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1  regulation of the CD8(+) T cell response to vaccinia virus infection.
2 ncreased and accelerated mortality following vaccinia virus infection.
3  most bone marrow T cells activate 3 d after vaccinia virus infection.
4 dly increase translation in the first day of vaccinia virus infection.
5 LECs toward MPECs, during the acute phase of vaccinia virus infection.
6 ty to localize infected cells and to control vaccinia virus infection.
7  which accelerates clearance of epicutaneous vaccinia virus infection.
8 e ability to act as a potent defense against vaccinia virus infection.
9 in a cell-intrinsic manner in the context of vaccinia virus infection.
10 infected HEK293T cells early and late during vaccinia virus infection.
11 e chemokine receptor CX3CR1 to an intranasal vaccinia virus infection.
12 control wild-type mice within 10 d following vaccinia virus infection.
13 ependent manner during both transfection and vaccinia virus infection.
14 tic choriomeningitis virus-immune mice after vaccinia virus infection.
15  on DNA replication and occurred late during vaccinia virus infection.
16 rate rate of diabetes after Coxsackie B4 and vaccinia virus infection.
17 e inhibition of this pathway observed during vaccinia virus infection.
18  were confirmed by examining the response to vaccinia virus infection.
19 necrotic RIP1-RIP3 complex is induced during vaccinia virus infection.
20 rded postexposure prophylaxis after systemic vaccinia virus infection.
21 CS-1 mimetics to protect mice against lethal vaccinia virus infection.
22 f CD8 T cells during the primary response to vaccinia virus infection.
23 cts C57BL/6 mice against overwhelming lethal vaccinia virus infection.
24 is expressed exclusively at late times after vaccinia virus infection.
25 port pathways were not adversely affected by vaccinia virus infection.
26 ses is required for the lethality of mice in vaccinia virus infection.
27 responses and viral clearance in the lung on vaccinia virus infection.
28 on of autoreactive cells was not detected in vaccinia virus infection.
29 al of the viral RNA polymerase late during a vaccinia virus infection.
30 ING pathway in response to dsDNA or modified vaccinia virus infection.
31 cific CD8(+) T cells responses to subsequent vaccinia virus infection.
32 e effects of antiviral agents on progressive vaccinia virus infections.
33 s that are considered essential for clearing vaccinia virus infections.
34 vidence for phosphotyrosine signaling during vaccinia virus infection and implicates the F10 kinase a
35 t a B12-VRK1-BAF signaling axis forms during vaccinia virus infection and is modulated via kinases B1
36 in multiple stages of CD8 T cell response to vaccinia virus infection and may help to design effectiv
37  A23R genes occurred between 1 and 5 h after vaccinia virus infection and was not prevented by an inh
38 r understanding of the pathogenesis of fetal vaccinia virus infections and aid in the development of
39 infection with either virus, after a cleared vaccinia virus infection, and during a persistent/latent
40 studies demonstrated that antibodies to live vaccinia virus infection are needed for optimal protecti
41 , we analyzed the responses of host cells to vaccinia virus infection at both the transcriptional and
42 ecific, demonstrating poor responsiveness to vaccinia virus infection but robust maturation following
43 minor groove of double-stranded DNA, inhibit vaccinia virus infection by blocking viral DNA replicati
44                We demonstrate that cutaneous vaccinia virus infection by scarification activates derm
45          This study highlights the fact that vaccinia virus infection can enhance cellular energy pro
46                                              Vaccinia virus infection causes a host shutoff that is m
47 of the changes in the target cell induced by vaccinia virus infection depends on the natural cytotoxi
48                                              Vaccinia virus infection does not induce expression of l
49  PD-1 in memory differentiation during acute vaccinia virus infection in intact mice.
50                 Using a model of respiratory vaccinia virus infection in mice, we could specifically
51                          In this study, with vaccinia virus infection in mice, we show that OX40 was
52  lethal toxin challenge in vitro and against vaccinia virus infection in vivo.
53 mune detection pathways, we performed serial vaccinia virus infections in primary human cells.
54                         By using a cutaneous vaccinia virus infection model, we demonstrate that regu
55                                         With vaccinia virus infection, neither the early nor late pha
56 inant and actually recognized in vivo during vaccinia virus infection of HLA-A*0201 transgenic mice.
57                                              Vaccinia virus infection of primary LCs harvested from m
58                                              Vaccinia virus infection of primary LCs strongly inhibit
59                                              Vaccinia virus infection of XS52 cells not only failed t
60 ease on the host response to intra-pulmonary vaccinia virus infection remain poorly defined.
61 nto paired recipients, we show here that, on vaccinia virus infection, similar levels of panniculitis
62           Although antibody protects against vaccinia virus infection, the mechanism is not understoo
63 dependent of infection or during a surrogate vaccinia virus infection to identify how MC159 prevented
64 tro and protect mice against lethal MPXV and vaccinia virus infection via both Fc-dependent and indep
65                             Using a model of vaccinia virus infection, we show that B7-2 but not B7-1
66 hat showed notable changes in abundance upon vaccinia virus infection were concentrated largely in ju
67 f oxidative phosphorylation increased during vaccinia virus infection, while inhibition of the cellul