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1 nd vice versa because of a phenomenon termed antibody-dependent enhancement.
2 erity of secondary flavivirus infections via antibody-dependent enhancement.
4 lusion, here we find that in the presence of Antibody Dependent Enhancement (ADE) heterogeneity can i
5 evere dengue disease focus on the process of antibody-dependent enhancement (ADE) as a primary risk f
6 p-regulated DENV infection by a mechanism of antibody-dependent enhancement (ADE) in a variety of Fc
7 investigates the complex dynamics induced by antibody-dependent enhancement (ADE) in multiserotype di
9 sed severity seen in secondary infections is antibody-dependent enhancement (ADE) leading to increase
13 protection against DENV disease and prevents antibody-dependent enhancement (ADE) of disease in mice.
14 mmune serum, it has been shown in vitro that antibody-dependent enhancement (ADE) of ZIKV infection c
15 cross-reaction to ZIKV and was able to drive antibody-dependent enhancement (ADE) of ZIKV infection.
16 ble of both cross-neutralization, as well as antibody-dependent enhancement (ADE) of ZIKV infection.
20 e virus (DENV) infections is associated with antibody-dependent enhancement (ADE), and it was recentl
28 tions in flavivirus immune vaccinees such as Antibody-Dependent Enhancement (ADE, a phenomenon involv
29 kly neutralizing they also may contribute to antibody-dependent enhancement and flavi virus pathogene
30 unopathology is thought to play a part, with antibody-dependent enhancement and massive immune activa
31 nteractions, arising from cross-immunity and antibody-dependent enhancement, between related pathogen
32 ovide statistical support for the process of antibody-dependent enhancement (but not original antigen
35 human sera (PHS) and the major mediators of antibody-dependent enhancement in the presence of PHS.
38 ion showed significant capacity for in vitro antibody dependent enhancement of Dengue-1, 2, 3 and 4 s
42 on in the Fc region which completely ablates antibody-dependent enhancement of DENV replication in vi
43 ted against DENV-2 by using a mouse model of antibody-dependent enhancement of infection (ADE)-induce
45 zed all four serotypes of DENV, and mediated antibody-dependent enhancement of infection in Fc recept
50 raction of FcgammaRI with A1H3 underlays the antibody-dependent enhancement of the cellular effects o
51 rceived wisdom, patterns generated solely by antibody-dependent enhancement or heterogeneity in virus
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