ライフサイエンスコーパス: EAV

1 EAV genomes amplified from the semen of these two stalli

2 e have demonstrated that EqCXCL16 acts as an EAV entry receptor in EAV-susceptible cells, equine mono

3 ddress these possibilities, we have analyzed EAV and ALV particles in a measles virus vaccine equival

4 PCR analysis of ALV and EAV proviral sequences in peripheral blood mononuclear c

5 In contrast, both ALV-E and EAV particle-associated RNA were detected at equivalent

6 ufacturer and confirm the presence of RT and EAV RNA.

7 Similar to other arteriviruses, EAV primarily targets cells of the monocyte/macrophage l

8 st, the present study demonstrates that both EAV and PRRSV nsp4 cleave NEMO at multiple sites and tha

9 eaving NEMO is a common strategy utilized by EAV and PRRSV nsp4 to antagonize IFN induction, EAV nsp4

10 manufacturers all have particles containing EAV genomes and various levels of defective or nondefect

11 We managed to predictably demonstrate EAV spread by droplets because of USS action.

12 This is the first study that describes EAV full-length genomic evolution during acute and long-

13 E-based Western blot assay or had detectable EAV or ALV-E RNA sequences by RT-PCR.

14 The various ORFs of the dominant EAV variants evolved independently, and there was appare

15 Identification of the cellular receptors for EAV may provide insights to design antivirals and better

16 ight different NEMO fragments resulting from EAV or PRRSV nsp4 scission to induce IFN-beta production

17 n the stallion reproductive tract.IMPORTANCE EAV can persist in the reproductive tract of infected st

18 er, the host-specified molecules involved in EAV binding and entry into monocytes/macrophages have no

19 at EqCXCL16 acts as an EAV entry receptor in EAV-susceptible cells, equine monocytes.

20 orm of EqCXCL16 likely plays a major role in EAV host cell entry processes, possibly acting as a prim

21 and PRRSV nsp4 to antagonize IFN induction, EAV nsp4 adopts a more complex substrate recognition mec

22 mentally infected and two naturally infected EAV carrier stallions were deep sequenced to elucidate t

23 lly demonstrate that the ampulla is the main EAV tissue reservoir rather than immunologically privile

24 rodimer developed antibodies that neutralize EAV.

25 h both antiviral agents used as coolants, no EAV-associated RK-13 cell infection was found.

26 imulated by heterotypic nsp1betas of all non-EAV arteriviruses tested.

27 ionarily conserved mechanism employed in non-EAV/-WPDV arteriviruses for the expression of additional

28 The results show the absence of EAV and ALV integrants in DNA prepared from MVVE-inocula

29 envelope proteins that affect the binding of EAV to different cell receptors on CD3(+) T lymphocytes

30 of infected stallions can become carriers of EAV and continue to shed virus in the semen.

31 ovel substrate recognition characteristic of EAV nsp4.

32 major challenge for the worldwide control of EAV is that this virus has the distinctive ability to es

33 esses the known neutralizing determinants of EAV.

34 ntal mechanisms associated with the entry of EAV into susceptible cells.

35 ovel insight into the intrahost evolution of EAV during acute and persistent infection and demonstrat

36 A distinctive feature of EAV infection is that it establishes long-term persisten

37 ing potential consequences of integration of EAV and ALV sequences in human DNA, which may result fro

38 insight into the evolutionary mechanisms of EAV and identified critical regions of the viral genome

39 In summary, an in vitro model of EAV persistence in cell culture was established for the

40 Overall, the nonstochastic nature of EAV evolution during persistent infection was driven by

41 F5 and ORF6 (which encodes the M protein) of EAV were cloned into two different VEE replicon vectors

42 have been implicated as the primary sites of EAV persistence, the viral host cell tropism and whether

43 es are infected with the virulent strains of EAV.

