ライフサイエンスコーパス: herpesviral

1 ily of Alloherpesviridae within the order of Herpesvirales.

2 shutoff phenotype is driven by the conserved herpesviral alkaline exonuclease, termed SOX in KSHV and

3 ill be needed to evaluate the performance of herpesviral and other persisting vectors for achieving l

4 Herpesviral capsids are assembled in the host cell nucle

5 red a new viable target for the treatment of herpesviral diseases.

6 AS cooperate in a novel way to sense nuclear herpesviral DNA and initiate innate signaling.

7 ase (cGAS) have both been proposed to detect herpesviral DNA directly in herpes simplex virus (HSV)-i

8 Proteins involved in the herpesviral DNA encapsidation process have become promis

9 Herpesviral DNA fragments isolated from AIDS-associated

10 Conventional nested PCR detected herpesviral DNA in brain tissue samples from two striped

11 te primers targeting a conserved region of a herpesviral DNA polymerase gene, a DNA fragment was ampl

12 uggest that consensus primer PCR targeted to herpesviral DNA polymerase may prove to be useful in the

13 r, exerts its antiviral effect by inhibiting herpesviral DNA polymerases through premature chain term

14 unreported amino acid-coding sequences from herpesviral DNA polymerases were obtained, including reg

15 rimer PCR method which amplifies a region of herpesviral DNA-directed DNA polymerase (EC 2.7.7.7) and

16 However, targets for the herpesviral DUBs have remained elusive.

17 that all the pCD41 RNA species belong to the herpesviral early-late family.

18 We found that, unique among herpesviral gB proteins, the HCMV fusion factor has a Cy

19 ese studies reveal the existence of a unique herpesviral gene expression program corresponding to nei

20 dy reports that inefficient codon usage in a herpesviral gene is strikingly correlated with the inabi

21 ells in vivo and may be useful for designing herpesviral gene therapy vectors and attenuated viral va

22 Nearly a decade ago, a novel herpesviral genome was discovered in KS biopsies, and si

23 eat sequences, which are commonly present in herpesviral genomes, to excise the BAC vector cassette.

24 ples and the initial characterization of new herpesviral genomes.

25 Cells treated with gB, but not other herpesviral glycoproteins, exhibited the same transcript

26 Finally, the morphogenesis of herpesviral growth in three-dimensional cultures reveals

27 gamma-Herpesviral immune evasion mechanisms are optimized to s

28 ecent progress in our understanding of gamma-herpesviral immune evasion strategies.

29 enotypes, and the presence of characteristic herpesviral inclusions in capillary endothelial cells at

30 rapeutic and prevention strategies to combat herpesviral infection and pathogenesis.

31 on is the first example of a consistent dual herpesviral infection in a human neoplasm and provides a

32 with EBV and likely play important roles in herpesviral infection in general.

33 Upon herpesviral infection of cells, the viral genome is chro

34 s 1 (HSV-1) causes one of the most prevalent herpesviral infections in humans and is the leading etio

35 During the 2-year follow-up, herpesviral infections were monitored clinically, by ser

36 rotein complex, providing new ways to combat herpesviral infections.

37 This is required for herpesviral late gene expression, a complex and poorly u

38 Transcription of herpesviral late genes is stimulated after the onset of

39 ovides further insight into the functions of herpesviral miRNAs in virus-induced oncogenesis and late

40 nd divergent evolutionary mechanisms, varied herpesviral miRNAs share the ability to decrease IFN sig

41 osea skin lesions, respectively, compared to herpesviral mRNA positivity in only 13% normal skin and

42 Herpesviral mRNAs are produced and translated by cellula

43 Herpesviral ORF57 (Rhadinovirus) and ICP27 (Simplexvirus

44 transcription during latency for a member of Herpesvirales outside Herpesviridae.

45 based lymphoma cell line, produces infective herpesviral particles carrying a linear 270-kb genome th

46 ally could help us to interfere with MDV and herpesviral pathogenesis.

47 The mechanism of herpesviral protease activation upon dimerization was st

48 ting to the tuned micromolar dissociation of herpesviral protease dimers.

49 As in all herpesviral proteases, the enzyme is active only as a we

50 V Pr is compared with the interface of other herpesviral proteases.

51 anged as in other structurally characterized herpesviral proteases.

52 tween the dimer interface and active site of herpesviral proteases.

53 ce it has been reversed only by provision of herpesviral proteins, such as ICP0, not by alteration of

54 triggers of latent viral infections, such as herpesviral reactivation and persistence in the host.

55 Physiological triggers of herpesviral reactivation are poorly defined.

56 , Abernathy et al. (2015) demonstrate that a herpesviral RNA endonuclease induces host transcriptiona

57 als to reconstruct their shared history with herpesviral sags, revealing that the acquisition is a co

58 s setting, other appropriately targeted anti-herpesviral strategies may prove to be more effective.

59 Host & Microbe, Wu et al. (2015) discover a herpesviral strategy for inhibiting the prominent host s

60 The herpesviral terminase complex is part of the intricate m

61 hibition of the viral protease in developing herpesviral therapeutics.

62 Chromatin-based regulation of herpesviral transcriptional programs is increasingly app

63 These studies indicate that the lytic herpesviral transcriptome resembles a microcosm of the h

64 s have revealed that the complexity of lytic herpesviral transcriptomes is significantly greater than

65 cluding Smi1/Knr4, PGs2, FBXO3, SKIP16, Syd, herpesviral US22, IRS1 and TRS1, and their bacterial hom

66 Herpesviral virions contain a tegument layer that consis

67 mission electron microscopy failed to reveal herpesviral virions in pityriasis rosea lesional skin.