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1 ls of exceptional stability that protect the viral genome.
2 lution at multiple loci dispersed across the viral genome.
3 acers) that target specific sequences in the viral genome.
4 ult in A3G signature G-to-A mutations in the viral genome.
5 ore efficiently transcribe and replicate the viral genome.
6 tein and a deletion within the 3'-UTR of the viral genome.
7 to form the convex shell that surrounds the viral genome.
8 L1 at the terminal repeat (TR) region of the viral genome.
9 ulence associated with rearrangements of the viral genome.
10 ds in the terminal repeat (TR) region of the viral genome.
11 d transcriptional output from the integrated viral genome.
12 pecifically to the 3' untranslated region of viral genome.
13 d to a reduced nucleosome positioning on the viral genome.
14 The primary role of capsid is to package the viral genome.
15 logenetic classification based on the entire viral genome.
16 sible because of the segmented nature of the viral genome.
17 vide a stable, genetically defined source of viral genome.
18 that encase the double-stranded DNA (dsDNA) viral genome.
19 functions and requires interaction with the viral genome.
20 by the first open reading frame (ORF) of the viral genome.
21 mal membrane, and permits the release of the viral genome.
22 em for UUKV that permits manipulation of the viral genome.
23 izes stem-loop sequences engineered into the viral genome.
24 n exonuclease-inactivating mutation into the viral genome.
25 y of a complex that is able to replicate the viral genome.
26 ognizes a poly-uridine/cytosine motif in the viral genome.
27 irus-like particle that does not contain the viral genome.
28 ecognition because of characteristics of the viral genome.
29 G2 phase is independent of the nature of the viral genome.
30 activity of cellular enzymes that mutate the viral genome.
31 ies, whose codons are overrepresented in the viral genome.
32 CTCF peaks relative to the Ser5P form in the viral genome.
33 hich are noninfectious because they lack the viral genome.
34 role during the strategic mutagenesis of the viral genome.
35 II and preventing silenced chromatin on the viral genome.
36 as found in the 2C/3A junction region of the viral genome.
37 some L1 protein remains associated with the viral genome.
38 to efficiently replicate and transcribe the viral genome.
39 L1, from the minor capsid protein L2 and the viral genome.
40 e reconstruction across large regions of the viral genome.
41 r model of infection, and sequenced the full viral genomes.
42 e-specific integration and excision of their viral genomes.
43 recapitulating RSE-mediated recoding within viral genomes.
44 nes may be important modulators of infecting viral genomes.
45 ber of CD4(+) T cells that harbor infectious viral genomes.
46 e decoding of mobile chromosomal element and viral genomes.
47 HPV) through epigenetic modifications of the viral genomes.
48 opulations of both viral particles and naked viral genomes.
49 recombination is an important factor shaping viral genomes.
50 cted cell lines containing highly methylated viral genomes.
51 offers direct and experimental annotation of viral genomes.
52 ion whereas other designs create chimeras of viral genomes.
53 nome similar to vAc(P35), while in the other viral genome, a 24.4 kbp-fragment containing 10 essentia
54 RNA replication observed for the 5'-deleted viral genomes-a less stable ribonucleoprotein complex fo
55 , we identified 10 complete or near complete viral genomes allowing, for the first time, an assessmen
56 addition, neutralization of IL-8 diminished viral genome amplification in differentiating HPV-positi
58 It inhibits reverse transcription of the viral genome and can also synthesize unanchored polyubiq
60 s, VP35, is essential for replication of the viral genome and for evasion of host immune responses.
62 ultifunctional protein that encapsidates the viral genome and functions as an adapter between the vir
66 SPR/Cas9 system disrupts latently integrated viral genome and provides long-term adaptive defense aga
68 iced viral RNA transcripts, which encode the viral genome and the genes encoding viral structural pro
72 rocess ensures rapid copying of the parental viral genome and will enable protein factors involved in
73 RE11-RAD50-NBS1 (MRN) DSB-sensing complex to viral genomes and activation of the ATM kinase can promo
75 ries to search for the presence of all known viral genomes and discover human T-lymphotropic virus 1
76 the history of virus dispersal from sampled viral genomes and infer the locations of ancestral infec
77 onal HSV-2 low-passage-number and laboratory viral genomes and initiated analysis of the genetic dive
80 nome synthesis, methylation of the 5'-cap of viral genome, and polyprotein processing among other act
81 on of Tax, which drives transcription of the viral genome, and Rex, which favors expression of incomp
82 ed with antiviral signaling, the presence of viral genome, and the absence of HSV protein expression
83 ral protein expression, encapsidation of the viral genome, and the release of mature virions were imp
86 escent infection resembling latency in which viral genomes are retained in a low number of neurons, v
87 , is critical for function, probably to wrap viral genome around the ring during packaging initiation
88 DNA to the host cell nucleus to maintain the viral genome as nuclear episomes, which are the basis fo
89 pparently coats but does not encapsidate the viral genome as visualized by atomic force microscopy.
