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1 her (synchrony) and the onset of inhalation (latency).
2  lifelong infection through establishment of latency.
3  SMAD3, which is required for maintenance of latency.
4 mRNA could be exploited for controlling KSHV latency.
5 ponents of a nonhuman primate model of HIV-1 latency.
6 otein kinase family is linked to maintaining latency.
7 population of the starting cells with a long latency.
8  infected cells or inhibit reactivation from latency.
9 e of infected cells and the establishment of latency.
10 tivate its replicative phase from quiescence/latency.
11 f reduced response variability and shortened latency.
12 transcription and blocking reactivation from latency.
13 suggesting co-regulated transcription during latency.
14  between zero and nonzero (possibly maximal) latency.
15 veral hallmarks of HIV and SIV infection and latency.
16 ting LXA4 secretion in the host to establish latency.
17 V disease and prevented the establishment of latency.
18 minal ganglia (TG) are an important site for latency.
19 t memory T cells, has been implicated in HIV latency.
20  control of viral episome maintenance during latency.
21 stability is always between zero and maximal latency.
22 rence in the establishment or maintenance of latency.
23  in lytic infections and associated with VZV latency.
24 rses HIV/simian immunodeficiency virus (SIV) latency.
25 onsistently induces BoHV-1 reactivation from latency.
26  HSV-1 latency in certain neuronal models of latency.
27 s acidic domain reader is critical for viral latency.
28 on factors are involved in establishing this latency.
29 ate-specification decisions, including viral latency.
30  protein kinases is linked to maintenance of latency.
31 f nuclear architecture and a marker of HIV-1 latency.
32 nvestigate the contribution of this locus to latency.
33 on drifts, and with only approximately 60 ms latency.
34 s to PD-1, CTLA-4, TIM-3, and TIGIT reversed latency.
35  N-803 by promoting the maintenance of viral latency.
36  viral infection characterized by periods of latency.
37  blocking IC molecules with Abs reverses HIV latency.
38 cetylase inhibitor reported to reverse HIV-1 latency.
39 er, during early stages of reactivation from latency.
40 nct but unknown mechanisms may promote viral latency.
41 ic bet hedging between viral replication and latency.
42 inhibit virus replication, but do not affect latency.
43 viral DNA replication, and reactivation from latency.
44 all target types, but with no change in N2pc latencies.
45 h-resolution structures has been hindered by latency-a hallmark of EBV infection-and atomic structure
46     However, little is known about how HIV-1 latency affects their function.
47 on, and sensorimotor interaction, i.e. short-latency afferent inhibition, were recorded from 15 healt
48 ) sleep, demonstrated as a shortening of REM latency, an increase of REM density, as well as total RE
49                           For ERPs, the mean latencies and amplitudes of the P100 VEP and P3 ERP show
50 und-driven firing rates, reduced first-spike latencies and wideband increases in excitability.
51 cer brain metastases (BCBM) have a 5-20 year latency and account for 30% of mortality; however, mecha
52 fication of small molecules that destabilize latency and allow immune clearance of infected cells cou
53  episomes form the molecular basis for viral latency and are etiologically linked to virus-associated
54  that infiltrate the ganglia at the onset of latency and contract to a stable activated tissue-reside
55 een examined for their suitability for HIV-1 latency and cure research.
56 promising reagents for a SHIV model of HIV-1 latency and cure.IMPORTANCE Simian-human immunodeficienc
57 ished infection can be recapitulated without latency and depends only on the ability to target initia
58  platforms suffer from high cost, read-write latency and error-rates that render them noncompetitive
59 nsive evaluation of deubiquitinases in HIV-1 latency and establishes that they may hold a critical ro
60 been developed for characterization of HIV-1 latency and high-throughput screening for latency-revers
61 expression of viral lytic transcripts during latency and impaired induced reactivation compared to th
62                 The reduction of sleep onset latency and increase in wakefulness later in the night m
63                           This shortening of latency and increased reproducibility may confer additio
64 nflux and AP failure rates, and increased AP latency and jitter during high frequency repetitive firi
65 cy III critical for the establishment of EBV latency and lifelong persistence within its host, wherea
66 rus (EBV) switches between four viral genome latency and lytic programmes to navigate the B-cell comp
67  sequence are deficient for establishment of latency and persistent infection.
