ライフサイエンスコーパス: viral

1 hout HCC (n = 309: 39% HBV, 39% HCV, 22% non-viral).

2 Stem-loop A (SLA), a part of the viral 5' untranslated region (UTR), is critical for the

3 ty of a novel combinatorial adeno-associated viral (AAV) gene therapy by expressing DAT selectively i

4 Viral adaptation and tissue response were assessed throu

5 form a transient intermediate that pulls the viral and cell membranes together as two heptad-repeat r

6 sted a tightly synchronized diel coupling of viral and cellular replication cycles in both photoautot

7 acturing of cytoreagents.Current widely used viral and electroporation methods for creating therapeut

8 hesis of dsRNA precursors of highly abundant viral and host siRNAs by the cellular RdRPs.

9 Here we compare viral and human promoter sequences and expression to tes

10 hematophagous insects that harbor bacterial, viral and parasitic agents like Bartonella sp., Phlebovi

11 with HCC (n = 102: 32% HBV, 54% HCV, 14% non-viral) and without HCC (n = 309: 39% HBV, 39% HCV, 22% n

12 induced-dendritic cells loaded with the pp65 viral antigen (iDCpp65) exhibited a faster development a

13 We identified viral antigen in multiple organ tissues where it was not

14 Given the well-documented viral archeology of human immunodeficiency virus (HIV) e

15 ring structure dynamics and heterogeneity of viral assemblies have revealed important insights into g

16 of HCV-infected cells to daclatasvir reduced viral assembly and induced clustering of structural prot

17 ional roles in the replication cycle such as viral assembly.

18 ell which maximizes its protection against a viral attack.

19 s of proinflammatory cytokines, resulting in viral attenuation in vivo This might represent an adapta

20 demonstrate that PGC1alpha alone can support viral biosynthesis independently of the expression of ad

21 ynthesis, it mediates a dramatic increase in viral capsid production and robust viral replication.

22 Viral capsids are a prototypical example, where coat pro

23 tures, ranging from self-assembling cages to viral capsids.

24 c vaccine.IMPORTANCE RSV and HPIV1 are major viral causes of acute pediatric respiratory illness for

25 orresponds to defects in the accumulation of viral cDNA in the nucleus.

26 omprehensive EBV regulome encompassing 1,992 viral/cellular genes and enhancers.

27 gered by ligand functions to protect against viral challenge, which probably accounts for its selecti

28 tion and lung viral reduction against lethal viral challenge.

29 short time (HTST) treatment, a commonly used viral clearance upstream strategy.

30 CD8(+) T cells are important for viral clearance, and although often ineffective in neona

31 iciency enhanced T cell responses to promote viral clearance, but increased IL-22 in vivo decreased T

32 te of recurrent infection and participate in viral clearance.

33 his defect, we tracked the fates of multiple viral components in infected cells.

34 Viral components target subcellular organelles to access

35 oans, including the selective elimination of viral components.

36 Viral concentrates (VCs), containing bioinformative DNA

37 Viral consensus sequences can be achieved in 1-2 d by st

38 HCV adaptive immunity, may contribute to HCV viral control following RG-101 therapy.

39 Findings confirm that viral crAssphage qPCR assays perform at a similar level

40 Human cytomegalovirus encodes 2 viral cytokines that are orthologs of human cellular int

41 After viral delivery of Cre recombinase to hepatocytes in vivo

42 The safe, non-viral delivery of CRISPR/Cas components would greatly im

43 The viral determinants of Lv2 susceptibility mapped to the H

44 s, infectious bovine rhinotracheitis, bovine viral diarrhea virus, Mannheimia haemolytica or Mycoplas

45 viruses are recognized as a leading cause of viral diarrhea worldwide in children, immunocompromised

46 Anti-HMGB1 mitigated both early-life viral disease and asthma-like features, highlighting HMG

47 et for therapeutic intervention against this viral disease.

48 information to facilitate the management of viral diseases.IMPORTANCE Tomato is an important source

49 in primary infection and greater changes in viral diversity generated more efficient antibodies.

