ライフサイエンスコーパス: proviral

1 The proviral action of PLK1 is associated with the biogenesi

2 pendent pathway in order to help promote the proviral activation and polarization of infected monocyt

3 ze DNA damage response pathways that possess proviral activities.

4 We map the proviral activity of ANP32 proteins to one region in par

5 We map the enhanced proviral activity of swine ANP32A to a pair of amino aci

6 Nearly full-length proviral amplification and sequencing (NFL-PAS) were per

7 Through nearly full-length proviral amplification and sequencing (NFL-PAS), we gene

8 FeLV proviral and antigen levels were also measured in 6 natu

9 n gammaherpesvirus infection, as it has both proviral and antiviral effects.

10 archers to identify evolutionarily conserved proviral and antiviral genes that function in nematodes

11 ly, we determined the expression of selected proviral and antiviral hsa-miRNAs in 242 transplant reci

12 e hCMV Towne strain, identifying a subset of proviral and antiviral hsa-miRNAs.

13 ATM is a unique host kinase that has both proviral and antiviral roles in the context of gammaherp

14 transcriptomics analyses, we identify three proviral and nine antiviral miRNAs that interact with HC

15 y significantly limits circulating levels of proviral and replication-competent HIV-1 and promotes co

16 as (Puma concolor) with FeLV and quantitated proviral and viral antigen loads.

17 The proviral and viral loads of the northern population were

18 Analyses of proviral and viral RNA levels demonstrate that PLVA fitn

19 A proviral burden of less than 10 copies per 1 million PBM

20 mmatory innate immune pathway resulting in a proviral cellular environment.

21 biosynthesis are specific and that PLK1 is a proviral cellular factor.

22 Simultaneous coexpression of proviral cellular factors with WW-domain protein partly

23 d SGS are not always sufficient to establish proviral clonality.

24 r used in this system is derived from an HIV proviral clone engineered to express two different fluor

25 ce, but this is obscured by the expansion of proviral clones.

26 ity and specificity, totally eliminating the proviral contamination.

27 ratory setting can be sensitive to low-level proviral contamination.

28 iral load (Rho = 0.3531; P = 0.0218) and the proviral copy number in the peripheral blood as an indir

29 axis as a predictor of plasma viral load and proviral copy number in the peripheral blood.

30 anthers and domestic cats had similar exFeLV proviral copy numbers, but Florida panther tissues have

31 method can be applied to both viral RNA and proviral DNA amplification templates, allowing genotypin

32 terized by sequencing near-full-length (NFL) proviral DNA and env from viral outgrowth assays (VOAs).

33 tion but before the formation of circular or proviral DNA and is independent of the previous characte

34 ly cell free HIV RNA, a DBS VL also measures proviral DNA as well as cell-associated RNA, potentially

35 e provirus landscape, we performed an intact proviral DNA assay (IPDA) and obtained 661 near-full-len

36 The intact proviral DNA assay (IPDA) is a novel approach to charact

37 antitative viral outgrowth assay, the intact proviral DNA assay, and total HIV gag DNA.

38 si and integrase, and negative by the intact proviral DNA assay, at 27 months.

39 maintains HIV-1 latency by associating with proviral DNA at the 5' long terminal repeat region, recr

40 ly, there was an inverse correlation between proviral DNA clone size and the probability of reactivat

41 vif/env-deficient luciferase-reporter HIV-1 proviral DNA clone.

42 The promoter in HIV type 1 (HIV-1) proviral DNA contains three sequential guanosines at the

43 IV variants exactly matched that of multiple proviral DNA copies from infected blood cells sampled be

44 g between 5' and 3' LTRs of integrated HIV-1 proviral DNA copies from latently infected human CD4+ T-

45 Retroviruses insert a proviral DNA copy into the host cell genome to produce n

46 ck down show increased HIV-1 replication and proviral DNA formation, while those overexpressing the f

47 requires clearance and removal of integrated proviral DNA from infected cells and tissues.

48 e and removal of fragments of the integrated proviral DNA from the genome of infected blood cells and

49 ent results in a reduction in the percent of proviral DNA in blood and tissues.

50 of infection and the reactivation of silent proviral DNA in latently infected cells.

