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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 cific CD8(+) T cells responses to subsequent vaccinia virus infection.
31 e effects of antiviral agents on progressive vaccinia virus infections.
32 s that are considered essential for clearing vaccinia virus infections.
33 vidence for phosphotyrosine signaling during vaccinia virus infection and implicates the F10 kinase a
34 in multiple stages of CD8 T cell response to vaccinia virus infection and may help to design effectiv
35 A23R genes occurred between 1 and 5 h after vaccinia virus infection and was not prevented by an inh
36 r understanding of the pathogenesis of fetal vaccinia virus infections and aid in the development of
37 infection with either virus, after a cleared vaccinia virus infection, and during a persistent/latent
38 studies demonstrated that antibodies to live vaccinia virus infection are needed for optimal protecti
39 , we analyzed the responses of host cells to vaccinia virus infection at both the transcriptional and
40 ecific, demonstrating poor responsiveness to vaccinia virus infection but robust maturation following
41 minor groove of double-stranded DNA, inhibit vaccinia virus infection by blocking viral DNA replicati
44 of the changes in the target cell induced by vaccinia virus infection depends on the natural cytotoxi
53 inant and actually recognized in vivo during vaccinia virus infection of HLA-A*0201 transgenic mice.
58 nto paired recipients, we show here that, on vaccinia virus infection, similar levels of panniculitis
60 dependent of infection or during a surrogate vaccinia virus infection to identify how MC159 prevented
62 hat showed notable changes in abundance upon vaccinia virus infection were concentrated largely in ju
63 f oxidative phosphorylation increased during vaccinia virus infection, while inhibition of the cellul
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