68  virtually all humans and establish lifelong latency and reactivate to infect other humans.
69 ized a human neuronal cell line model of HSV latency and reactivation (LUHMES) to characterize the la
70  the complex molecular mechanisms underlying latency and reactivation continues to evolve.
71 of HVEM plays an important role in the HSV-1 latency and reactivation cycle that is independent of HV
72 VEM immunomodulatory functions contribute to latency and reactivation or whether its binding to gD is
73 d cells sense environmental cues to regulate latency and reactivation, and emphasize the role of cont
74 peutic approaches should focus on preventing latency and reactivation.
75 ity to bind gD, is required for WT levels of latency and reactivation.
76 ted in primary and cell line models of HIV-1 latency and reactivation.
77 HPCs from TGF-beta-mediated effects on viral latency and reactivation.
78  mechanisms of virus-mediated pain linked to latency and reactivation.IMPORTANCE The reactivation of
79 n the sensory neurons and to reactivate from latency and then cause disease in peripheral tissues, su
80 n IRF-7 restricts the establishment of viral latency and viral reactivation.
81 es have a functional role in maintaining HIV latency and whether blocking IC molecules with Abs rever
82         We performed whole gut transit, bead latency, and geometric center studies.
83 l studies, as well as in vitro models of HIV latency, and has been shown to effectively induce HIV RN
84 HIV and acquired knowledge on HIV infection, latency, and host response.
85     Ideally, such tools are noninvasive, low-latency, and provide interfaces to trigger external hard
86  (HPCs) support human cytomegalovirus (HCMV) latency, and their differentiation along the myeloid lin
87  cellular subsets and establishment of viral latency, and viral rebound with return to pretreatment s
88               The mechanisms contributing to latency are diverse and depend on the nature of both the
89 ease in spike number and a decrease in spike latency are observed with increasing stimulation intensi
90                                              Latency-associated nuclear antigen (LANA), the most abun
91 esses a small subset of genes, including the latency-associated nuclear antigen (LANA), which mediate
92 uous to the protease cleavage sites, and the latency-associated structural elements.
93 urthermore, Abeta(42) colocalized with HSV-1 latency-associated transcript (LAT) expression.
94 RNAs (miR-H1/H6) that are encoded within the latency-associated transcript (LAT) region, a portion of
95 nase is crucial for the ability of the HSV-1 latency-associated transcript (LAT) to inhibit apoptosis
96 n depend on the anti-apoptotic activities of latency-associated transcript (LAT).
97 ering in and near ORF61 and antisense to the latency-associated transcript of VZV can positively infl
98     HSV expressing the epitope from the full latency-associated transcript promoter did not efficient
99  benefit from less variability and shortened latencies at subsequent synapses.
100  well as lower and less variable first-spike latencies at suprathreshold intensities.
101 specific DNA-binding protein can disrupt EBV latency by driving the transcription of target genes and
102     A quiescent state of infection mimicking latency can be achieved in the presence of acyclovir (AC
103 esting that (i) a variant of classical HSV-1 latency can be established during earlier stages of neur
104                   Although reactivation from latency can cause life-threatening disease, our molecula
105                              The presence of latency can dramatically decrease infection clearance, b
106 knockout screen using CRISPR-Cas9 in a HIV-1 latency cell line model.
107 form gamma (AtLEGgamma) is controlled by the latency-conferring dimer state, the activation of the mo
108 hasize the stochastic nature of lytic versus latency decision of HSV-1 in nonneuronal cells.
109  tuning," i.e., their response magnitude and latency depended on the whisker's deflection angle.
110 ative stress do not increase with increasing latency duration suggesting a lack of host or bacterial
111 rate, the generation time increases over the latency duration.
112 DAC) inhibitor vorinostat disrupts EBV/HHV-8 latency, enhances chemotherapy-induced cell death, and m
113 thway in productively infected cells, before latency establishment and after reactivation.
