severely att

73 Postinoculation treatment did not block the initial infection, but we identified treatment regimens

74 ing epithelial cells, may be targets for the initial infection by HIV-1.

75 ulation structure within patients, confirmed initial infection by one or a few viral particles.

76 antagonistic virus-virus interaction whereby initial infection by one virus prevents subsequent infec

77 and the EBV BMRF-2 protein; and (iii) after initial infection, by virus spread directly across later

78 ies have a pivotal role in the prevention of initial infection, cellular immune responses to HPV anti

79 between approximately 1 to 5 years following initial infection compared to 18 women with similar risk

80 ining quiescent d109 genomes weeks after the initial infection, demonstrating the functionality of th

81 Since initial infection depends on binding of the viral envelo

82 nes infection was primarily dependent on the initial infection dose or amount of antigen displayed, a

83 ing systemic infections disseminate from the initial infection focus to the target organs usually thr

84 Transmitted variants that established initial infection harbored key substitutions in E1E2 out

85 T cells persist in the brain even after the initial infection has been cleared.

86 IBS patients is sensitized 2 years after the initial infection has resolved.

87 Several possible routes for the initial infection have been suggested [1-6], including t

88 After initial infection, HIV-1 rapidly replicated and depleted

89 times after infection, including the time of initial infection immediately following transmission whe

90 pse parasite genotypes were different to the initial infection in 13 of 20 (65%) mothers compared wit

91 ic and antigenic variation within 28 days of initial infection in C3H/HeN mice.

92 uctural specificities that may influence the initial infection in mammalian hosts.

93 est that increasing ASL pH might prevent the initial infection in patients with CF, and that assaying

94 role in viral immunosurveillance at sites of initial infection in response to local cDC1-derived proi

95 Recent studies suggest that initial infection in the middle ear cleft may be key to

96 halus was equally successful at establishing initial infections in both host populations.

97 A substantial proportion of initial infections in both men and women are asymptomati

98 infectious cycle in vivo: in the gut during initial infection, in the liver where it replicates robu

99 responsible for most HPV-related cancers, an initial infection increases the 1-year probability of re

100 We discovered that compared to the initial infection isolate, the strain recovered during a

101 rsistent S. aureus bacteremia cases with the initial infection isolates and with three resolved S. au

102 cancers arise years if not decades after the initial infection, it has been estimated that there will

103 In some cases, initial infection leads to chronic and reactivating bruc

104 Initial infection levels affecting less than 10 % of cel

105 ion and persistence threshold depends on the initial infection levels.

106 hile such virulence factors are important in initial infection, many become dysregulated or nonfuncti

107 eoformans cells are melanized and imply that initial infection may involve exposure to melanized cell

108 elopment of stronger immune responses to the initial infection may protect from superinfection.

109 Initial infection occurred on the filaments, which preve

110 In addition if initial infection occurs during the growth phase then an

111 lls and showed the ability to expand from an initial infection of 1% of hypoxic cells to spread throu

112 ctiforme exist which show elevated levels of initial infection of A. punctatus as a consequence of re

113 utation in sigH resulted in a sixfold-higher initial infection of A. punctatus tissue without a paral

114 During the initial infection of B lymphocytes by Epstein-Barr virus

115 near normal numbers of target cells and the initial infection of bone marrow occurs normally in vivo

116 ecular processes that might occur during the initial infection of cells with exogenous transmissible

117 ikely need to induce antibodies that prevent initial infection of host cells or that limit early even

118 Prevention of the initial infection of mucosal dendritic cells (DC) and in

119 y the heretofore unknown length of time from initial infection of newly developing cluster of young l

120 self-amplify and spread in the tumor from an initial infection of only a few cells.

121 After the initial infection of peripheral tissues such as mucosal

122 of thrips, but they are not required for the initial infection of plants.

123 M. tuberculosis from the lung following the initial infection of the host.

124 in Vero cells could dramatically reduce the initial infection of the respiratory tract in animal mod

125 maA mutant was 10-fold less effective in the initial infection of the traumatized aortic valve.

126 Our data show that, during the initial infections of epithelial cells with respiratory

127 In 1999, 18 years after the initial infection, one of the members (D36) developed AI

128 in axons to either sensory ganglia following initial infection or back out to peripheral sites of inn

129 velope proteins were not detected during the initial infection or during rechallenge.