51 red because the virus persists as integrated proviral DNA in long-lived cells despite years of suppre

52 Proviral DNA in lymph node CD4 T cells was also diminish

53 ood and also substantially reduced levels of proviral DNA in lymph nodes and gastrointestinal mucosa

54 These data suggest that intact proviral DNA in PBMC and LNMC during ART suppression is

55 day 3 blocked the emergence of viral RNA and proviral DNA in peripheral blood and also substantially

56 ome cases, clonal expansion is driven by HIV proviral DNA integrated into one of a handful of genes.

57 the tumors carry both somatic mutations and proviral DNA integrated into the tumor genome.

58 irus (ALV) induces tumors by integrating its proviral DNA into the chicken genome and altering the ex

59 he chain of events leading to integration of proviral DNA into the host genome.

60 ot CD4, correlated positively with post-cART proviral DNA levels (Spearman's R = 0.61, P = 0.0004) an

61 Acitretin also decreases proviral DNA levels in CD4(+) T cells from HIV-positive

62 nistration resulted in significantly reduced proviral DNA levels in PBMCs after 2 weeks and in lymph

63 in peripheral blood mononuclear cell (PBMC) proviral DNA levels was also measured over time in the E

64 eduction in cell-associated DNA load, intact proviral DNA levels, and in inducible SIV reservoir in l

65 blood mononuclear cell (PBMC) or lymph node proviral DNA levels.

66 eservoir size was quantified in terms of the proviral DNA loads as well as the levels of replication-

67 Residual proviral DNA may confound interpretation in virologicall

68 uman immunodeficiency virus (HIV)-integrated proviral DNA necessitates lifelong suppressive antiretro

69 envelope (env) genes could be amplified from proviral DNA or RNA derived from brain tissue of 12 indi

70 based on polymerase chain reaction to detect proviral DNA regardless of transcriptional status, but t

71 Most of the proviral DNA resides in CD4(+)T cells.

72 Although uracilated proviral DNA showed few mutations, the viral genomic RNA

73 increased sequencing of samples enriched for proviral DNA such as dried blood spots and increased use

74 cted cells through viral DNA integration and proviral DNA transcription.

75 We also analysed the presence of intact proviral DNA using multiplex ddPCR targeting the packagi

76 The long-range HIV genotyping from proviral DNA was successful in about 90% of 212 targeted

77 d viral outgrowth of cultured cells and from proviral DNA were amplified by PCR and sequenced for evi

78 onal "bursts" of nascent RNA from integrated proviral DNA, and concomitant HIV-1, HIV-2 transcription

79 reased APOBEC3G signature mutations in HIV-1 proviral DNA, and higher frequencies of TRAIL(+) NK cell

80 Donor and recipient HIV proviral DNA, and viral RNA from the viraemic timepoint

81 identical expanded sequences made up 54% of proviral DNA, and, as might be expected, the sequences o

82 rvoir showed limited overlap with integrated proviral DNA, most of which is known to represent defect

83 a viremia, replication-competent reservoirs, proviral DNA, or 2-long-terminal repeat circles, althoug

84 e astrocyte HIV reservoirs, without excising proviral DNA, will likely lead to detrimental neuropatho

85 tone marks and methylation of the integrated proviral DNA.

86 eplication, they do not eliminate integrated proviral DNA.

87 tion but before formation of circular DNA or proviral DNA.

88 ated Moloney murine leukemia virus (Mo-MuLV) proviral DNA.

89 ntiretroviral concentrations, HIV-1 RNA, and proviral DNA.

90 nome of infected cells in the form of latent proviral DNA.

91 vivo, resulting in elimination of integrated proviral DNA; virus is not detected in blood, lymphoid t

92 tus, completeness of the KoRV genome and the proviral (DNA) and viral (RNA) loads of 71 northern and

93 Proviral DNAs are formed normally but are then silenced

94 and used them to show that hypermutation of proviral DNAs from seven patients was induced by A3G, A3

95 encing and promote transcription of chimeric proviral DNAs.

96 proteins were observed, it appeared that the proviral effect of ROS overcame the antiviral effects of

97 To explain how autophagic flux could exert a proviral effect on the VZV infectious cycle, we postulat

98 irect a classically antiviral protein into a proviral effector.

99 m to the interferon response and demonstrate proviral effects for polyamines.

100 y, we investigated whether they also exerted proviral effects.

101 t remained unclear whether they also exerted proviral effects.