114 anges of VGSCs during the processes of HSV-1 latency establishment and reactivation using human dorsa
115 upon infection but steadily recovered during latency establishment and that latent neurons exhibited
116 germinal center (GC) B cell responses during latency establishment, an understanding of how viral gen
117 ed by subthalamic stimulation revealed short latency events indicative of monosynaptic connectivity b
118                             Widespread short latency excitation, compatible with monosynaptic transmi
119 xity with a high temporal resolution and low-latency feedback.
120  HSV-2 skin or vaginal disease and prevented latency following active or passive immunization in prec
121                                     Response latencies for these cells were compatible with a contrib
122 rast to acyclovir, treatment of cells during latency for 24 h with TAF still inhibited EBV lytic DNA
123                                          The latency from the end of an effective stimulus to the sta
124 e transcriptionally upregulated, while viral latency genes are downregulated ahead of expression of t
125 cells, EBV promoters drive the expression of latency genes, while oriP functions as an enhancer for t
126 ess MSI-related reduction of the visual P100 latency, greater MSI-related slowing of the auditory P20
127                                              Latency has advantages for both host and microbe.
128       We demonstrate that in vitro models of latency have higher levels of the P-TEFb subunit cyclin
129 s the change in cold pressor hand withdrawal latency (HWL) before and after drug injection.
130                                           In latency I BL xenografts, decitabine followed by EBV-CTLs
131                      Decitabine treatment of latency I EBV+ Burkitt lymphoma (BL) sensitized cells to
132 widespread among B-cell lines supporting the latency I or III program of EBV protein expression and i
133 as been that most EBV+ lymphomas express the latency I program, in which the single Epstein-Barr nucl
134 imately transitioned to the more restrictive latency I program, whereas cells infected with wild-type
135 d latency III or transitioned more slowly to latency I.
136 lated by a long noncoding RNA, that supports latency III critical for the establishment of EBV latenc
137  infection of primary B cells, which require latency III for growth in vitro, both BHLF1 (-) viruses
138 fected with wild-type virus either sustained latency III or transitioned more slowly to latency I.
139 infected lymphomas that express the full EBV latency III program, a critical barrier has been that mo
140 re initially indistinguishable in supporting latency III.
141 ults in a reduced ability to reactivate from latency.IMPORTANCE Herpes simplex virus 1 (HSV-1) establ
142  cellular factors that may contribute to HIV latency.IMPORTANCE The ability of HIV to establish a rev
143  in facilitating efficient reactivation from latency.IMPORTANCE While HSV antivirals reduce the sever
144 portantly, SP inhibits HIV reactivation from latency in both cell line models and resting CD4(+)T cel
145  signaling correlates with maintaining HSV-1 latency in certain neuronal models of latency.
146 ress viral genes more proximately to promote latency in dorsal root ganglion (DRG) neurons.
147 ation according to cortical region, response latency in each neuronal cluster was correlated with the
148 BV strain was recently reported to establish latency in humanized mice but not cause tumors.
149 inflammatory LXA4 secretion to maintain KSHV latency in infected cells.
150 timulation increased AP failure rates and AP latency in LSO neurons from the Kv3.3KO, underlining the
151 single cell RNA-seq analysis to characterize latency in monocytes and hematopoietic stem and progenit
152 tial for productive replication and also for latency in particular cell types.
153 roinvasive pathogens that establish lifelong latency in peripheral ganglia following the initial infe
154 l IRFs 1, 2, and 3 are also expressed during latency in primary effusion lymphoma (PEL) cells, and vI
155 toxin B, Abs to CTLA-4 and PD-1 reversed HIV latency in proliferating and nonproliferating CD4(+) T c
156 ortant bovine pathogen, establishes lifelong latency in sensory neurons.
157 t it is unclear what mechanisms maintain HIV latency in the blood or gut.
158 del to study the molecular mechanisms of HIV latency in the gut and reveal new cellular factors that
159 thways for its survival advantage during its latency in the infected human host.
