ライフサイエンスコーパス: lytic

1 vestigated 230 A. baumannii strains using 17 lytic A. baumannii phages and the phage susceptibility w

2 Lytic activation from latency is a key transition point

3 To ensure that lytic activation is not prematurely terminated, expressi

4 EspF are required for virulence and promote lytic activity independently of the major EsxA and EsxB

5 e charge of this helix is crucial for tuning lytic activity of CDCs.

6 of peptidoglycan protects bacteria from the lytic activity of lysozyme, a mammalian innate immune en

7 A newly isolated phage, MMI-Ps1, with strong lytic activity was used for treatment of acute lung infe

8 -class antistaphylococcal lysin, is a direct lytic agent that is rapidly bacteriolytic, eradicates bi

9 es proof of concept for exebacase and direct lytic agents as potential therapeutics and supports cond

10 CD4-MBL CAR-T cells displayed potent lytic and functional responses to Env-expressing cell li

11 n factor that governs the switch between the lytic and latent forms of Toxoplasma gondii, a parasite

12 y of these pelagiphages to propagate by both lytic and lysogenic infection.

13 s, resulting in subpopulations of responsive/lytic and refractory cells.

14 a priori conditions under which exposure to lytic and temperate phage and conjugative plasmids will

15 deletion, resulting in the loss of multiple lytic and virion genes.

16 by accommodating for the negative effects of lytic bacteriophage and antibiotic exposure on diagnosti

17 shed, and the predatory relationship between lytic bacteriophage and the etiologic agent Vibrio chole

18 ic performance was assessed as a function of lytic bacteriophage detection and exposure to the first-

19 where bacterial pathogens are vulnerable to lytic bacteriophage predation.

20 A custom-made, lytic bacteriophage preparation was administered to the

21 95% CI, 0.022 to 0.649), respectively, when lytic bacteriophage were detected.

22 tal, clinical, and scientific concern is how lytic bacteriophage, as well as antibiotics, impact diag

23 target strains and tested them against novel lytic bacteriophages (n = 65).

24 Use of lytic bacteriophages (phages) for the treatment of drug-

25 encounter selection by both antibiotics and lytic bacteriophages.

26 dividual vIL-6-protein interactions to HHV-8 lytic biology.

27 vIRF-2-USP7 interaction in HHV-8 latent and lytic biology.IMPORTANCE Human herpesvirus 8-encoded IRF

28 The standard treatment for patients with lytic BKPyV infection is to reduce immunosuppressive the

29 nts with T2Candida panel positive and myco/f lytic blood culture negative results, while 6 patients h

30 ctive values of the panel compared to myco/f lytic blood culture.

31 tal of 433 paired T2Candida panel and myco/f lytic blood cultures were identified.

32 T2Candida panel and mycolytic/fungal (myco/f lytic) blood culture collected simultaneously during hos

33 ice for the initial assessment of MM-related lytic bone lesions.

34 ed by chemicals and immunologic ligands, the lytic cascade is activated only when expression of the E

35 essential for successful completion of EBV's lytic cascade.

36 e level of viral replication or later in the lytic cascade.

37 and disruption of this loop disables the EBV lytic cascade.

38 g of ZEBRA-dependent activation of the viral lytic cascade.IMPORTANCE The binding of ZEBRA to methyla

39 ment components C5b-9, has been connected to lytic cell death and implicated in secondary injury afte

40 the disruption of the early coordinated non-lytic cell death response, ultimately supports the infla

41 ffector of necroptosis, a form of programmed lytic cell death.

42 Continuous lytic cell lysis and de novo infection allowed LEC cultu

43 s and two cellular proteins, ATM and KAP1, a lytic cycle amplification loop is established, and disru

44 in key to effective replication in the HSV-1 lytic cycle and reactivation in the latent cycle.

45 DNA binding, recognition of DNA methylation, lytic cycle DNA replication, and viral late gene express

46 s of temperate phages that are locked in the lytic cycle have shown that CRISPR-Cas systems can effic

47 key factors for KSHV genome maintenance and lytic cycle in lymphatic endothelial cells, supporting K

48 tently reactivates from latency and enters a lytic cycle in which numerous lytic mRNAs and proteins a

49 eplication and suppressed its looping to the lytic cycle initiator BZLF1 promoter.

