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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
57                                              Viral genome analysis indicates unusually low CpG dinucl
58     It inhibits reverse transcription of the viral genome and can also synthesize unanchored polyubiq
59  proteins that leads to amplification of the viral genome and expression of late viral genes.
60 s, VP35, is essential for replication of the viral genome and for evasion of host immune responses.
61 or significant accumulation of mutations per viral genome and for intracellular selection.
62 ultifunctional protein that encapsidates the viral genome and functions as an adapter between the vir
63 leus, thereby promoting nuclear entry of the viral genome and infection.
64  vaccine platform, due to the absence of the viral genome and its high protein density.
65                             Variation in the viral genome and negative effects of serial vaccination
66 SPR/Cas9 system disrupts latently integrated viral genome and provides long-term adaptive defense aga
67           These capsids help to organize the viral genome and replicative complex(es).
68 iced viral RNA transcripts, which encode the viral genome and the genes encoding viral structural pro
69 s tethering by binding simultaneously to the viral genome and to chromatin during mitosis.
70                    We have characterized the viral genome and used this information to take steps tow
71  virus in cell culture before search for the viral genome and viral antigens.
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
74 lopment of novel antiviral drugs that target viral genomes and block viral replication.
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
78 virus capsids, which encapsidate and protect viral genomes and mediate entry into host cells.
79  identification of transmitted/founder (T/F) viral genomes and their progeny.
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
84      How chromatin is initially assembled on viral genomes, and which variant forms of the core histo
85                                 Furthermore, viral genomes are highly diverse, and using only the cur
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
93 res for a large-scale comparison of complete viral genomes available in RefSeq.
94 ost for 1 year demonstrated mutations in the viral genome become fixed over time.
95 ggest that some L1 protein may accompany the viral genome beyond the endosomal compartment.
96                       HIRA co-localizes with viral genomes, binds to incoming viral and plasmid DNAs
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
106 NA replication complex and is brought to the viral genome by the viral proteins E1 and E2.
107 ane perturbation and recognition of incoming viral genomes by cytosolic nucleic acid receptors are re
108                                     Recoding viral genomes by numerous synonymous but suboptimal subs
109 ich the structure, function, and fate of the viral genome can be modulated by the transcriptionally c
110                             Rapidly evolving viral genomes can adapt to this pressure by acquiring ge
111 se results, the alanine substitutions in the viral genome caused exaggerated syncytium formation, red
112                                  Once at the viral genome, CDK11 phosphorylated serines at position 2
113 rstones toward viral sequence annotation and viral genome classification.
114                         Analysis of complete viral genomes collected from patients in western Africa
115 re, using deep genome sequencing 13 distinct viral genome constellations were differentiated.
116 70.8-kb circular double-stranded DNA (dsDNA) viral genome content, and identification of its cellular
117 cell transmission, only a minute fraction of viral genomes contribute to the progeny.
118 eveloped markedly larger lesions with higher viral genome copies in skin than did wild-type mice.
119 lts in the reduction of viral transcription, viral genome copy number and virus yield.
120 n human neurons than in MRC-5 cells, and the viral genome copy number-to-PFU ratio for VZV in human n
121 fluorescence microscopy, indicating a higher viral genome copy number.
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
126 ributed to mutations that accumulated in the viral genome during its derivation.
127 ssures exist to maintain the fidelity of the viral genome during repeated reactivations from its late
128  cells are programmed to retain the incoming viral genomes during primary infection.
129 therwise acute viruses.Replication defective viral genomes (DVGs) can facilitate persistence of param
130                        Replication defective viral genomes (DVGs) generated during virus replication
131  step of genome recognition is mediated by a viral genome-encoded RNA rather than a protein.
132 dditionally, miR-122 reduces the fraction of viral genomes engaged in protein translation.
133 s recruited to nuclear sites associated with viral genome entry in a SIM-dependent manner, consistent
134 act of A3B on productive BKPyV infection and viral genome evolution.
