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1 s to the understanding of the history of the Herpesvirales.
2 ily of Alloherpesviridae within the order of Herpesvirales.
3 shutoff phenotype is driven by the conserved herpesviral alkaline exonuclease, termed SOX in KSHV and
4                                The conserved herpesviral alkaline exonucleases play an important role
5 ill be needed to evaluate the performance of herpesviral and other persisting vectors for achieving l
6 o evaluate such hypothesis, we used over 600 Herpesvirales and 2000 Caudovirales complete genomes to
7                                              Herpesvirales are an ancient viral order that causes lif
8                                              Herpesviral capsids are assembled in the host cell nucle
9             Our data suggest that MxB senses herpesviral capsids, mediates their disassembly, and the
10 hey allowed to propose a core genome for the Herpesvirales, composed of 4 proteins, including the ATP
11 pproach yielded the first structure of gamma-herpesviral core NEC, namely the 1.56 angstrom structure
12 riking structural similarity to its a- and y-herpesviral counterparts despite apparent differences in
13 red a new viable target for the treatment of herpesviral diseases.
14 AS cooperate in a novel way to sense nuclear herpesviral DNA and initiate innate signaling.
15 ase (cGAS) have both been proposed to detect herpesviral DNA directly in herpes simplex virus (HSV)-i
16                     Proteins involved in the herpesviral DNA encapsidation process have become promis
17                                              Herpesviral DNA fragments isolated from AIDS-associated
18             Conventional nested PCR detected herpesviral DNA in brain tissue samples from two striped
19 te primers targeting a conserved region of a herpesviral DNA polymerase gene, a DNA fragment was ampl
20 uggest that consensus primer PCR targeted to herpesviral DNA polymerase may prove to be useful in the
21 r, exerts its antiviral effect by inhibiting herpesviral DNA polymerases through premature chain term
22  unreported amino acid-coding sequences from herpesviral DNA polymerases were obtained, including reg
23 rimer PCR method which amplifies a region of herpesviral DNA-directed DNA polymerase (EC 2.7.7.7) and
24                     However, targets for the herpesviral DUBs have remained elusive.
25 that all the pCD41 RNA species belong to the herpesviral early-late family.
26 herpesvirus responsible for oral lesions and herpesviral encephalitis.
27                                    The order Herpesvirales encompasses a wide variety of important an
28 equencing (RNA-seq) upon expression of these herpesviral endonucleases in order to characterize their
29                  We found that, unique among herpesviral gB proteins, the HCMV fusion factor has a Cy
30 ese studies reveal the existence of a unique herpesviral gene expression program corresponding to nei
31 ilencing of the viral genome and facilitates herpesviral gene expression.
32 dy reports that inefficient codon usage in a herpesviral gene is strikingly correlated with the inabi
33 ells in vivo and may be useful for designing herpesviral gene therapy vectors and attenuated viral va
34                 Nearly a decade ago, a novel herpesviral genome was discovered in KS biopsies, and si
35 eat sequences, which are commonly present in herpesviral genomes, to excise the BAC vector cassette.
36 ples and the initial characterization of new herpesviral genomes.
37         Cells treated with gB, but not other herpesviral glycoproteins, exhibited the same transcript
38                Finally, the morphogenesis of herpesviral growth in three-dimensional cultures reveals
39 ient cellular membrane fusion mechanism that Herpesvirales have hijacked or co-opted for capsid expor
40                                        gamma-Herpesviral immune evasion mechanisms are optimized to s
41 ecent progress in our understanding of gamma-herpesviral immune evasion strategies.
42 enotypes, and the presence of characteristic herpesviral inclusions in capillary endothelial cells at
43 rapeutic and prevention strategies to combat herpesviral infection and pathogenesis.
44 on is the first example of a consistent dual herpesviral infection in a human neoplasm and provides a
45  with EBV and likely play important roles in herpesviral infection in general.
46                                         Upon herpesviral infection of cells, the viral genome is chro
47                                              Herpesviral infection reflects thousands of years of coe
48                     Conclusions: First-onset herpesviral infection within 100 days after allogeneic h
49 s 1 (HSV-1) causes one of the most prevalent herpesviral infections in humans and is the leading etio
50                 During the 2-year follow-up, herpesviral infections were monitored clinically, by ser
51 argeted for therapeutic intervention against herpesviral infections.