50 contrast to those of EBV and HCMV, the KSHV lytic cycle occurs while the APC/C is active.

51 Pinholin S(21)68 triggers the lytic cycle of bacteriophage phi21 in infected Escherich

52 While the lytic cycle of EBV can be triggered by chemicals and imm

53 y reported to act as restrictive factors for lytic cycle transcription and virion production.

54 rs (GR and KLF4) correlates with stimulating lytic cycle viral gene expression following stressful st

55 important for MYC expression reactivated the lytic cycle, including in Burkitt xenografts.

56 ted viral DNA triggers activation of the EBV lytic cycle, leading to viral replication and, in some p

57 ose gene products, ensures completion of the lytic cycle.

58 and secretion of a hexapeptide (AimP) during lytic cycle.

59 highlighting their significance in the KSHV lytic cycle.

60 y at 72 particles per cell at the end of its lytic cycle.

61 ) is necessary for phage DT1 to complete its lytic cycle.

62 nd other diseases, most of which require the lytic cycle.

63 a subpopulation of cells to support the EBV lytic cycle.IMPORTANCE Transition from latency to the ly

64 gulate viral transcription during latent and lytic cycles of replication.

65 he dependence of EBV late gene expression on lytic DNA amplification, and suggest some directions for

66 atency for 24 h with TAF still inhibited EBV lytic DNA replication at 72 h after drug was removed.

67 d clinically for HIV prevention, inhibit EBV lytic DNA replication, with respective IC(50) values of

68 ssion by EBNA-antisense transcription during lytic EBV infection.

69 ut not FG-4592, induced accumulation of both lytic EBV proteins and phosphorylated p53 in cell lines

70 Lytic EBV transcription differs from cellular transcript

71 ne protease CspB, which processes the cortex lytic enzyme SleC, leading to degradation of the spore c

72 ires the activities of a family of cell-wall lytic enzymes called resuscitation-promoting factors (Rp

73 otechnological potential of phages and their lytic enzymes is of interest for their ability to select

74 poprotein (HDL) complexes called trypanosome lytic factors (TLFs) 1 and 2.

75 These lytic forms of cell death are distinct from apoptosis du

76 roaches predict that genes involved in phage lytic function are preferentially lost, resulting in sho

77 l prophages that retain a full complement of lytic-function genes.

78 ransactivation activity and KSHV spontaneous lytic gene expression and infectious virus release.

79 ly results in a significant decrease in late lytic gene expression and virion production, indicating

80 These new compounds also increase viral lytic gene expression in PEL cells.

81 viral RNAs (including microRNAs) to suppress lytic gene expression or regulate cellular protein expre

82 the positive effect of DHX9 depletion on EBV lytic gene expression was not confined to SM-dependent g

83 led temporal gene regulation, in which early lytic gene expression was terminated in late protein-exp

84 s of an RNA quality control pathway and KSHV lytic gene expression, and demonstrates that NMD can fun

85 oma-associated herpesvirus (KSHV) latent and lytic gene replication.

86 By 6 days postinfection, there is a loss of lytic gene transcription and an increase in the numbers

87 ng how one insulator site in HSV-1 modulates lytic gene transcription and heterochromatin deposition

88 RNA transfection, inhibits SM-dependent late lytic gene transcription but not transcription of other

89 -1s can also directly activate KSHV ORF21, a lytic gene.

90 However, there is evidence that some lytic genes can be directly activated by certain cellula

91 Expression of 15 late lytic genes that are important for virion production and

92 Immediately after LCL establishment, EBV lytic genes were also expressed in LCLs, and ~4% of the

93 support spontaneous expression of oncogenic lytic genes, high viral genome copies, and release of in

94 ly interacted with RTA protein to coregulate lytic genes.

95 tiates transcription from promoters of viral lytic genes.

96 igenetic modifications and silencing of KSHV lytic genes.

97 strict or activate the transcription of KSHV lytic genes.

98 l, which was associated with defects in both lytic granule biogenesis and synaptic actin remodeling.