135 cumulated at nuclear pores that retained the viral genome for at least 4 h postinfection.
136 H motifs enables specific recognition of the viral genome for initiation of DNA packaging during viru
137 he palindromic structures at the ends of the viral genome for their replication.
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
140  pUL25 protein is required for releasing the viral genome from capsids docked at nuclear pores.
141  system with a spacer that matched a partial viral genome from the metagenome.
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
146 fluenced by events that occur soon after the viral genome has entered the host cell nucleus.
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
149                          While many of those viral genomes have become inactivated, some copies of th
150 icular, the protein containers encapsulating viral genomes have been determined to high resolution us
151                   Colinear alignments of the viral genomes identified segmental homologies to ERVs of
152 lay between the innate immune system and the viral genome in HCV control.
153 f EBV lytic promoters and helps maintain the viral genome in its latent state.
154  been linked to reverse transcription of the viral genome in target cells, the mechanism by which unc
155 te was observed, along with the detection of viral genome in the air at low copy numbers.
156 virus (IAV) life cycle is replication of the viral genome in the host cell nucleus.
157 d L1 proteolysis and retention of L2 and the viral genome in the late endosome/lysosome.
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
160 ripts, we visualized active transcription of viral genomes in naturally infected cells.
161 n of PML NB proteins, which are recruited to viral genomes in order to repress viral transcription.
162 s used to determine k for all 3,905 complete viral genomes in RefSeq.
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
168 ction, with the detection of negative strand viral genome, indicating viral replication.
169 s the recruitment process, the newly formed, viral-genome-induced PML NB-like foci can fuse with exis
170                                 Packaging of viral genomes inside empty procapsids is driven by a pow
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.
173          To maximize the coding potential of viral genomes, internal ribosome entry sites (IRES) can
174       This process involves packaging of the viral genome into chromatin, which is often assumed to o
175 e intricate machinery that delivers a single viral genome into empty preformed capsids (encapsidation
176 in is responsible for the integration of the viral genome into the host cell chromosome.
177                         HIV-1 integrates its viral genome into the host cell, leading to persistent i
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
180 ges the NPC and what triggers release of the viral genome into the nucleus.
181 lex (NPC), a key step during delivery of the viral genome into the nucleus.
182 e of the NPC, a key step for delivery of the viral genome into the nucleus.
183 capsid at a nuclear pore, and release of the viral genome into the nucleus.
184 ranscription initiation and packaging of the viral genome into viral nucleocapsids.
185               To identify the regions of the viral genome involved in this process, we used SELEX (sy
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
189               Replication of the hepatitis C viral genome is catalyzed by the NS5B (nonstructural pro
190      As a result, expression of the incoming viral genome is delayed.
191                                    After one viral genome is encapsidated, the internal pressure sign
192            In papillomavirus infections, the viral genome is established as a double-stranded DNA epi
193 us infection, a histone-free DNA copy of the viral genome is synthesized that must be loaded with nuc
194                                 The complete viral genome is transcriptionally active during infectio
195                    Upon host cell entry, the viral genome is translated on endoplasmic reticulum (ER)
196                  Characterization of unknown viral genomes is hindered by the many genomes populating
197                             This property of viral genomes is unexplained.
198 pon viral injection, a small sequence of the viral genome, known as a spacer, is integrated into the
199  the determinants of SBVp32 virulence to the viral genome M segment.
200  the structural and functional features of a viral genome maturation complex, an essential intermedia
201                               As part of its viral genome, MERS-CoV encodes a papain-like protease (P
202 onstrate detection of a soluble nucleic acid viral genome mimic.
203 ustering affects both viral partitioning and viral genome numbers of KSHV.
204                           Propagation of the viral genome occurs within replication complexes, and un
205 egion (nucleotides [nt] 5199 to 5338) of the viral genome of positive sense.
206          The specific infectivities (PFU per viral genome) of HSV(chol) and HSV(des) were similar, su
207                                              Viral genomes often encode genes derived from their host
208 th the detection of serum viremia and plasma viral genomes on day 4 p.e.