160 estricting establishment of gammaherpesvirus latency in the peritoneal cavity and, to a lesser extent
161 f these viruses is the capacity to establish latency in the sensory neurons and to reactivate from la
162                       While KSHV establishes latency in virtually all susceptible cell types, LECs su
163 ymptomatic behavior of pathogens (hereafter "latency") in order to unify epidemiology and evolution f
164 a power patterns revealed that late (>500 ms latency) in the cue-to-target foreperiod, only EEG alpha
165 rnal stressors can trigger reactivation from latency, in part because activation of the glucocorticoi
166 F1, indeed contributes to key aspects of EBV latency, including its ability to promote the continuous
167      Such beta-bursts were followed by short-latency increases of bilateral sensorimotor beta-burst r
168                     In vitro models of HIV-1 latency involving cell lines or primary cells have been
169                               Although viral latency is a critical factor in this persistence, recent
170                        Lytic activation from latency is a key transition point in the life cycle of h
171                                        HIV-1 latency is a major barrier to cure.
172                                       Hence, latency is a temporally unstable state with an eventual
173                                              Latency is an integral part of the pathogenic strategies
174                            Reactivation from latency is controlled by processes that restrict or acti
175 munodeficiency virus (SHIV)-macaque model of latency is critical to investigate eradicative and suppr
176 disease, our molecular understanding of HCMV latency is incomplete.
177  establishes, maintains and reactivates from latency is largely unknown.
178           Understanding of the mechanisms of latency is leading to novel approaches to destroy latent
179                                              Latency is not antigenically silent, and viral proteins
180 tive viral outgrowth assays (QVOAs) in which latency is reversed with T cell activation to allow vira
181 rtant site for bovine herpesvirus 1 (BoHV-1) latency is sensory neurons within trigeminal ganglia (TG
182 us, one way in which BHLF1 may contribute to latency is through a mechanism, possibly mediated or reg
183 tioxidant responses on viral replication and latency is unknown.
184 the most abundantly expressed protein during latency, is a multifunctional protein which is absolutel
185                                       During latency, KSHV expresses a small subset of genes, includi
186 nts induced short-latency (SAI) but not long-latency (LAI) afferent inhibition of face M1, while faci
187 ection of nonneuronal cells and results in a latency-like state in the infected cells.
188 at high temporal resolution (70 Hz) with low latencies (&lt;30 milliseconds), while being affordable (<U
189 ependent mechanism, revealing a proteostatic latency mechanism common to polyomaviruses.
190                                  In an HIV-1 latency model using autologous CD8(+) T cell clones as b
191                                     Stopping latencies, motor evoked potentials, and frontal beta pow
192           These data suggest that our murine latency ("mu-Lat") model enables efficient determination
193 attack and are proposed to contribute to the latency of cryptococcal infection.
194 deration in future vaccine design.IMPORTANCE Latency of HSV-1 in host neurons enables long-term persi
195  DR(Sert) neurons dramatically increased the latency of mice to arouse during hypercapnia, as did sil
196 TP, primarily through shifts in the relative latency of Pyr and inhibitory neurons.
197         Consistent with this prediction, the latency of stable units was significantly shorter than t
198 des and are more precise than the behavioral latency of stopping.
199 ble strategy (ESS) at zero, some, or maximal latency of the first stage or, perhaps surprisingly, at
200    Overall, these findings indicate that the latency of the rodent VEP is sensitive to changes mediat
201 rallel, there was a significant delay in the latency of the transient VEPs from the affected side of
202 scue the VEP delay and instead increased the latency of the VEP waveform.