99 ole for septins in regulating the release of lytic granule contents during NK cell-mediated killing.

100 oteins had no impact on conjugate formation, lytic granule convergence, or MTOC polarization to the c

101 Cytotoxicity, lytic granule exocytosis, and the phosphorylation of Pyk

102 otency and specificity of killing by driving lytic granule fusion at the synapse and thereby the rele

103 n with syntaxin binding protein 2 to promote lytic granule fusion.

104 s expected but surprisingly had no effect on lytic granule polarization and directional secretion.

105 poxin A(4) promoted NK cell LIMK expression, lytic granule polarization to the immune synapse and cyt

106 ytic granules at the CS, where they regulate lytic granule release.

107 letal rearrangement is necessary for NK cell lytic granule trafficking and immune synapse formation t

108 F-actin accumulation at the immune synapse, lytic granule trafficking, and cytotoxicity.

109 d displayed superior capacity to degranulate lytic granules against KIR ligand-matched primary leukem

110 s copurify and accumulate near the polarized lytic granules at the CS, where they regulate lytic gran

111 a target cell triggers NK cell cytotoxicity, lytic granules containing proteins including perforin an

112 ith antigen-specific CD8(+) T cells in which lytic granules had been destroyed by pretreatment with C

113 ne synapses by promoting the polarization of lytic granules toward the microtubule-organizing center

114 is observed, including the Golgi apparatus, lytic granules, and mitochondria.

115 ion and have severely impaired exocytosis of lytic granules.

116 ng involves the membrane fusion of preformed lytic granules.

117 d-cell microscopy showed poor convergence of lytic granules.

118 summary, Listeria phages inactivate Cas9 in lytic growth using variable, narrow-spectrum inhibitors,

119 phage genes are small, are not required for lytic growth, and are of unknown function.

120 are critical for the switch from lysogeny to lytic growth.

121 Lytic HSV-1 infections impaired NPC migration, which rep

122 ermination of the P(R') late promoter during lytic induction of the phage.

123 ctious virions may have particular value for lytic induction strategies in the clinical setting.IMPOR

124 To develop a lytic-induction therapy for treating patients with EBV-a

125 tabilizing drugs may be helpful as part of a lytic-induction therapy for treating patients with EBV-p

126 rd nonhuman primate cell lines while causing lytic infection and cell death.

127 events that activate CMV gene expression and lytic infection and viral dissemination are then facilit

128 reased virulence, virus replication rate and lytic infection dynamics in laboratory experiments, but

129 ence of the immune activator interferon, and lytic infection in the absence of interferon.

130 Lytic infection of human parvovirus B19 (B19V) takes pla

131 JC virus (JCV) infection is a lytic infection of oligodendrocytes in progressive multi

132 owever, depletion of CD8 T cells resulted in lytic infection of the choroid plexus and ependymal lini

133 s that drive cell survival during a normally lytic infection remained unclear.

134 e viral transcriptome and translatome during lytic infection with base-pair resolution by computation

135 ellular pathways, modulates HHV-8 latent and lytic infection, and is targeted by vIRFs 1, 3, and 4.

136 During lytic infection, however, AcrIIA1 fails to block Cas9 du

137 cells, can be significantly induced by viral lytic infection, suggesting potential regulation of vira

138 boosts E1A transcription, E3-19K levels and lytic infection.

139 aperone that functions with Hsc70 to promote lytic infection.

140 virus, suggesting that these sncRNA promoted lytic infection.

141 as playing a key role in B2 induction during lytic infection.

142 rococcal polysaccharide antigen to engage in lytic infection.

143 Neural progenitor cells are permissive for lytic infection.

144 rectly to suppress viral gene expression and lytic infection.

145 aperone that functions with Hsc70 to promote lytic infection.IMPORTANCE Viruses have evolved a variet

146 t are antisense to VLT, a transcript made in lytic infections and associated with VZV latency.

147 nal layer of complexity of VZV regulation of lytic infections.

148 PROX1 expression correlated with latent and lytic KSHV protein expression.

149 replication and sensitivity to rapamycin in lytic KSHV-infected cells.