90 viruses observed, suggesting that both core viral genomes as well as viral community structure were
91 sid proteins and secondary structures in the viral genome, as exemplified by the RNA bacteriophage MS
92 anism by which the viral core containing the viral genome associates with dynein and induces its peri
97 SET also allows ATM to localize to incoming viral genomes bound by protein VII during infection with
98 ced approximately 80% of the backbone of the viral genome, built atomic models for 16 RNA stem-loops,
99 orm this shell must be stable to protect the viral genome but also sufficiently flexible to disassemb
100 isolated HPAI H5N1 viruses that had similar viral genomes but differed substantially in their lethal
101 t a DNA damage response (DDR) is directed to viral genomes but is distinct from the response to cellu
102 infection, KAP1 is still associated with the viral genome, but its heterochromatin-inducing activity
103 not in cDCs, indicating that sensing of the viral genome by pDCs activates cDCs in trans to cross-pr
104 cological reagents, specific mutation in the viral genome by reverse genetics and confocal microscopy
105 Using differential staining of an incoming viral genome by small molecular dyes in selectively perm
107 ane perturbation and recognition of incoming viral genomes by cytosolic nucleic acid receptors are re
109 ich the structure, function, and fate of the viral genome can be modulated by the transcriptionally c
111 se results, the alanine substitutions in the viral genome caused exaggerated syncytium formation, red
116 70.8-kb circular double-stranded DNA (dsDNA) viral genome content, and identification of its cellular
118 eveloped markedly larger lesions with higher viral genome copies in skin than did wild-type mice.
120 n human neurons than in MRC-5 cells, and the viral genome copy number-to-PFU ratio for VZV in human n
122 for amplification of two large fragments of viral genome covering about 80% of the unique HIV-1 geno
123 DNA), which is a stable episomal form of the viral genome decorated with host histones and nonhistone
124 Here we provide evidence that the incoming viral genome dissociates from the TGN and associates wit
125 separation of reverse transcriptase from the viral genome during early steps of infection.IMPORTANCE
127 ssures exist to maintain the fidelity of the viral genome during repeated reactivations from its late
129 therwise acute viruses.Replication defective viral genomes (DVGs) can facilitate persistence of param
133 s recruited to nuclear sites associated with viral genome entry in a SIM-dependent manner, consistent
136 H motifs enables specific recognition of the viral genome for initiation of DNA packaging during viru
138 ified infectious virus for up to 185 dpi and viral genomes for up to 400 dpi in lymphoid tissues of t
139 nces of integration for the evolution of the viral genome, for the telomere, and for the risk of dise
142 a of (i) archaeal, bacterial, eukaryotic and viral genomes from cultured organisms, (ii) single cell
143 rotein that is suggested to protect incoming viral genomes from detection by the cellular DNA damage
144 on multiplex PCR for targeted enrichment of viral genomes from samples containing as few as 50 genom
145 equences in their respective donors and that viral genomes generally evolved early in infection accor
147 to suppress viral gene expression after the viral genome has integrated into the host cell genome, w
148 and breaks (DSBs) targeted to the integrated viral genome have been shown to decrease production of p
150 icular, the protein containers encapsulating viral genomes have been determined to high resolution us
154 been linked to reverse transcription of the viral genome in target cells, the mechanism by which unc
158 e proteins can accumulate on or close to the viral genomes in a sequential manner which may lead to t
159 and suggests that the exchange of RNA among viral genomes in an infected host occurs in multiple loc
161 n of PML NB proteins, which are recruited to viral genomes in order to repress viral transcription.
163 the MRN complex consistently colocalize with viral genomes in replication compartments (RCs), whereas
164 ent targeting results in a sharp increase of viral genomes in the host cell when the target is locate
165 sviruses 6A/B (HHV-6A/B) can integrate their viral genomes in the telomeres of human chromosomes.
166 r sites [serine (S)220 and S239] in the full viral genome increase LT levels and promote MCV virion p
167 tion of nucleotide substitution rates in the viral genome indicated an increase in the frequency of t
169 s the recruitment process, the newly formed, viral-genome-induced PML NB-like foci can fuse with exis
171 ion of the minor capsid protein, L2, and the viral genome instead of trafficking into the nucleus.
172 n of complex genomic rearrangements, such as viral genome integration, in paired-end sequence data.