44 tification of tissue and cellular tropism of EAV is critical for understanding the molecular basis of

45 do not support transmission of either ALV or EAV to recipients of the U.S.-made vaccine and provide r

46 sence of evidence of infection with ALV-E or EAV in 43 YF vaccine recipients suggests low risks for t

47 Persistent EAV infection is associated with moderate, multifocal ly

48 s exerted on the V1 region during persistent EAV infection led to the emergence of virus variants wit

49 with far-Western blotting, gradient-purified EAV particles were shown to bind directly to the EqCXCL1

50 tribute value with classes and relationship (EAV/CR), which supports the SenseLab project as a whole.

51 that the EV and endogenous avian retroviral (EAV) genes were methylated in both the SL and BL subline

52 particles, the endogenous avian retrovirus (EAV) and the endogenous avian leukosis virus (ALV-E), wh

53 cles containing endogenous avian retrovirus (EAV-0) RNA and originates from the chicken embryonic fib

54 rvoir of the virus as they continuously shed EAV in their semen.

55 In these stallions, EAV is detectable only in the reproductive tract, and vi

56 ntral Kentucky subsequently became long-term EAV carriers.

57 Furthermore, we demonstrate that EAV has specific tropism for stromal cells (fibrocytes a

58 Here, we demonstrated that EAV nsp4 also inhibited virus-induced IFN-beta productio

59 Finally, the results demonstrated that EAV preferentially infects subpopulations of horse CD14(

60 Moreover, we reveal that EAV nsp4 also cleaves NEMO at glutamine 205 (Q205), whic

61 Altogether, our findings suggest that EAV and PRRSV nsp4 cleave NEMO at multiple sites and tha

62 This study suggests that EAV employs complex immune evasion mechanisms that warra

63 With saline coolant, the EAV-induced cytopathic effect on RK13 cells was found up

64 nificantly enhances our understanding of the EAV carrier state in stallions by unequivocally identify

65 The major variants of the EAV population that sequentially arose within the reprod

66 Thus, evolution of the EAV quasispecies that occurs during persistent infection

67 em from one database to another based on the EAV representation of the basic database objects.

68 Therefore, EAV persistence provides a powerful new natural animal m

69 sceptibility of equine CD3+ T lymphocytes to EAV infection have a genetic basis.

70 tibility/resistance of CD3+ T lymphocytes to EAV infection.

71 portion of the cell population permissive to EAV infection from <3% to almost 100%.

72 been changed from traditional relational to EAV/CR (Entity-Attribute-Value with Classes and Relation

73 lly simple model-the entity-attribute-value (EAV) model-to describe uniformly metadata relating to in

74 The binding of biotinylated virulent EAV strain Bucyrus at 4 degrees C was significantly high

75 Equine arteritis virus (EAV) and porcine reproductive and respiratory syndrome v

76 arteriviruses except equine arteritis virus (EAV) and wobbly possum disease virus (WPDV).

77 me virus (PRRSV) and equine arteritis virus (EAV) are economically important veterinary pathogens.

78 nt and suspension of Equine Arteritis Virus (EAV) delivered to the USS tip.

79 cyrus (VB) strain of equine arteritis virus (EAV) established persistent infection in high-passage-nu

80 Equine arteritis virus (EAV) has a global impact on the equine industry as the c

81 (+) T lymphocytes to equine arteritis virus (EAV) infection and establishment of persistent infection

82 Equine arteritis virus (EAV) is the causative agent of equine viral arteritis (E

83 cyrus (VB) strain of equine arteritis virus (EAV) to produce the modified live virus (MLV) vaccine st

84 natural reservoir of equine arteritis virus (EAV), as venereal infection of mares frequently occurs a

85 eins (G(L) and M) of equine arteritis virus (EAV), both individually and in heterodimer form (G(L)/M)

86 l entry receptor for equine arteritis virus (EAV).

87 cells infected with equine arteritis virus (EAV).

88 (E51) of the ancient endogenous avian virus (EAV) family of proviruses or that appear unique to subgr

89 nging to the ancient endogenous avian virus (EAV) family or to the avian sarcoma-leukosis virus (ALV)

90 iruses (ALV-E) and endogenous avian viruses (EAV).

91 phocyte susceptibility phenotype to in vitro EAV infection may be at higher risk of becoming carriers

92 cation-defective particles or infection with EAV and ALV pseudotypes bearing measles virus envelopes.