209 ata sets than published metagenome-assembled viral genomes or isolates.
210 icate within the lungs or generate defective viral genomes or to differences in levels of costimulato
211 n is replication-competent with no change in viral genome over time.
212 ed in this paper reveals a new mechanism for viral genome packaging and will provide a tractable syst
213 ay be excluded as an essential mechanism for viral genome packaging.
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
217                 In this quiescent state, the viral genome persists as a circular, histone-associated
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
226  protein during latency and is important for viral genome replication and transcription.
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
229 duce sumoylation and the assembly of SUMO2/3 viral genome replication domains.
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
233 els of KSHV lytic transcripts, proteins, and viral genome replication.
234 ns in inactivating MRN and ATM to facilitate viral genome replication.
235  of hepatitis C virus (HCV) is essential for viral genome replication.
236 -acting function of 3D that is essential for viral-genome replication.
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
239 ne expression and excision of the integrated viral genome resulting in reactivation.
240               At least some of the quiescent viral genomes retain the capacity to reactivate, resulti
241                 Sequencing of plasma and CSF viral genome revealed only two non-coding changes compar
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
244              By analysing 92 newly generated viral genome sequences from blood donors and recipients,
245                   Two novel influenza A-like viral genome sequences have recently been identified in
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
248                       Partial or full-length viral genome sequences were generated in 86% of RNA-seq-
249             We report the first use of whole viral genome sequencing to identify nosocomial transmiss
250 e data are consistent with a model involving viral genome sequestration into such structures, thereby
251                                          The viral genome shares 75.4% nucleotide identity with a pro
252                 Phylogenetic analysis of the viral genome showed that SFTS virus represents a new lin
253 cting viral genomes to cooperatively promote viral genome silencing.
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
256 is also involved in the transcription of the viral genome that it delivers to the nucleus.
257 formation and excision to release a circular viral genome that was subsequently lost.
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
260                     Lassa virus protects its viral genome through the formation of a ribonucleoprotei
261 omeres, remains associated with the incoming viral genome throughout mitosis and transiently resides
262 s viral assembly by blocking transfer of the viral genome to assembly sites.
263 hingolipid biosynthesis, not reported in any viral genome to date.
264 oncert to convert single-stranded RNA of the viral genome to double-stranded DNA that is then integra
265          Some designs merely modify a single viral genome to improve on the age-old method of attenua
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
268 evolved a unique strategy for delivering the viral genome to the nucleus of dividing cells.
269 rt that some L1 protein traffics with L2 and viral genome to the nucleus.
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
273 of biologically important RNAs, ranging from viral genomes to long noncoding regulatory RNAs.
274 V requires the viral protein, LANA1, to bind viral genomes to nucleosomes arrayed on both cellular an
275 the MTOC, potentially aiding in the delivery viral genomes to the nucleus.
276      Daclatasvir greatly reduced delivery of viral genomes to these core clusters without altering HC
277       Some host factors are diverted for the viral genome translation, some are recruited to improvis
278 gic degradation, whereas PLA2G16 facilitates viral genome translocation and prevents clearance.
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
283 P) is known to mediate the nuclear import of viral genome via its nuclear localization signals.
284 to 24 months after infection, from which the viral genome was also sequenced; (ii) we compared 2 mode
285 otiorum, a full-length cDNA of the 14,538-nt viral genome was cloned.
286                                              Viral genome was detected in 21 (2.3%) samples from 9 he
287 ng a conserved 3' untranslated region of the viral genome was evaluated.
288                 Ultra-deep sequencing of the viral genome was performed on 11 entecavir-treated and p
289                                     The full viral genome was sequenced by primer walking.
290 ns, while low numbers of copies of influenza viral genome were detected in the air, predominantly at
291                         Complete and partial viral genomes were assembled and used to measure the num
292 Rep-encoding single-stranded DNA (CRESS DNA) viral genomes, were identified.
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
298                                  Analyses of viral genomes with ecological and epidemiological data y
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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