203 l vanilloid family member 1 (TRPV1), and the latency of TRPV1-mediated Ca(2+) responses can be contro
204 1, and TGM2 as potential regulators of HIV-1 latency, of which PSMD1 and TMG2 could be confirmed phar
205 alphaherpesviruses can establish spontaneous latency only in neuronal cells and emphasize the stochas
206  of PML NBs were restored upon transition to latency or by decreasing oxidative stress or iron conten
207 and HVEM(-/-) mice, HSV-1 does not establish latency or reactivate effectively in mice lacking HVEM,
208 ution to differences in the establishment of latency (or ability to spread back to the periphery) and
209  by greater amplitude (p = .012) and shorter latency (p = .029) of the N2 component of event-related
210 ugment ART with therapies that reverse viral latency, paired with immunotherapies to clear infection,
211 ons to model selection, spatial control, and latency period as well as estimating the exposure-respon
212 lth risks remains challenging because of the latency period for many chronic diseases that take years
213 ilateral disease, pineal gland tumors, and a latency period of at least 1 year.
214 s 9.8 months (IQR 3.6-17.4; n=96) and median latency period since first exposure to a PARP inhibitor
215 els of >=85 dB for at least 15 years (5-year latency period), showed no increased risk of VS (odds ra
216 cal course, involved drugs, daily drug dose, latency periods, test results of skin test and cellular
217 as interneurons were strongly activated at a latency preceding that found in projection neurons.
218 een excluded from consideration of a role in latency, primarily because of the general incompatibilit
219  the view on insomnia, i.e., prolonged sleep latency, problems to maintain sleep, and early morning a
220 ecular link between B-cell state and the EBV latency programme.
221 ild-type (WT) herpes simplex virus 1 (HSV-1) latency reactivation depend on the anti-apoptotic activi
222 ike inhibitory protein) gene restored the WT latency reactivation phenotype to that of a LAT-minus [L
223 s expressing CD80 in place of LAT had higher latency reactivation than a LAT-null virus.
224 ession of CD80 fully rescues LAT function in latency reactivation, apoptosis, and immune exhaustion,
225  can restore the ability of LAT to establish latency, reactivation, and immune exhaustion as well as
226 l CD8(+) T cells and HSV-1 appear to control latency/reactivation cycles.
227                            By contrast, long-latency reflex components are typically assumed to origi
228 that spinal circuits also contribute to long-latency reflexes in distal and forearm muscles, alongsid
229  with a contribution to both short- and long-latency reflexes.
230 7, USP14, OTULIN, and USP5 as possible HIV-1 latency regulators.
231 es of spatially identified units, ordered by latencies relative to each other (with minimal effects o
232 ny of activation across neurons, but not the latency relative to inhalation.
233                                              Latency requires multiple functions: maintaining the her
234 ng pathways, was observed, as well as longer latency responses likely reflecting a mixture of slower
235                                  However, no latency reversal agent (LRA) to date effectively clears
236 rosis factor (TNF)-alpha, an established HIV latency reversal agent, significantly induced GFP expres
237 ectively viral eradication agents, including latency reversal agents, penetrate, and function in dive
238 despite CTLA-4/PD-1 blockade inducing robust latency reversal and reducing total levels of integrated
239 molecule inhibition of HSF1 attenuated HIV-1 latency reversal by histone deactylase inhibitors, prote
240 d individuals, inhibition of HSF1 attenuated latency reversal by phorbol ester+ionomycin but not by a
241                                     However, latency reversal by second mitochondria-derived activato
242 le for CD8(+) lymphocytes in suppressing the latency reversal effect of N-803 by promoting the mainte
243  virus type 1 (HIV-1) cure strategy involves latency reversal followed by immune-mediated clearance o
244                                  The lack of latency reversal in the model used in this study may be
245 vivo, attributed to the lack of quantifiable latency reversal in this model with low levels of persis
246 other cellular factors play key roles in HIV latency reversal in vivo despite robust HDACi pharmacolo
247 they happen could provide clues to stimulate latency reversal more effectively and safely or to preve
248         We show here that, for diverse LRAs, latency reversal observed in model systems involves a he
249 ]) has been employed in several clinical HIV latency reversal studies, as well as in vitro models of
250 adout of B cell state and highlights Burkitt latency reversal therapeutic targets.
251                               The potency of latency reversal was significantly higher following comb
252                   This promising approach to latency reversal-in combination with appropriate tools f
253 en the host transcriptional response and HIV latency reversal.
254   We investigated the combined impact of the latency reversing agent vorinostat (VOR) and AGS-004, an
255  cells successfully reactivated by different latency reversing agents.