150 Since these T cells can influence lytic/latent decisions in reactivating neurons, we argue

151 bacteriophage switch is unable to choose the lytic life cycle showing that the CI:MOR complex is esse

152 on of a sensitive host: the lysogenic or the lytic life cycle.

153 pite the death of individual host cells from lytic lysis.

154 ages utilize antitermination to regulate the lytic/lysogenic switch and our results demonstrate that

155 A highly sensitive and selective non-lytic M13 phage-based electrochemical impedance spectros

156 We demonstrate that lytic MHV68 infection of B cells, macrophages, and fibro

157 was directly proportional to the content of lytic molecules, which required antigenic stimulation ov

158 y and enters a lytic cycle in which numerous lytic mRNAs and proteins are produced, culminating in in

159 eafter referred to as phages) enter either a lytic or a lysogenic cycle.

160 ence is dependent upon infection mode, be it lytic or lysogenic.

161 target genes and by interacting with the EBV lytic origin of replication.

162 ion ensures that the P(LIT) promoter and the lytic P(L) and P(R) promoters are synchronously activate

163 VI indicates that in the absence of VII the lytic peptide is trapped inside the hexon cavity, and cl

164 Recently, the well-studied lytic peptide melittin has formed the basis for the deve

165 tion as a new strategy to transform membrane-lytic peptides (MLPs) into cytocompatible intracellular

166 The ability of lytic peptides to engage with cell membranes has been ex

167 PLEs parasitize the lytic phage ICP1, excising from the bacterial chromosome

168 mal island-like element (PLE), sabotages the lytic phage ICP1, which triggers PLE excision from the b

169 acterium Synechococcus was challenged with a lytic phage under nitrogen (N) or phosphorus (P) limitat

170 clusters corresponding to both temperate and lytic phages and representing novel genera with a large

171 When lytic phages encountered motile host bacteria in our exp

172 We isolated eight lytic phages that target the core microbiota member Bifi

173 However, while HCMV enters the lytic phase and produces virus in salivary epithelial ce

174 This lytic phase is also essential for EBV to cause infectiou

175 le.IMPORTANCE Transition from latency to the lytic phase is necessary for herpesvirus-mediated pathol

176 factors regulating the KSHV latent phase-to-lytic phase switch can provide insights into the pathoge

177 The Epstein-Barr virus (EBV) lytic phase, like those of all herpesviruses, proceeds v

178 Since many of these diseases rely on EBV's lytic phase, we developed a high-throughput assay that i

179 inflammasomes to activate its replicative or lytic phase.

180 of the virus to transit from latency to the lytic phase.

181 ically switch from a latent to a replicative/lytic phase.

182 f interaction-altered vIL-6 variants and the lytic phenotypes of recombinant viruses expressing selec

183 n, with a drastic reduction in the number of lytic plaques in MAL-silenced cells.

184 Lytic polysaccharide monooxygenase (LPMO) and copper bin

185 esembles copper centers in CopC proteins and lytic polysaccharide monooxygenase (LPMO) enzymes.

186 at Jd1381 contains an N-terminal family AA10 lytic polysaccharide monooxygenase (LPMO), a family 5 ch

187 Lytic polysaccharide monooxygenases (LPMOs) are a recent

188 Lytic polysaccharide monooxygenases (LPMOs) are microbia

189 Lytic polysaccharide monooxygenases (LPMOs) have a uniqu

190 Lytic polysaccharide monooxygenases (LPMOs) have been pr

191 e cell membrane in a linear order, forming a lytic pore and inducing activation of the NLRP3 inflamma

192 t B and subunit A, thus forming a tripartite lytic pore that is permissive to efflux of potassium.

193 L) and alpha-toxin are exotoxins that create lytic pores in the host cell membrane.

194 which directly correlates to a reduction in lytic potential but only minimally affects cell entry.

195 ells, and downregulation of cytotoxic T cell lytic potential.

196 In these diseases, lytic (productive) replication, in addition to viral lat

197 itches between four viral genome latency and lytic programmes to navigate the B-cell compartment and

198 e detection, EBV switches between latent and lytic programs.

199 that binds to TATT motifs unique to EBV late lytic promoters.

200 dronized side chains to enhance the membrane lytic property.

