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1 egions in the membrane fusion protein of the Visna virus.
2 er region of the prototype lentivirus, maedi visna virus.
3 protein (SU) gp135 of the lentiviruses maedi-visna virus and caprine arthritis-encephalitis virus (CA
4 s activators of two nonprimate lentiviruses, visna virus and equine infectious anemia virus, revealed
5 s), ERK-1/2, in primary cells susceptible to visna virus and report that virus infection induces and
6 unodeficiency virus, Jembrana disease virus, visna virus, and caprine arthritis encephalitis virus.
7 ases of human immunodeficiency virus type 1, visna virus, and Rous sarcoma virus exhibited different
8 ns of human immuno- deficiency virus type 1, visna virus, and Rous sarcoma virus exhibited distinct p
9 itive, biologically relevant system to study visna virus cell entry and envelope-receptor interaction
10 type viruses, supporting the notion that the visna virus cellular receptor is a widely expressed prot
11     Based on those results, additional HIV-1/visna virus chimeric integrases were designed and purifi
12 alpha- and gamma-retroviruses, and the maedi visna virus dimer linkage region is capable of forming h
13  virus (MuLV) particles pseudotyped with the visna virus envelope glycoprotein and encoding a green f
14 re obtained when the cytoplasmic tail of the visna virus envelope TM protein was truncated to 3, 7, o
15 s of human immunodeficiency virus type 1 and visna virus guided the quantitative testing of oligonucl
16 rs not only in cells classically infected by visna virus (i.e., macrophages and microglia), but also
17                        In addition, although visna virus-induced activation of MAPK is detectable wit
18 of ERK-1/2 activation in brains derived from visna virus-infected sheep demonstrates a strong correla
19                                        Maedi-Visna virus infection in sheep, which targets these cell
20 an immunodeficiency virus type 1 (HIV-1) and visna virus integrase (IN) proteins.
21  substitutions at the analogous positions in visna virus integrase and Rous sarcoma virus integrase c
22                              The activity of visna virus integrase was more dependent on the identity
23 d for efficient viral transcription from the visna virus long terminal repeat (LTR).
24                        AP-1 sites within the visna virus LTR, which can be bound by the cellular tran
25       In transient-transfection assays using visna virus LTR-CAT as a reporter construct, the activit
26 th Fos and/or Jun bound to AP-1 sites in the visna virus LTR.
27  The small-ruminant lentiviruses ovine maedi-visna virus (MVV) and caprine arthritis-encephalitis vir
28 m bovine immunodeficiency virus (BIV), maedi-visna virus (MVV) and equine infectious anemia virus (EI
29                   Lentiviruses such as Maedi Visna virus (MVV) in sheep, and human immunodeficiency v
30                                        Maedi-visna virus (MVV) is a natural pathogen of sheep with a
31                                        Maedi-visna virus (MVV) Vif is similarly promiscuous, degradin
32                                         MuLV/visna virus particles were used to transduce a panel of
33                         Once targeted to the visna virus promoter, the Tat protein could then interac
34 n interactions with cellular proteins at the visna virus promoter, we used an in vitro protein affini
35  We produced human MPO-Tg mice with use of a Visna virus promoter.
36            The production of functional MuLV/visna virus pseudotypes has provided a sensitive, biolog
37                              Functional MuLV/visna virus pseudotypes were obtained when the cytoplasm
38 ter as a tool to study the expression of the visna virus receptor.
39 inhibitor of the ERK/MAPK pathway, abolishes visna virus replication, as evidenced by extremely low l
40  cells not considered to be major targets of visna virus replication, suggesting that activation of t
41 at proximal to the viral TATA box, where the visna virus Tat activation domain could contact TBP to a
42 reviously described by our laboratory as the visna virus Tat activation domain.
43                                    Thus, the visna virus Tat protein appears to target AP-1 sites in
44           A potential mechanism by which the visna virus Tat protein could target the viral promoter
45                                          The visna virus Tat protein is a strong transcriptional acti
46                                          The visna virus Tat protein is required for efficient viral
47 n in vivo two-hybrid assay, to show that the visna virus Tat protein specifically interacts with the
48                                          The visna virus Tat protein was also able to interact with c
49 ike other lentiviral transactivators such as visna virus Tat, is unable to transactivate from minimal
50 from human immunodeficiency virus type 1 and visna virus were able to substitute for the EIAV slipper

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