52  present with atypical, recurrent, or severe herpesviral infections.
53 rotein complex, providing new ways to combat herpesviral infections.
54 ovel mode of regulation, and argue for a pro-herpesviral KAP1 function that ensures transition from t
55 er, we identified MHV68 ORF36, the conserved herpesviral kinase, as playing a key role in B2 inductio
56                         This is required for herpesviral late gene expression, a complex and poorly u
57                             Transcription of herpesviral late genes is stimulated after the onset of
58  (EBV) is a human tumor virus and a model of herpesviral latency.
59 ovides further insight into the functions of herpesviral miRNAs in virus-induced oncogenesis and late
60 nd divergent evolutionary mechanisms, varied herpesviral miRNAs share the ability to decrease IFN sig
61 osea skin lesions, respectively, compared to herpesviral mRNA positivity in only 13% normal skin and
62                                              Herpesviral mRNAs are produced and translated by cellula
63 itical details of the molecular mechanism of herpesviral NEC interactions and highlight their potenti
64 cificity and permissivity so far observed in herpesviral NEC interactions.
65  (VZV) is an alphaherpesvirus that lacks the herpesviral neurovirulence protein ICP34.5.
66 nteraction between vFLIP, a Kaposi's sarcoma herpesviral oncoprotein, and NEMO using small molecule s
67                                              Herpesviral ORF57 (Rhadinovirus) and ICP27 (Simplexvirus
68       We also present the structure of its B-herpesviral ortholog, revealing a striking structural si
69 transcription during latency for a member of Herpesvirales outside Herpesviridae.
70 based lymphoma cell line, produces infective herpesviral particles carrying a linear 270-kb genome th
71 ally could help us to interfere with MDV and herpesviral pathogenesis.
72                             The mechanism of herpesviral protease activation upon dimerization was st
73 ting to the tuned micromolar dissociation of herpesviral protease dimers.
74                                    As in all herpesviral proteases, the enzyme is active only as a we
75 V Pr is compared with the interface of other herpesviral proteases.
76 anged as in other structurally characterized herpesviral proteases.
77 tween the dimer interface and active site of herpesviral proteases.
78 and that this activity is conserved in other herpesviral protein kinase homologs.IMPORTANCE Viral inf
79 B2 SINEs, revealing a role for the conserved herpesviral protein kinase ORF36.
80 ce it has been reversed only by provision of herpesviral proteins, such as ICP0, not by alteration of
81 ork and function modal features of human and herpesviral proteins.
82  transplantation mouse model to test whether herpesviral reactivation after transplant causes organ i
83 triggers of latent viral infections, such as herpesviral reactivation and persistence in the host.
84                    Physiological triggers of herpesviral reactivation are poorly defined.
85                                 In the order Herpesvirales, RLFS were presented in all members wherea
86 , Abernathy et al. (2015) demonstrate that a herpesviral RNA endonuclease induces host transcriptiona
87 this question, we compared the effect of the herpesviral RNases on the human transcriptome and identi
88 als to reconstruct their shared history with herpesviral sags, revealing that the acquisition is a co
89 ers associated to these proteins grouped the Herpesvirales strains accordingly to the established fam
90 s setting, other appropriately targeted anti-herpesviral strategies may prove to be more effective.
91  Host & Microbe, Wu et al. (2015) discover a herpesviral strategy for inhibiting the prominent host s
92                                          The herpesviral terminase complex is part of the intricate m
93             We also find that the genomes of Herpesvirales that infect mollusks and fish encode CLCC1
94 hibition of the viral protease in developing herpesviral therapeutics.
95                Chromatin-based regulation of herpesviral transcriptional programs is increasingly app
96        These studies indicate that the lytic herpesviral transcriptome resembles a microcosm of the h
97 s have revealed that the complexity of lytic herpesviral transcriptomes is significantly greater than
98 cluding Smi1/Knr4, PGs2, FBXO3, SKIP16, Syd, herpesviral US22, IRS1 and TRS1, and their bacterial hom
99                                              Herpesviral virions contain a tegument layer that consis
100 mission electron microscopy failed to reveal herpesviral virions in pityriasis rosea lesional skin.