256 ected individuals upon cell stimulation with latency reversing agents.
257 eservoirs when tested either alone or with a latency-reversing agent (LRA).
258 -1 latency and high-throughput screening for latency-reversing agents (LRAs).
259 eacetylase inhibitors are widely studied HIV latency-reversing agents (LRAs).
260  combination IC blockade compared with other latency-reversing agents, including vorinostat and bryos
261 ure with CD8(+) T cells blocked the in vitro latency-reversing effect of N-803 on primary human CD4(+
262 lation of trigeminal afferents induced short-latency (SAI) but not long-latency (LAI) afferent inhibi
263 previously shown that rats with short-defeat latencies (SL/vulnerable rats) show increased anxiety- a
264 eep quality, subjective sleep quality, sleep latency, sleep duration, sleep efficacy, sleep medicatio
265 establish lifelong, transcriptionally silent latency states in sensory neurons to escape host detecti
266                                      If not, latency strongly decreased clearance even at low latent
267  larger receptive fields and longer response latencies than basal dendrite inputs, suggesting a domin
268 is detected in more TG neurons during BoHV-1 latency than in reactivation and uninfected calves.
269 ice to pick up pellets of standard chow with latencies that varied based on stimulation intensity; on
270 still have high computational costs and high latency that is a serious impediment for applications, s
271 ctivity features (such as neuron identity or latency) that are consequential for perception remains c
272 nnate immune responses to establish lifelong latency throughout a susceptible individual's lifetime,
273 elective for attack action and exhibit short-latency, time-locked spiking relative to the activity of
274   Contrary to our expectations, 'Avoidance' (latencies to approach and eat the novel food) did not pr
275 her half of socially defeated rats show long-latencies to defeat (LL/resilient) and are similar to co
276  sounds and reduced behavioral reaction time latencies to high-intensity sounds.
277 increased sound-evoked responses and reduced latencies to higher-intensity sounds.
278 y participated in more trials, showed little latency to approach the boxes and mainly manipulated fun
279 al inhibition of BF-PV neurons increased the latency to arousal produced by exposure to hypercarbia o
280 stent sleep disturbances, including a longer latency to fall asleep, more time awake during the night
281 Gs) had a more hyperpolarized VP with longer latency to fire action potentials on depolarization comp
282  potentially involved in the transition from latency to lytic VZV infection.
283    Secondary outcome measures were change in latency to persistent sleep from baseline to days 1 and
284  the reduction of wake after sleep onset and latency to persistent sleep from baseline to days 1 and
285  wake time after sleep onset, and subjective latency to sleep onset from baseline to week 4.
286 ective wake after sleep onset and subjective latency to sleep onset.
287 N neuron, and (3) the interneuron's response latency to strong, synchronous LGN input.
288 e EBV lytic cycle.IMPORTANCE Transition from latency to the lytic phase is necessary for herpesvirus-
289 a key role in regulating the transition from latency to the lytic replication stages of EBV infection
290 ure TCR gene-therapy to treat EBV-associated latency type II/III malignancies.
291 imulus dimension (i.e., rate, synchrony, and latency) using holographic two-photon optogenetic stimul
292  which are well-known EHV1 dissemination and latency vessels.
293 y the establishment and maintenance of viral latency, viral reactivation, and changes in the function
294 ds of glaucoma; however, the AUC for saccade latency was only 0.635 compared to 0.914 for SVOP sensit
295 investigate host factors which promote HIV-1 latency, we conducted a genome-wide functional knockout
296 cone a-wave amplitude and a prolonged b-wave latency were observed in both disorders, whereas a reduc
297            There is an increase in selection latency when the disk's color changed smoothly compared
298 ase in weight most prominent and of shortest latency with 10 mg/kg/d GenX exposure.
299             We found that KOS(M) established latency with a higher number of viral genomes than strai
300 ry infection of the cornea, the virus enters latency within the trigeminal ganglion (TG), from which
301            The model predicted that a unit's latency would be related to its temporal profile.

 
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