102 ification (MDA) of cellular DNA diluted to a proviral endpoint to obtain full-length proviral sequenc

103 l factors that unexpectedly act as important proviral enhancers during influenza virus infection.

104 ses are needed to investigate differences in proviral expansion and virus production following latenc

105 tic change was not associated with increased proviral expression in latently infected resting cells.

106 is a useful tool to characterize fractional proviral expression in single infected cells that persis

107 (CARD-SGS) method to investigate fractional proviral expression of HIV RNA (1.3-kb fragment of p6, p

108 toward centromeres, dampening the resulting proviral expression without affecting the overall effici

109 monstrate for the first time that SIRT1 is a proviral factor for MERS-CoV replication and that ORF4a

110 monstrate for the first time that SIRT1 is a proviral factor for MERS-CoV replication and that ORF4a

111 -CoV replication, suggesting that SIRT1 is a proviral factor for MERS-CoV.

112 Thus, TRAF2 is a proviral factor for VACV that plays a role in promoting

113 We have discovered that TRAF2 is a proviral factor in vaccinia virus replication in both He

114 ation of downstream effectors, including the proviral factor TiPARP, and to modulation of cytokine ge

115 s (DENV) infection requires cholesterol as a proviral factor, although statin treatment did not show

116 most previous studies established DHX9 as a proviral factor, we demonstrate that DHX9 may act as an

117 commonly found in two forms, the full-length proviral form, and the more numerous solo-LTR form, thou

118 hanged viral infectivity kinetics, decreased proviral formation, and preferentially decreased integra

119 etic analysis revealed that more than 80% of proviral forms lack the intron of the UBC promoter.

120 y apparent and easily distinguished from low proviral frequency, an advantage of the IPDA over standa

121 phatase SHP1, which plays a B cell-intrinsic proviral function during MHV68 infection.

122 ntrinsic mechanism by which HCV exploits the proviral function of CRABP1 to establish an efficient vi

123 This is also the first report of a proviral function of IFITMs in DNA virus replication.

124 or LepB lipid kinase to confirm the critical proviral function of PI(3)P phosphoinositide and the ear

125 In sum, we documented a proviral function of the pleiotropic factor RelA linked

126 rovide evidence that P-FAK interaction has a proviral function.

127 t abundant PE in subcellular membranes has a proviral function.

128 The proviral functions of Sac1 include manipulation of lipid

129 ping binding sites in CHIKV HVD and additive proviral functions.

130 ese reservoirs are thus needed to reactivate proviral gene expression in latently infected cells.

131 can stimulate T-cell activation that induces proviral gene expression in latently infected T cells.

132 and anvilone A (14) were found to induce HIV proviral gene expression similar to the control compound

133 The antisense strand of the HTLV-2 proviral genome also encodes a protein termed APH-2.

134 s that control the folding of this region of proviral genome by inducing/stabilizing G-quadruplex str

135 s a protein from the antisense strand of its proviral genome, the HTLV-1 basic leucine zipper factor

136 significantly higher fraction of intact SIV proviral genomes compared to ART-treated HIV-1 or HIV-2

137 unbiased method to amplify near-full-length proviral genomes from HIV-1-infected adults treated at d

138 by the frequency of G-to-A mutations in the proviral genomes in the contexts of A3G (GG-to-AG) and A

139 radication because transcriptionally dormant proviral genomes persist in long-lived reservoirs of res

140 Quiescent proviral genomes that persist during human immunodeficie

141 d over 30 complete or near complete viral or proviral genomes with diverse genome structure, genome s

142 s a conserved molecular pattern that directs proviral genomic transcripts to the piRNA biogenesis mac

143 e independent predictors of higher levels of proviral HIV DNA in blood.

144 equences were phylogenetically distinct from proviral HIV-1 DNA detected in circulating PBMCs before

145 he immune factors associated with changes in proviral HIV-1 DNA levels during treatment with the pote

146 The relative frequencies of X4-tropic proviral HIV-1 variants were determined by means of next

147 < 0.0001) and are positively correlated with proviral HIV-DNA copy numbers in peripheral blood mononu

148 IMPORTANCE DDX3X is a proviral host factor for HCV infection.

149 or capsid protein L2 and was identified as a proviral host factor required for HPV16 endocytosis into

150 viral protease and describe GPx8 as a novel proviral host factor targeted by the HCV NS3-4A protease

151 PLK1 is a proviral host factor that could be envisaged as a target

152 1 in CHIKV nsP3 HVD overlaps that of another proviral host factor, CD2AP.