50 ve DNA and proteins, have been used to study viral diversity, viral metagenomics and virus-host inter

51 significant roles in the replication of the viral DNA and the production of progeny virions in HEK29

52 -integration complex (PIC) that contains the viral DNA as well as several cellular and HIV proteins,

53 hi2-1 assembled a compartment that separated viral DNA from the cytoplasm.

54 hine, the large terminase protein, processes viral DNA into constituent units utilizing its nuclease

55 es formed in the nucleus are locations where viral DNA is copied to support virus persistence and amp

56 We have also observed that newly replicated viral DNA is not associated with cellular histones.

57 C) 3 proteins have been identified as potent viral DNA mutators and have broad antiviral activity.

58 nsfection of a duplex HBoV1 genome initiates viral DNA replication and produces progeny virions that

59 localization and BFL-1 transcription by the viral EBNA3A protein.

60 Here we review the pro- and anti-viral effects of methyl-6-adenosine in distinct viral li

61 dicate that sorafenib causes a disruption in viral egress by targeting VCP and the secretory pathway,

62 of severe hand, foot, and mouth disease and viral encephalitis in children across the Asia-Pacific r

63 We found that strong viral enhancers/promoters placed in foamy viral vectors

64 the endoplasmic reticulum that could impact viral entry and replication.

65 Viral entry in CIN85-depleted cells was only moderately

66 cy virus (SIV) envelope spike (Env) mediates viral entry into host cells.

67 in an N-linked glycosylation site within the viral envelope (E) protein, whereas many isolates of the

68 equently gained through analyses of isolated viral envelope antigens, host CD4 receptors, and cognate

69 rime repair exonuclease 1 (TREX1) is an anti-viral enzyme that cleaves nucleic acids in the cytosol,

70 rs, such as B lymphocytes, gammaHVs exist as viral episomes and express few viral genes.

71 rget sequence cause immune failure and allow viral escape.

72 tivation is selected for by both somatic and viral events during NPC pathogenesis.

73 This approach defines potential pathways of viral evolution, beyond those already observed in natura

74 us virus 1 (KRCV-1) and assessed within-host viral evolution.

75 ignaling pathway inhibit activation of lytic viral expression but do not inhibit several other lytic

76 hose analysis might illuminate mechanisms of viral extinction.

77 erfere with the conformational change in the viral F protein that is required to elicit membrane fusi

78 authors show that a chemical inhibitor to a viral fusion protein is effective in reducing viral titr

79 Paramyxovirus viral fusion proteins (F) insert into the target cell me

80 omplementarity to the mRNA for the important viral gene activator ICP0, inhibition of ICP0 expression

81 e an important site of HCMV latency, and one viral gene expressed by latently infected myeloid cells

82 the inhibition of early and immediate early viral gene expression.

83 and it blocks repressor complexes to enable viral gene transcription.

84 aHVs exist as viral episomes and express few viral genes.

85 fenses consisting of RNAi-based silencing of viral genes.

86 variation in this phenotype attributable to viral genetic variation.

87 Viral genome analysis indicates unusually low CpG dinucl

88 ultifunctional protein that encapsidates the viral genome and functions as an adapter between the vir

89 ggest that some L1 protein may accompany the viral genome beyond the endosomal compartment.

90 g the virus to an F-pilus and delivering the viral genome into the host during infection, but how the

91 capsid at a nuclear pore, and release of the viral genome into the nucleus.

92 ges the NPC and what triggers release of the viral genome into the nucleus.

93 to naive cells, it is not clear whether the viral genome is also transferred via this mechanism and

94 the structural and functional features of a viral genome maturation complex, an essential intermedia

95 The specific infectivities (PFU per viral genome) of HSV(chol) and HSV(des) were similar, su

96 II and preventing silenced chromatin on the viral genome.

97 some L1 protein remains associated with the viral genome.

98 a of (i) archaeal, bacterial, eukaryotic and viral genomes from cultured organisms, (ii) single cell

99 on multiplex PCR for targeted enrichment of viral genomes from samples containing as few as 50 genom

100 bserved in ISAV HE are not seen in any other viral glycoprotein.

