ライフサイエンスコーパス: mouse cytomegalovirus

1 Ds prevented necroptosis upon infection with mouse cytomegalovirus.

2 ccinia virus, but dispensable in the case of mouse cytomegalovirus.

3 ntiation, we have analyzed an infection with mouse cytomegalovirus, a persistent-latent virus that el

4 both profound susceptibility to infection by mouse cytomegalovirus and approximately 20,000-fold sens

5 f LPS, AIM2 activators Francisella novicida, mouse cytomegalovirus and DNA, and the infectious agents

6 o Francisella tularensis, vaccinia virus and mouse cytomegalovirus and had a partial role in the sens

7 o caused hypersusceptibility to infection by mouse cytomegalovirus and other microbes.

8 similar to that of the miRNAs described for mouse cytomegalovirus, but they do not share any substan

9 es simplex virus 1 (HSV-1), HSV-2, HCMV, and mouse cytomegalovirus, by 30- to 700-fold, depending on

10 vely replicate in human cells and found that mouse cytomegalovirus can produce infectious particles a

11 This finding demonstrates that mouse cytomegalovirus can undergo all processes of its l

12 We reexamined the dogma that mouse cytomegalovirus cannot productively replicate in h

13 During mouse cytomegalovirus (CMV) infection, a population of L

14 importance for detecting cells infected with mouse cytomegalovirus (CMV) via recognition of the viral

15 ions, we challenged old mice carrying latent mouse cytomegalovirus (CMV), herpes simplex virus 1 (HSV

16 We observed that the mouse cytomegalovirus encoded protein m18 is necessary a

17 The mouse cytomegalovirus encodes an MHC-like protein, m157,

18 effects of LPS, and are hypersusceptible to mouse cytomegalovirus, failing to produce type I interfe

19 s as a transgene vector, manipulation of the mouse cytomegalovirus genome to allow limited spread to

20 Tlr9(CpG1) allele are highly susceptible to mouse cytomegalovirus infection and show impaired infect

21 ither pathway offers full protection against mouse cytomegalovirus infection in the absence of the ot

22 ain mediators of NK cell-mediated control of mouse cytomegalovirus infection in vivo.

23 s replication, were dependent on AIM2 during mouse cytomegalovirus infection in vivo.

24 fect NK cell function in vivo in response to mouse cytomegalovirus infection.

25 ls are defective in protecting the host from mouse cytomegalovirus infection.

26 lso observed after Listeria monocytogenes or mouse cytomegalovirus infection.

27 or the expansion of Ly49H(+) NK cells during mouse cytomegalovirus infection.

28 The mouse cytomegalovirus M33 protein is highly homologous t

29 The mouse cytomegalovirus major immediate-early (IE) transcr

30 By screening a panel of deletion mutants of mouse cytomegalovirus (MCMV) a mutant was identified tha

31 infection by the double-stranded DNA viruses mouse cytomegalovirus (MCMV) and human adenovirus.

32 nce of the major immediate-early gene ie3 of mouse cytomegalovirus (MCMV) and that of the correspondi

33 Mouse cytomegalovirus (MCMV) and Toll-like receptor-medi

34 ies specificity and similar tropisms suggest mouse cytomegalovirus (mCMV) as a potential vector for t

35 daptive and innate immune cells critical for mouse cytomegalovirus (MCMV) clearance.

36 Mouse cytomegalovirus (MCMV) encodes an MHC-like protein

37 Mouse cytomegalovirus (MCMV) encodes two potential seven

38 ne, we selectively deleted 32 genes from the mouse cytomegalovirus (MCMV) genome.

39 The mouse cytomegalovirus (MCMV) immediate early 3 protein (

40 Transcription of mouse cytomegalovirus (MCMV) immediate early ie1 and ie3

41 We investigated the mouse cytomegalovirus (MCMV) immediate-early 1 protein (

42 49D receptor impacts the NK cell response to mouse cytomegalovirus (MCMV) infection by comparing the

43 is up-regulated in activated NK cells during mouse cytomegalovirus (MCMV) infection in response to si

44 During mouse cytomegalovirus (MCMV) infection, the first wave o

45 investigated how NOD NK cells respond after mouse cytomegalovirus (MCMV) infection, using NOD mice c

46 ygotes displayed increased susceptibility to mouse cytomegalovirus (MCMV) infection.

47 -18 stimulation and by mouse NK cells during mouse cytomegalovirus (MCMV) infection.

48 in expansion and memory cell formation after mouse cytomegalovirus (MCMV) infection.

49 sion to become long-lived memory cells after mouse cytomegalovirus (MCMV) infection; therefore, we ex

50 ller (NK) cell receptor Ly49H recognizes the mouse cytomegalovirus (MCMV) m157 glycoprotein expressed

51 ng NK cells in Nfil3(-/-) mice infected with mouse cytomegalovirus (MCMV) or recombinant viruses expr

52 ereas engagement of the AIM2 inflammasome by mouse cytomegalovirus (MCMV) or transfected double-stran

53 Mouse cytomegalovirus (MCMV) susceptibility often result

54 scovered the first two epitopes derived from mouse cytomegalovirus (MCMV) that are recognized by CD4

55 Mouse cytomegalovirus (MCMV), a beta-herpesvirus that es

56 focuses on genes required for resistance to mouse cytomegalovirus (MCMV), as identified through unbi

57 rs, including the Ly49H molecule recognizing mouse cytomegalovirus (MCMV), can stimulate NK cell expa

58 In infections with mouse cytomegalovirus (MCMV), MCMV-specific NK cells und

59 Ly49H binds with high affinity to a mouse cytomegalovirus (MCMV)-encoded glycoprotein, m157,

60 t have arisen from these recent studies: (i) mouse cytomegalovirus (MCMV)-induced memory; (ii) cytoki

61 Currently, no mouse cytomegalovirus (MCMV)-specific CD4 T cell respons

62 interleukin-12 (IL-12) is indispensible for mouse cytomegalovirus (MCMV)-specific NK cell expansion

63 V-7, than to another murine betaherpesvirus, mouse cytomegalovirus (MCMV).

64 While the possibility that mouse cytomegalovirus might replicate in human cells rai