201 ged stimulation over days to achieve maximal lytic protein expression and cytotoxic capacity.IMPORTAN

202 hey displayed similarly delayed kinetics for lytic protein expression, with significant increases occ

203 of VI, and is responsible for releasing the lytic protein from the hexon cavity during entry and ste

204 These lytic proteins may also contribute to tumorigenesis.

205 IV Tat has been found to synergize with KSHV lytic proteins to induce angiogenesis.

206 l role for two of the core RIGs in efficient lytic reactivation and replication, highlighting their s

207 tion and sustained ERK-RSK activation during lytic reactivation and subsequently results in a signifi

208 of antivirals as suppressive therapy for EBV lytic reactivation may aid efforts aimed at disease prev

209 effects on viral gene expression 24 h after lytic reactivation of wild-type virus.

210 Lytic reactivation plays a central role in the developme

211 -infected endothelial cells undergoing viral lytic reactivation remain unclear.

212 in, a nuclear protein expressed early during lytic reactivation that binds to viral RNAs and enhances

213 posi sarcoma tumor cells undergo spontaneous lytic reactivation to produce viral progeny for infectio

214 ases with plasma cell differentiation, a key lytic reactivation trigger.

215 particularly effective as inhibitors of EBV lytic reactivation, and that clinical studies to address

216 LINC00313, an lncRNA upregulated during KSHV lytic reactivation, as a novel HIV Tat-interacting lncRN

217 On lytic reactivation, BORF2-null viruses were susceptible

218 ified a network of host factors that repress lytic reactivation, centered on the transcription factor

219 nses against infected human cells undergoing lytic reactivation.

220 ent to disrupt KSHV latency and induce viral lytic reactivation.

221 Here, we demonstrate that NMD restricts KSHV lytic reactivation.

222 ic state, turn expression of the replication/lytic/reactivation switch protein on to enter the replic

223 Such non-lytic release of beta-coronaviruses results in lysosome

224 induction event triggers the production and lytic release of free viruses.

225 Like other herpesviruses, it has latent and lytic repertoires.

226 posi's sarcoma-associated herpesvirus (KSHV) lytic replication and directly activate viral interleuki

227 hypoxia-induced, or chemically induced KSHV lytic replication and enhances the inhibitory effect of

228 s 1 to 4), all of which are expressed during lytic replication and inhibit a variety of antiviral sig

229 by systemic inflammation caused, in part, by lytic replication and overproduction of KSHV vIL-6 in XB

230 hances the inhibitory effect of rapamycin on lytic replication and sensitivity to rapamycin in lytic

231 MYC bound the EBV genome origin of lytic replication and suppressed its looping to the lyti

232 e both positive and negative effects on KSHV lytic replication as well as effects on the host cell th

233 nvestigated the activity of APC/C during the lytic replication cycle of KSHV and found that, in contr

234 th impair the activity of APC/C during their lytic replication cycle through virus-encoded protein ki

235 deregulates the activity of APC/C during the lytic replication cycle.

236 The EBV vPIC requires an origin of lytic replication in cis, implying that the vPIC mediate

237 capsid maturation into the cytoplasm during lytic replication in infected cells.

238 of KSHV's close relatives EBV and HCMV, KSHV lytic replication occurs while the APC/C is active.

239 The transition into the lytic replication stage, at which virus is produced, is

240 EBV undergoes latency and lytic replication stages in its life cycle.

241 egulating the transition from latency to the lytic replication stages of EBV infection.

242 revalent betaherpesviruses with intermittent lytic replication that can be pathogenic in immunocompro

243 ely independently of USP7 interaction, while lytic replication was inhibited by vIRF-2, in part or in

244 nteracted with ORF50, the viral initiator of lytic replication, and bound to the KSHV genome in the p

245 e epigenetic silencing of their genes during lytic replication, and they can also take advantage of e

246 ause of the strong propensity of LECs toward lytic replication, LECs maintained virus as a population

247 y responsible for MIE gene expression during lytic replication, remains silent during reactivation.

248 st, KSHV-infected LECs predominantly entered lytic replication, underwent cell lysis, and released ne

249 eed a way to efficiently reactivate EBV into lytic replication.

