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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  manufacturers all have particles containing EAV genomes and various levels of defective or nondefect
9 E-based Western blot assay or had detectable EAV or ALV-E RNA sequences by RT-PCR.
10             The various ORFs of the dominant EAV variants evolved independently, and there was appare
11 Identification of the cellular receptors for EAV may provide insights to design antivirals and better
12 er, the host-specified molecules involved in EAV binding and entry into monocytes/macrophages have no
13 at EqCXCL16 acts as an EAV entry receptor in EAV-susceptible cells, equine monocytes.
14 orm of EqCXCL16 likely plays a major role in EAV host cell entry processes, possibly acting as a prim
15 lly demonstrate that the ampulla is the main EAV tissue reservoir rather than immunologically privile
16 rodimer developed antibodies that neutralize EAV.
17              The results show the absence of EAV and ALV integrants in DNA prepared from MVVE-inocula
18 envelope proteins that affect the binding of EAV to different cell receptors on CD3(+) T lymphocytes
19 major challenge for the worldwide control of EAV is that this virus has the distinctive ability to es
20 esses the known neutralizing determinants of EAV.
21 ntal mechanisms associated with the entry of EAV into susceptible cells.
22                     A distinctive feature of EAV infection is that it establishes long-term persisten
23 ing potential consequences of integration of EAV and ALV sequences in human DNA, which may result fro
24             In summary, an in vitro model of EAV persistence in cell culture was established for the
25 F5 and ORF6 (which encodes the M protein) of EAV were cloned into two different VEE replicon vectors
26 have been implicated as the primary sites of EAV persistence, the viral host cell tropism and whether
27 es are infected with the virulent strains of EAV.
28 tification of tissue and cellular tropism of EAV is critical for understanding the molecular basis of
29 do not support transmission of either ALV or EAV to recipients of the U.S.-made vaccine and provide r
30 sence of evidence of infection with ALV-E or EAV in 43 YF vaccine recipients suggests low risks for t
31                                   Persistent EAV infection is associated with moderate, multifocal ly
32 s exerted on the V1 region during persistent EAV infection led to the emergence of virus variants wit
33 with far-Western blotting, gradient-purified EAV particles were shown to bind directly to the EqCXCL1
34 tribute value with classes and relationship (EAV/CR), which supports the SenseLab project as a whole.
35 that the EV and endogenous avian retroviral (EAV) genes were methylated in both the SL and BL subline
36  particles, the endogenous avian retrovirus (EAV) and the endogenous avian leukosis virus (ALV-E), wh
37 cles containing endogenous avian retrovirus (EAV-0) RNA and originates from the chicken embryonic fib
38 rvoir of the virus as they continuously shed EAV in their semen.
39                          In these stallions, EAV is detectable only in the reproductive tract, and vi
40 ntral Kentucky subsequently became long-term EAV carriers.
41             Furthermore, we demonstrate that EAV has specific tropism for stromal cells (fibrocytes a
42       Finally, the results demonstrated that EAV preferentially infects subpopulations of horse CD14(
43                     This study suggests that EAV employs complex immune evasion mechanisms that warra
44 nificantly enhances our understanding of the EAV carrier state in stallions by unequivocally identify
45                    The major variants of the EAV population that sequentially arose within the reprod
46                       Thus, evolution of the EAV quasispecies that occurs during persistent infection
47 em from one database to another based on the EAV representation of the basic database objects.
48                                   Therefore, EAV persistence provides a powerful new natural animal m
49 sceptibility of equine CD3+ T lymphocytes to EAV infection have a genetic basis.
50 tibility/resistance of CD3+ T lymphocytes to EAV infection.
51 portion of the cell population permissive to EAV infection from <3% to almost 100%.
52  been changed from traditional relational to EAV/CR (Entity-Attribute-Value with Classes and Relation
53 lly simple model-the entity-attribute-value (EAV) model-to describe uniformly metadata relating to in
54         The binding of biotinylated virulent EAV strain Bucyrus at 4 degrees C was significantly high
55 cyrus (VB) strain of equine arteritis virus (EAV) established persistent infection in high-passage-nu
56                      Equine arteritis virus (EAV) has a global impact on the equine industry as the c
57 (+) T lymphocytes to equine arteritis virus (EAV) infection and establishment of persistent infection
58 cyrus (VB) strain of equine arteritis virus (EAV) to produce the modified live virus (MLV) vaccine st
59 natural reservoir of equine arteritis virus (EAV), as venereal infection of mares frequently occurs a
60 eins (G(L) and M) of equine arteritis virus (EAV), both individually and in heterodimer form (G(L)/M)
61 l entry receptor for equine arteritis virus (EAV).
62  cells infected with equine arteritis virus (EAV).
63 (E51) of the ancient endogenous avian virus (EAV) family of proviruses or that appear unique to subgr
64 nging to the ancient endogenous avian virus (EAV) family or to the avian sarcoma-leukosis virus (ALV)
65 iruses (ALV-E) and endogenous avian viruses (EAV).
66 phocyte susceptibility phenotype to in vitro EAV infection may be at higher risk of becoming carriers
67 cation-defective particles or infection with EAV and ALV pseudotypes bearing measles virus envelopes.

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