153 C8 inhibits the function of eEF1A, a coopted proviral host factor.

154 In contrast, six of eight proviral hsa-miRNAs showed a decrease during viral decli

155 eron (IFN) alfa plus ribavirin decreases the proviral human immunodeficiency virus type 1 (HIV) DNA l

156 rpesviruses in vitro, suggesting that ATM is proviral in the context of infected cell cultures.

157 h RNAP II, and its level increases following proviral induction.

158 l frequency of latent, replication-competent proviral infection, we assessed the specific contributio

159 Pan proviral insertion site of Moloney murine leukemia (PIM)

160 The high expression of proviral insertion site of Moloney murine leukemia virus

161 in our knowledge of the mechanisms by which proviral integration and clonal expansion sustain the HI

162 plex promotes ALV integration activity, with proviral integration frequency varying directly with cel

163 While the extent of proviral integration in HIV-1-infected MDDCs was unaffec

164 on, after reverse transcription but prior to proviral integration into host DNA.

165 ted cells, proliferation is a consequence of proviral integration into host genes associated with cel

166 Surprisingly, PF74 markedly reduced proviral integration owing to inhibition of nuclear entr

167 Clones were confirmed by host-proviral integration site analysis.RESULTSHIV-1 genomic

168 expression of the NFkappaB-dependent kinase proviral integration site for Moloney murine leukemia vi

169 pro-oncogenic, serine-threonine kinase PIM1 (Proviral Integration site for Moloney murine leukemia vi

170 Reed-Sternberg cells overexpress oncogenic (proviral integration site for Moloney murine leukemia vi

171 rease the expression of the oncogenic kinase proviral integration site for Moloney-murine leukemia 1

172 , the Gfi1 locus is frequently found to be a proviral integration site in retrovirus-induced lymphoma

173 node and blood cells, and characterized the proviral integration sites in paired lymph node and bloo

174 ployed high-throughput sequencing to analyze proviral integration sites in these tumors.

175 Twenty-six unique proviral integration sites were mapped between 46 and 3,

176 cted cell populations with identical genomic proviral integration sites).

177 HIV reservoir as shown by the duplication of proviral integration sites.

178 of infected-cell proliferation and sites of proviral integration to HIV persistence.

179 titute a reserve supply of HIV-1 genomes for proviral integration.

180 log of HS38, with inhibitory activity toward proviral integrations of Moloney (PIM) virus 3 kinase bu

181 ing cure strategies. However, the persisting proviral landscape in ART-treated NHPs is uncharacterize

182 .IMPORTANCE There are limited data about the proviral landscape in children exhibiting long-term supp

183 ength sequencing to longitudinally study the proviral landscape of four subjects on ART to investigat

184 reservoir but does not profoundly affect the proviral landscape.

185 ical models illuminating the balance between proviral latency and activation in the target cell popul

186 Proviral latency is a major barrier to a cure for HIV.

187 HIV's fate decision between replication and proviral latency lacks self-cooperativity and determinis

188 s and that more effective means of reversing proviral latency will likely be required to deplete HIV-

189 model that cellular sterols are essential as proviral lipids during viral replication.

190 dependent suppression of mTORC1 activity for proviral lipophagy.IMPORTANCE Dengue virus alters host c

191 l load showed that females and patients with proviral load >50,000 copies/10(6) peripheral blood mono

192 Higher cerebrospinal fluid HTLV-1 proviral load (p = 0.01) was associated with thinner spi

193 stics of individuals with low or high HTLV-1 proviral load (pVL), symptomatic disease, and the impact

194 Blood was drawn for HTLV-1 serology and proviral load (PVL).

195 Correlations between proviral load and markers of active HIV production (ie,

196 ons there was a positive association between proviral load and neoplasia (P = 0.009).

197 during chronic infection, even after HTLV-1 proviral load has reached its set point, and we estimate

198 e measures of gait, quantification of HTLV-1 proviral load in peripheral blood mononuclear cells, and

199 Kaplan-Meier curves stratified by sex and proviral load showed that females and patients with prov

200 Lower proviral load was associated with undetectable 2-long te

201 PBMC proviral load was significantly lower in ET youth (media

202 ition of HIV-1 expression and a reduction in proviral load within macrophage cultures.