101 Consistent with these findings, viral glycoproteins fail to mature in SPCA1-deficient ce

102 Our results suggest that viral glycoproteins induce a strong innate antiviral res

103 metry analysis, we found that VLVs contained viral glycoproteins required for cellular entry, as well

104 different phylogenetic methods, we analyzed viral gp120 sequences obtained from extensive longitudin

105 nderstand the relationship between these two viral groups.

106 HBV is a major cause of viral hepatitis, liver cirrhosis, and hepatocellular car

107 r other diseases, including tuberculosis and viral hepatitis.

108 and MAVS, in the presence or absence of two viral IFN antagonistic proteins.

109 vironmental factors that promote more severe viral illnesses might lead to new strategies for the pre

110 pha/beta) are critical mediators of any anti-viral immune response and IFNbeta has been implicated in

111 r cells and serves as an innate link between viral infection and B cell immunity.

112 t that an exaggerated interferon response to viral infection by airway epithelial cells may be a mech

113 ytes sequentially throughout the course of a viral infection in vivo.

114 irect causative link was established linking viral infection to herbicide resistance, transcriptome s

115 ough activating the ER stress pathway during viral infection.

116 H) cells, but not TH1 effectors, elicited by viral infection.

117 ory origins of T cell dysfunction in chronic viral infection.

118 i), suggesting a unique neuronal response to viral infection.

119 ry have long been an effective treatment for viral infections because of the strong D-stereoselectivi

120 Many viral infections cause host shutoff, a state in which ho

121 Viral infections have been proposed to elicit pathologic

122 Viral infections kill millions yearly.

123 Influenza viral infections often lead to increased mortality in ol

124 the host transcriptional response to various viral infections provides a wealth of data but utilizati

125 Viral infections typically used in other lab animals to

126 To treat patients suffering from such viral infections, broadly reactive and highly sensitive

127 imary isolates of HIV-1 to the inhibition of viral infectivity by IFITMs.

128 -1 Vif, interfered with HIV-1 production and viral infectivity even in the absence of APOBEC3.

129 Despite success in viral inhibition and CD4 T cell recovery by highly activ

130 ases in the plasma drug concentration of the viral integrase inhibitor dolutegravir.

131 verified experiments show that more than 90% viral integration sequences detected by seeksv are true.

132 The gene ectopic viral integration site 1 (EVI) and its variant myelodysp

133 te gene expression in late events during the viral life cycle, RNA-Seq was carried out on triplicate

134 encode only four proteins to accomplish the viral life cycle, so each arenavirus protein likely play

135 ssembly, cell entry, and other stages of the viral life cycle.

136 al effects of methyl-6-adenosine in distinct viral life cycles, the role of 2' O-methyl modifications

137 tegorized as nonmelanoma skin cancer (NMSC), viral-linked and "other" cancers.

138 Viral-linked cancer had the largest inpatient and outpat

139 not have cirrhosis, and have a pretreatment viral load <6,000,000 IU/mL.

140 Although WHO recommends viral load (VL) monitoring for those on antiretroviral t

141 hedding among women with undetectable plasma viral load (VL).

142 e breastfeeding; ART treatments can suppress viral load and are key to preventing transmission to the

143 ody levels, ASCs and HAI titers with reduced viral load and inflammatory responses in the cVLP group.

144 % of those on treatment to have a suppressed viral load by 2020, with each individual target reaching

145 Effective viral load monitoring and point-of-care resistance tests

146 Landon Myer and colleagues discuss viral load monitoring for pregnant HIV-positive women an

147 ange, 2.8-16.8 months) in this setting where viral load monitoring was available.

148 enrolment, the proportion who died or had a viral load of 400 copies/mL or higher at 12 months post-

149 We monitored the viral load of MJNV RNA in various tissues of shrews, whi

150 nd patients, which will be vital in ensuring viral load tests are appropriately used to improve the q

151 HHV-6 shedding rate and viral load were similar between children with primary or

152 Viral serology, viral load, and liver biochemistry were performed at reg

153 must quantify the heritability of set-point viral load, which is the fraction of variation in this p

154 and drives CD4 decline independently of the viral load.

