ライフサイエンスコーパス: visna

1 Unlike prototypical lentiviruses like visna and caprine arthritis-encephalitis viruses, which

2 an 23% sequence identity, the ectodomains in Visna and HIV-1 envelope glycoproteins show detailed str

3 scopy, we now visualize the functional maedi-visna lentivirus intasome at 4.9 angstrom resolution.

4 nt caprine arthritis-encephalitis (CAEV) and visna lentiviruses and the betaretroviruses Jaagsiekte s

5 tif in a 10-amino-acid sequence derived from visna leukemia virus results in wild-type release of vir

6 sive pneumonia virus (OPPV) in the U.S., and Visna/Maedi virus (VMV) elsewhere, these viruses reduce

7 A major route of transmission of Visna/maedi virus (VMV), an ovine lentivirus, is thought

8 ere synthesized, and the soluble core of the Visna membrane fusion protein was reconstituted in solut

9 the cells examined were susceptible to MuLV/visna pseudotype viruses, supporting the notion that the

10 rs not only in cells classically infected by visna virus (i.e., macrophages and microglia), but also

11 The small-ruminant lentiviruses ovine maedi-visna virus (MVV) and caprine arthritis-encephalitis vir

12 m bovine immunodeficiency virus (BIV), maedi-visna virus (MVV) and equine infectious anemia virus (EI

13 Lentiviruses such as Maedi Visna virus (MVV) in sheep, and human immunodeficiency v

14 Maedi-visna virus (MVV) is a natural pathogen of sheep with a

15 Maedi-visna virus (MVV) sequesters CypA as the noncanonical co

16 cofactor to stabilize the complex, the maedi-visna virus (MVV) Vif hijacks cyclophilin A (CypA) inste

17 Maedi-visna virus (MVV) Vif is similarly promiscuous, degradin

18 econstitution of the intasome from the maedi-visna virus (MVV), an ovine lentivirus, revealed a large

19 protein (SU) gp135 of the lentiviruses maedi-visna virus and caprine arthritis-encephalitis virus (CA

20 s activators of two nonprimate lentiviruses, visna virus and equine infectious anemia virus, revealed

21 s), ERK-1/2, in primary cells susceptible to visna virus and report that virus infection induces and

22 itive, biologically relevant system to study visna virus cell entry and envelope-receptor interaction

23 type viruses, supporting the notion that the visna virus cellular receptor is a widely expressed prot

24 Based on those results, additional HIV-1/visna virus chimeric integrases were designed and purifi

25 alpha- and gamma-retroviruses, and the maedi visna virus dimer linkage region is capable of forming h

26 virus (MuLV) particles pseudotyped with the visna virus envelope glycoprotein and encoding a green f

27 re obtained when the cytoplasmic tail of the visna virus envelope TM protein was truncated to 3, 7, o

28 tative receptor binding site in the CAEV and visna virus gp135.

29 s of human immunodeficiency virus type 1 and visna virus guided the quantitative testing of oligonucl

30 Maedi-Visna virus infection in sheep, which targets these cell

31 an immunodeficiency virus type 1 (HIV-1) and visna virus integrase (IN) proteins.

32 substitutions at the analogous positions in visna virus integrase and Rous sarcoma virus integrase c

33 The activity of visna virus integrase was more dependent on the identity

34 d for efficient viral transcription from the visna virus long terminal repeat (LTR).

35 AP-1 sites within the visna virus LTR, which can be bound by the cellular tran

36 In transient-transfection assays using visna virus LTR-CAT as a reporter construct, the activit

37 th Fos and/or Jun bound to AP-1 sites in the visna virus LTR.

38 MuLV/visna virus particles were used to transduce a panel of

39 Once targeted to the visna virus promoter, the Tat protein could then interac

40 n interactions with cellular proteins at the visna virus promoter, we used an in vitro protein affini

41 We produced human MPO-Tg mice with use of a Visna virus promoter.

42 The production of functional MuLV/visna virus pseudotypes has provided a sensitive, biolog

43 Functional MuLV/visna virus pseudotypes were obtained when the cytoplasm

44 ter as a tool to study the expression of the visna virus receptor.

45 inhibitor of the ERK/MAPK pathway, abolishes visna virus replication, as evidenced by extremely low l

46 cells not considered to be major targets of visna virus replication, suggesting that activation of t

47 at proximal to the viral TATA box, where the visna virus Tat activation domain could contact TBP to a

48 reviously described by our laboratory as the visna virus Tat activation domain.

49 Thus, the visna virus Tat protein appears to target AP-1 sites in

50 A potential mechanism by which the visna virus Tat protein could target the viral promoter

51 The visna virus Tat protein is a strong transcriptional acti

52 The visna virus Tat protein is required for efficient viral

53 n in vivo two-hybrid assay, to show that the visna virus Tat protein specifically interacts with the

54 The visna virus Tat protein was also able to interact with c

55 ike other lentiviral transactivators such as visna virus Tat, is unable to transactivate from minimal

56 from human immunodeficiency virus type 1 and visna virus were able to substitute for the EIAV slipper

57 unodeficiency virus, Jembrana disease virus, visna virus, and caprine arthritis encephalitis virus.

58 ases of human immunodeficiency virus type 1, visna virus, and Rous sarcoma virus exhibited different

59 ns of human immuno- deficiency virus type 1, visna virus, and Rous sarcoma virus exhibited distinct p

60 In addition, although visna virus-induced activation of MAPK is detectable wit

61 of ERK-1/2 activation in brains derived from visna virus-infected sheep demonstrates a strong correla

62 er region of the prototype lentivirus, maedi visna virus.

63 egions in the membrane fusion protein of the Visna virus.