175 e intricate machinery that delivers a single viral genome into empty preformed capsids (encapsidation
178 g the virus to an F-pilus and delivering the viral genome into the host during infection, but how the
179 retroviruses must direct the movement of the viral genome into the nucleus to complete their replicat
186 Terminal deletions at the 5' end of the viral genome involving an RNA secondary structure requir
187 to naive cells, it is not clear whether the viral genome is also transferred via this mechanism and
188 transcriptional activity across most of the viral genome is associated with high viral loads in infe
193 us infection, a histone-free DNA copy of the viral genome is synthesized that must be loaded with nuc
198 pon viral injection, a small sequence of the viral genome, known as a spacer, is integrated into the
200 the structural and functional features of a viral genome maturation complex, an essential intermedia
210 icate within the lungs or generate defective viral genomes or to differences in levels of costimulato
212 ed in this paper reveals a new mechanism for viral genome packaging and will provide a tractable syst
214 ein controls replication, transcription, and viral genome partitioning during the viral infectious li
215 proteins expressed from the L4 region of the viral genome perform essential roles in moving the infec
216 of B cells is predominantly latent, with the viral genome persisting as a multicopy episome and expre
218 A packaging signals mapping along the entire viral genome" play the critical role in poliovirus packa
219 C3H preferentially binds to sequences in the viral genome predicted to contain duplexes, a property t
220 either the reverse transcription step of the viral genome prior to HK2 viral particle formation and/o
221 miRNAs, the interactions of miR-122 with the viral genome promote viral RNA accumulation in cultured
222 fections were also identified, and assembled viral genomes provided additional information on genotyp
223 d progenitors was not associated with robust viral genome replication and progeny production, while m
224 knockdown of NAP1L1, Bin1 or VAP-A impaired viral genome replication and recapitulated the perinucle
225 essing of MVC mRNAs at (pA)p is critical for viral genome replication and the optimal expression of N
227 sis and glutaminolysis, but not FAS, inhibit viral genome replication and, interestingly, are require
228 demonstrate that SUMO2/3 is recruited to E2A viral genome replication domains through noncovalent int
230 and will enable protein factors involved in viral genome replication to be specifically localised in
231 stimulate cellular proliferation to support viral genome replication with minimal activation of the
232 Deleting ORF7 did not affect viral entry, viral genome replication, or the expression of typical v
237 Streptococcus pyogenes Cas9 cleavage of the viral genome requires the presence of a 5'-NGG-3' protos
238 nomic coverage between different loci in the viral genome, respectively, due to large deletions in th
242 opens unprecedented opportunities to analyse viral genomes, revealing conserved structural features a
243 rmation (NCBI) database contained >2 million viral genome sequences and a reference set of 4000 vira
246 led to a dramatic increase in the number of viral genome sequences identified primarily from metagen
247 enome sequences and a reference set of 4000 viral genome sequences that cover a wide range of known
250 e data are consistent with a model involving viral genome sequestration into such structures, thereby
254 is a complex event where the latent episomal viral genome springs back to active transcription of lyt
255 ever, transgenic CRISPR/Cas9 system-mediated viral genome targeting has not been reported as an antiv
258 ow us to quantitate myeloid cells containing viral genomes that lead to productive infection in SIV-i
259 o release the contained reverse-transcribing viral genome, the capsid must disassemble in a process t
261 omeres, remains associated with the incoming viral genome throughout mitosis and transiently resides
264 oncert to convert single-stranded RNA of the viral genome to double-stranded DNA that is then integra
266 suggesting strong selective pressure on the viral genome to maintain sequence fidelity during reacti
267 structure that associates with the condensed viral genome to produce the mature infectious conical co
270 a pH of ~5 to clear a physical path for the viral genome to transit from the viral interior to the c
271 sm to translate viral proteins and replicate viral genomes to avoid or disable the host defense mecha
272 ed to nuclear domains that contain infecting viral genomes to cooperatively promote viral genome sile
274 V requires the viral protein, LANA1, to bind viral genomes to nucleosomes arrayed on both cellular an
276 Daclatasvir greatly reduced delivery of viral genomes to these core clusters without altering HC
279 volutionary rate estimates across almost all viral genome types and replication strategies, and we ex
280 ng on newly incorporated genetic elements in viral genomes, under conditions of energy limitation.
281 rus RNA in CSF and plasma, and sequenced the viral genome using an unbiased metagenomic approach.
282 The protocol can be used to sequence other viral genomes using the online Primal Scheme primer desi
284 to 24 months after infection, from which the viral genome was also sequenced; (ii) we compared 2 mode
290 ns, while low numbers of copies of influenza viral genome were detected in the air, predominantly at
293 data for cytidine deaminase activity on the viral genome, which causes an asymmetric increase in G t
294 enriched on the nontranscribed stand of the viral genome, which is also the lagging strand during vi
295 mary role is to promote transcription of the viral genome, which persists as an extrachromosomal DNA
296 in these factories and served to transcribe viral genomes, which coincided with an overall decrease
297 MCC tumors contain integrated copies of the viral genome with persistent expression of the MCPyV lar
299 ikely arranged as capsomeres, stabilizes the viral genome within the subviral complex during intracel
300 r class, which appear to directly target the viral genome without affecting cell viability.IMPORTANCE
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