155 spiratory symptoms, lung function, and nasal viral load.

156 atients with CMV pneumonia had higher median viral loads (3.9 log10 IU/mL; interquartile range [IQR],

157 itis B virus and hepatitis delta virus (HDV) viral loads (VL) during tenofovir-containing antiretrovi

158 ce the nucleoside analogue entecavir reduced viral loads and decreased liver inflammation.

159 ficient for the virus to evolve intermediate viral loads consistent with maximising transmission, as

160 Patients with higher peripheral blood viral loads in primary infection and greater changes in

161 ssion, as is observed, and not the very high viral loads that previous models have predicted, an effe

162 ome and postulated the existence of multiple viral long noncoding RNAs (lncRNAs).

163 of Vpr, the transcriptional activity of the viral long terminal repeat (LTR) from Vpr-deficient prov

164 bout whether it plays any role in regulating viral lytic reactivation.

165 However, the structure of the viral major capsid protein, elucidated at near-atomic re

166 d to the site of cell-cell contact where the viral material is efficiently translocated to target cel

167 ic protein surfaces of the inner face of the viral matrix and at the Cyclophilin A binding loop of th

168 onses, suggesting the involvement of complex viral mechanisms of immune evasion.

169 We used viral-mediated gene transfer to block the transcription

170 ld, and the association of EFC proteins with viral membranes.IMPORTANCE Poxviruses comprise a large f

171 ns, have been used to study viral diversity, viral metagenomics and virus-host interactions in natura

172 Ever since miR-H2's discovery as a viral microRNA bearing complete sequence complementarity

173 megalovirus signal-anchored protein known as viral mitochondria-localized inhibitor of apoptosis (vMI

174 rray of glycans that coat the surface of the viral molecule.

175 The association of viral movement proteins with microtubules facilitates th

176 to minimize the development of resistance by viral mutations.

177 crocycle threading until they are removed by viral neuraminidase.

178 The viral nonstructural 5A protein (NS5A) is the target for

179 resent during different stages of infection (viral nonstructural protein 1 and immunoglobulin M) has

180 The viral nucleocapsid, which is minimally composed of the p

181 mples positive for HPV-DNA were screened for viral oncoprotein expression using western blot and dot

182 utaneous candidiasis disease might also have viral or intracellular pathogen infections.

183 s shown that TNTs facilitate the exchange of viral or prion proteins from infected to naive cells, it

184 ections stemming from bacterial, fungal, and viral origins.

185 a public health emergency and designated the viral outbreak and related microcephaly clusters as a lo

186 s on the composition and organization of the viral particle.IMPORTANCE Tailless viruses of the family

187 eir transcriptional functions, work to drive viral pathogenesis.

188 e function will provide greater insight into viral pathogenicity and antiviral responses.

189 It is well established that viral pathogens exploit PD to spread between cells, but

190 ct to identify inhibitors for the many other viral pathogens of significance that require IMPalpha/be

191 s in the modulation of host defences against viral pathogens.

192 e qualitative detection of model amphipathic viral peptide on a screen-printed electrode.

193 re limited and immunological determinants of viral persistence remain largely unexplored.

194 n of HIV-1-infected cells may play a role in viral persistence, but little is known about the kinetic

195 tifying the ampullae as the primary sites of viral persistence, combined with the fact that persisten

196 clinical sensitivity (100%) but, because of viral persistence, low specificity (76%).

197 However, DVGs can also facilitate viral persistence.

198 HIV-1 pathogenesis and the evolution of the viral population, we must quantify the heritability of s

199 Consequently, we hypothesize that viral products expressed during latency cooperate with n

200 s of HSV-1 DNA replication and production of viral progeny in SCG neurons, but no significant differe

201 ion from latency, and they stimulate certain viral promoters and productive infection.