130 ccines generate antibodies that either block initial infection or help eradicate the virus before it

131 se; however, whether it acts at the level of initial infection or in promoting clinical progression i

132 hisms may have been present from the time of initial infection or may have appeared in response to im

133 er this transformation tropism occurs during initial infection or subsequently during the cellular tr

134 endent viral amplification at local sites of initial infection, perhaps through a macrophage-dependen

135 of the inflammatory responses at the site of initial infection (peritoneal cavity) revealed that CLP

136 potentially fundamental to understanding the initial infection process, intracellular survival, virul

137 the virus, not the target cell, to abort the initial infection process.

138 ediate not only virion assembly but also the initial infection processes of cell entry and nuclear en

139 Both initial infection rate constants, k, and decay constants

140 ently within nonciliated cells despite a low initial infection rate.

141 ed infection was due to recrudescence of his initial infection rather than reinfection by another str

142 After this initial infection resolves, the virus remains in a laten

143 However, the initial infection resulted in lasting elevation of antib

144 Unknown initial infection site and 72-hour surveillance cultures

145 grammed cell death in tissue surrounding the initial infection site limits pathogen spread.

146 panied by rapid cell death in and around the initial infection site, a reaction known as the hypersen

147 wing colonization of host tissues beyond the initial infection site.

148 itment of CX3CR1(hi) patrolling monocytes to initial infection sites in the mouse.

149 lipids to regulate macrophage recruitment to initial infection sites.

150 rophils do not interact with mycobacteria at initial infection sites.

151 subtype C isolates may be less fit following initial infection (T-cell and macrophage data) and may l

152 ted girls had a shorter mean time to loss of initial infection than did HIV-infected girls (403 days

153 infection may play a more important role in initial infection than previously appreciated.

154 After initial infection, the virus establishes latent reservoi

155 After the initial infection, the virus remains inactive or latent

156 then gradually, for the first 10 years after initial infection; the risk is relatively constant from

157 However, only in Arabidopsis did this initial infection then spread into the developing siliqu

158 r infection status, and that at the stage of initial infection there was no support for the dilution

159 ty of the urothelial barriers at the time of initial infection, these QIRs were established within te

160 arrier to understanding the progression from initial infection to cancer has been the lack of in vitr

161 at this virus cannot spread from the site of initial infection to neighboring cells.

162 to C. jejuni, we assessed the ability of an initial infection to prevent clinical illness after a se

163 The time from initial infection to reinfection was <1 year in 11 (41%)

164 n vary widely with respect to the outcome of initial infection to self-resolving acute or chronic dis

165 l of pathways that JCV may use from sites of initial infection to the brain.

166 scribing the sequence of events leading from initial infection to the induction of defense genes.

167 a target-cell-limited model from the time of initial infection until shortly after the peak in viremi

168 a result, the host's ability to control the initial infection was greatly enhanced.

169 vaccines elicited similar protection in that initial infection was not prevented, but subsequent ampl

170 elative risk of superinfection compared with initial infection was therefore 0.0 (95% confidence inte

171 No association between chronic fatigue and initial infections was seen in primary care practices.

172 coons reveals the long lasting effect of the initial infection wave in determining how viral populati

173 The SI variants that were associated with initial infection were dual tropic, with efficient repli

174 9-4.3) significantly increased the odds that initial infections were HSV-1 rather than HSV-2.

175 he pathogen abundantly expresses OspC during initial infection when the antigen is required, but down

176 ic T cells was moderately reduced during the initial infection, which might be a consequence of reduc

177 notion that OspC plays a unique role during initial infection while the antigenically variant VlsE p

178 nd pig showed comparable susceptibilities to initial infection with a highly pathogenic avian influen

179 Furthermore, initial infection with a low dosage (10(6) CFU/ml) of L.

180 e found that PAM were readily susceptible to initial infection with all five avian and mammalian infl

181 ccine candidates potentially able to prevent initial infection with either of these two hepatotropic

182 Initial infection with HIV-1 is transmitted by macrophag

183 A high incidence of initial infection with human papillomavirus (HPV) was pr

184 Initial infection with the BI/NAP1/027 epidemic clone wa

185 ablished cohort of 40 persons >6 years after initial infection with WNV.

186 During initial infection, within-host HA diversity increased dr

187 6 months from initial dose (ie, clearance of initial infection without subsequent microscopically con