250 ittently produces infectious virions through lytic replication.

251 kely contributes to the progression of viral lytic replication.

252 l of dTTP for viral replication and enhances lytic replication.

253 cation and transcription activator (RTA) and lytic replication.

254 RSK activation plays a critical role in KSHV lytic replication.

255 nds and recruits XPB to EBV promoters during lytic replication.

256 the production of dTTP and is important for lytic replication.

257 Periodic activation into the lytic/replicative phase allows such viruses to propagate

258 Influenza A virus (IAV) is a lytic RNA virus that triggers receptor-interacting serin

259 In the marine environment, only a few lytic single-stranded DNA (ssDNA) phages have been isola

260 viral transmission prior to their canonical lytic spread of virus.

261 In contrast, the lytic ssDNA and ssRNA phages have a single lysis protein

262 temperate phase in healthy hosts to a lethal lytic stage as host cells become physiologically stresse

263 between Si stress and the early, active and lytic stages of viral infection.

264 iruses) do so by switching from fast-growing lytic states to slow-growing latent states.

265 These genes regulate lytic susceptibility to various degrees in latently infe

266 These cellular genes contribute to lytic susceptibility to various degrees.

267 moter of Epstein-Barr virus's (EBV's) latent-lytic switch BZLF1 gene, Zp, inducing viral reactivation

268 ential against KSHV.IMPORTANCE The latent-to-lytic switch in KSHV infection is one of the critical ev

269 erminated, expression of the virally encoded lytic switch protein needs to be sustained.

270 d that a viral kinase activated by the viral lytic switch protein partners with a cellular kinase to

271 ed only when expression of the EBV latent-to-lytic switch protein ZEBRA is turned on.

272 lular kinase to deactivate a silencer of the lytic switch protein, thereby providing a positive feedb

273 d ahead of expression of the viral latent-to-lytic switch protein.

274 rments in early activation events in NK cell lytic synapse formation.

275 As predicted, delivery of lytic toxins is highly effective, whereas nonlytic toxin

276 ority of T6SS-wielding species do indeed use lytic toxins, indicative of a general principle underlyi

277 indicates that CTCF primarily activates KSHV lytic transcription, whereas cohesin has primarily inhib

278 cts, with cohesin primarily restricting KSHV lytic transcription.

279 s study reports the profiling of the dynamic lytic transcriptome of BoHV-1 using two long-read sequen

280 relates with the reduced expression of viral lytic transcripts during latency and impaired induced re

281 A few years ago, the conserved lytic transglycosylase MltG was identified as a potentia

282 Lytic transglycosylases (LT) are enzymes involved in pep

283 ell wall-modifying enzymes such as bacterial lytic transglycosylases (LTs) and expansins present in b

284 strate that the Rpfs function as endo-acting lytic transglycosylases, cleaving within the peptidoglyc

285 the activity of amidases, deacetylases, and lytic transglycosylases.

286 lear (PAN) RNA, which promotes the latent to lytic transition by repressing host genes involved in an

287 ot every latently infected cell exposed to a lytic trigger turns on the expression of ZEBRA, resultin

288 ascent transcriptome following exposure to a lytic trigger, we find that several cellular genes are t

289 r virus (EBV) indicate that upon exposure to lytic triggers, certain cellular genes are transcription

290 lation of latently infected cells respond to lytic triggers, resulting in subpopulations of responsiv

291 lls that respond to mechanistically distinct lytic triggers.

292 cells and emphasize the stochastic nature of lytic versus latency decision of HSV-1 in nonneuronal ce

293 metabolic reprogramming of host cells during lytic viral infection alters the flow of energy and nutr

294 An agent that upregulates lytic viral protein expression but that does not lead to

295 pe I interferon response in cells undergoing lytic virus replication.

296 between unicellular cyanobacteria and their lytic viruses (cyanophages) in the oceans is thought to

297 rimental approach for effective selection of lytic viruses for therapy, we have fully characterized t

298 bacteriophage will require mixes of diverse lytic viruses targeting relevant cps variants and allowi

299 Influenza A viruses (IAV) are lytic viruses that have recently been found to activate

300 y involved in the transition from latency to lytic VZV infection.