202 Additionally, rather than relying on natural viral properties, efforts are underway to engineer virus

203 Ebola viral protein 30 (eVP30) plays a critical role in EBOV t

204 luence of posttranslational modifications on viral protein function and provides additional insight i

205 anslation mechanism might selectively impact viral protein synthesis, suggesting that an NP-mediated

206 During T cell VS formation, viral proteins are actively recruited to the site of cel

207 Three related latency-associated viral proteins EBNA3A, EBNA3B, and EBNA3C are transcript

208 As our detailed knowledge of these viral proteins improves, we will undoubtedly uncover how

209 tter understanding of the roles of different viral proteins in coordinating the intercellular movemen

210 at interactions of the N domain with cognate viral proteins may be critical for virion assembly.IMPOR

211 standing the molecular mechanism(s) by which viral proteins such as HIV-1 Transactivator of Transcrip

212 ll (Pawluk et al. and Rauch et al.) identify viral proteins that suppress Cas9 and may function like

213 y sheds light on a conserved strategy by the viral proteins Vpx and Vpr to recruit host CRL4 (DCAF1)

214 ive capacity, is predictive of expression of viral proteins, and downregulating Ki67 leads to concurr

215 m ClO2-labile to ClO2-stable residues in the viral proteins, which likely increased the chemical stab

216 ads to concurrent decreases in expression of viral proteins.

217 nal activities have been attributed to these viral proteins.

218 rfere with the expression of immuno-dominant viral proteins.

219 sults provide a functional view of the Bam35 viral proteome, with a focus on the composition and orga

220 These data suggest that viral RCs can be marked and antagonized by a universal i

221 r frequency, 16S abundance, prokaryotic- and viral-read abundance.

222 s with episodes of cerebrospinal fluid (CSF) viral rebound or sustained plasma and CSF viremia during

223 on, they showed superior protection and lung viral reduction against lethal viral challenge.

224 Viral replication and cellular responses were measured u

225 bility of the host immune system to suppress viral replication and the ability of a virus to countera

226 increases survival of bees while decreasing viral replication following infection with FHV, whereas

227 he fact that persistence involves continuous viral replication in fibrocytes (possibly including tiss

228 Antiretroviral therapy (ART) suppresses viral replication in HIV-infected individuals but does n

229 ealing a role for NS1 and characteristics of viral replication in the URT that were associated with a

230 of antibody titer has been shown to enhance viral replication in vitro and severe disease in animal

231 munity can control both early and persistent viral replication independently of adaptive immune effec

232 Because cellular resistance to viral replication is marked by expression of antiviral r

233 Interestingly, the transient activation of viral replication led to HIV-1 reservoir reduction after

234 ded DNA (ssDNA) genome to the nucleus, where viral replication occurs.

235 D), there was no direct impact of the TBD on viral replication or virulence in mice.

236 n coordinating the intercellular movement of viral replication vesicles.

237 d capable of expressing reporter genes while viral replication was blocked.

238 tant roles in metabolism, tumor progression, viral replication, and skin barrier formation.

239 duction in DENV-infected cells and decreases viral replication.

240 thesis was also observed as a sign of active viral replication.

241 ducing gammadelta T cells, without affecting viral replication.

242 tolbutamide decreases survival and increases viral replication.

243 crease in viral capsid production and robust viral replication.

244 ndicating that this pathway is important for viral replication.

245 pes; furthermore, we propose that the poorer viral replicative capacity of subtypes A and C may parad

246 sing strategy to reduce if not eradicate the viral reservoir.

247 nge to HIV eradication is the elimination of viral reservoirs in germinal center (GC) T follicular he

248 g) assay also allows parallel phenotyping of viral reservoirs, including reactivated latent reservoir

249 Atopy and viral respiratory tract infections synergistically promo

250 The viral restriction factor SERINC5 inhibits HIV-1 infectio

251 hibited by human DNA polymerases relative to viral reverse transcriptases.

252 at the specific interactions between Gag and viral RNA are required for the enhancement of particle p

253 ch is the enzyme responsible for copying the viral RNA genome.

254 ' deletions greatly reduced the synthesis of viral RNA in vitro, which was detected only for the 7- a

255 iency of genome packaging when a packageable viral RNA is not required for virus assembly is currentl

256 Experimentally, we could detect small viral RNA polymerase molecules, distributed randomly amo

257 onse, and antiviral mechanisms affecting the viral RNA sequence and/or an RNA modification act on vir

258 The mean levels of influenza viral RNA shedding in asymptomatic and paucisymptomatic

259 ur previous hypothesis that specific dimeric viral RNA-Gag interactions are the nucleation event of i

260 Many viral RNAs are modified by methylation of the N(6) posit

261 danger of self-sustained epidemics from any viral sequence data.

262 Finally, viral sequences corresponding to anelloviruses, human pe

263 tocol for accurate detection and grouping of viral sequences from microbiome samples.

264 By assigning unique tags to individual viral sequences, we accurately reconstructed HBV haploty

265 Viral serology, viral load, and liver biochemistry were

266 The presence of influenza viral shedding in patients with influenza who have very

267 d mild to moderate diarrhea, lower titers of viral shedding, and no mortality, whereas the icPC22A vi

268 infection in CD4(+) T could be inhibited by viral-specific CD8(+) T cells, a result with implication

269 Thus, the viral SPI-1 protein and the host IRF2, FAM111A, and RFC

270 o mature in SPCA1-deficient cells preventing viral spread, which is evident even in cells with partia

271 or studies associating Merkel cell carcinoma viral status with prognosis have inconsistent findings.

272 cytokine responses to specific microbial and viral stimuli are associated with the development of all

273 es with limited potency against heterologous viral strains and genotypes.

274 ided insights into their precursors, and the viral strains that engage them, as well as defined how s

275 increased antiviral activity when exposed to viral strains with differential abilities to downmodulat

276 ve naturally relied extensively on available viral structural information.

277 Rates of HIV viral suppression and adherence to ART were similar in t

278 we identified 53 national care continua with viral suppression estimates representing 19.7 million (5

279 h 24 weeks and 48 weeks without compromising viral suppression or increasing toxic effects.

280 ns met primary criteria for comparability in viral suppression relative to the oral comparator group.

281 ng the 90-90-90 target for "on ART" and for "viral suppression," respectively.

282 rhagic fever (CCHF) is a widely distributed, viral, tickborne disease.

283 ng NAI drug efficacy using only the observed viral titer decay rates seen in patients.

284 iral fusion protein is effective in reducing viral titre and ameliorating infection in rodents and ne

285 In dual retrograde viral tracing and c-Fos immunostaining experiments, we f

286 ng CD4+ T-cell, as indicated by an increased viral transcription rate in these cells.

287 peptides therefore represent a new family of viral transduction enhancers for potential use in gene t

288 verse viruses, it is not feasible to build a viral tree of life using traditional phylogenetic method

289 , the study demonstrates the efficacy of non-viral TUS-based hSef-b gene delivery approach for the tr

290 tcome was the number of laboratory-confirmed viral upper respiratory tract infections based on parent

291 nses in the human host; forcing selection of viral variants that escape cellular and antibody (Ab)-me

292 Tbx20, using a cardiotropic adeno-associated viral vector 9.

293 PIV5 is a promising live viral vector and has been used to develop vaccines.

294 achment for the delivery of adeno-associated viral vector encoding Rab Escort Protein 1 is described

295 An adeno-associated viral vector was also used to reconstitute ORMDL3 expres

296 we used local injection of adeno-associated viral vectors (AAVs) encoding ligand-specific antagonist

297 so achieved by combining R21 with TRAP-based viral vectors and protective efficacy was significantly

298 ng viral enhancers/promoters placed in foamy viral vectors caused extremely low immortalization of pr

299 s for transgene induction involve the use of viral vectors prone to silencing and insertional mutagen

300 lead to new strategies for the prevention of viral wheezing illnesses and perhaps reduce the subseque