203 tion and promotes cell proliferation, a high proviral load, and persistence in vivo.

204 The 2 groups had a similar HTLV-1 proviral load, but there was a significant increase in c

205 ammatory disease is strongly correlated with proviral load, which in turn is correlated with the numb

206 tion of the TCR clonal expansion with HTLV-I proviral load.

207 ty of IFN-alpha14 to reduce both viremia and proviral loads in vivo suggests that it has strong poten

208 roduce greater reductions in HIV-1 viral and proviral loads than ART alone.

209 m than ARVs and has been shown to reduce HIV proviral loads, clinical trials are under way to test wh

210 o results in increased viral replication and proviral loads, suggesting that HBZ and APH-2 modulate t

211 gnificantly suppressed HIV-1 replication and proviral loads.

212 ct HIV-1 DNA in infant whole blood with high proviral loads.

213 also amplified, albeit more weakly than most proviral loci and with nondiscrete boundaries.

214 s, although the identities of the individual proviral loci contributing to this expression as well as

215 identify the boundaries of amplification for proviral loci.

216 This proviral locus does not produce piRNAs in undomesticated

217 ssion, suggesting that TiPARP functions in a proviral manner during MHV infection.

218 (BMP4) as a candidate endothelial-expressed proviral molecule.

219 tocellular response to ATRA creates either a proviral or an antiviral environment depending on its en

220 nsic mechanism by which ATRA exerts either a proviral or antiviral effect, depending on how it engage

221 Whether autophagy is proviral or antiviral for ZIKV is controversial and depe

222 NAi identified cellular proteins with either proviral or antiviral roles.

223 earest quantitative picture to date of HIV-1 proviral persistence on ART.

224 ollowing transfection of an HBoV1 infectious proviral plasmid and viral infection of polarized human

225 ng specificity on replication, we engineered proviral plasmids encoding diverse RTs within the backbo

226 fections in which autophagy constituents are proviral (poliovirus, dengue, and Zika), we developed a

227 vise our understanding of the composition of proviral populations and estimate the true reservoir siz

228 the impact of experimental interventions on proviral populations and their expression.

229 We characterized proviral populations in lymph nodes and peripheral blood

230 ed reverse transcription intermediates, with proviral products diagnostic of mismatch resolution mech

231 is recruited by Tat to the integrated HIV-1 proviral promoter in TNF-alpha signaling 2D10 T cells an

232 ment of epigenetic barriers inactivating the proviral promoter, and blockage of the assembly of the h

233 f CG and CHG sites in the promoter region of proviral PVCV decreased in aged plants, suggesting that

234 Transcripts and episomal DNAs derived from proviral PVCVs accumulated in aged plants, indicating th

235 We measured the proviral reservoir (CD4(+) T-cell-associated HIV-1 DNA)

236 T within the first 12 weeks of life showed a proviral reservoir 6-fold smaller than children initiati

237 suggest that a distinct configuration of the proviral reservoir represents a structural correlate of

238 e and as robust correlates of viral load and proviral reservoir size in PBMC.IMPORTANCE The detailed

239 y of HIV serostatus as a biomarker for small proviral reservoir size, although not necessarily for cu

240 V but cannot target and eradicate the latent proviral reservoir.

241 me to initiation of cART and the size of the proviral reservoir.

242 irologic parameters, including the inducible proviral reservoir.

243 d that it can significantly reduce the HIV-1 proviral reservoir.

244 fection leads to negligible peripheral blood proviral reservoirs in adolescence and is associated wit

245 -1 cure research, but the characteristics of proviral reservoirs in elite controllers remain to be de

246 Biomarkers of restricted proviral reservoirs may aid in the monitoring of HIV rem

247 It has been proposed that low-level proviral reservoirs might predict longer virologic contr

248 omosomal integration sites, we show that the proviral reservoirs of elite controllers frequently cons

249 rative due to the persistence of CD4+ T-cell proviral reservoirs that chronically resupply active vir

250 iency virus (HIV) infection in adults limits proviral reservoirs that preclude HIV cure.

251 Early antiretroviral therapy (ART) limits proviral reservoirs, a goal for human immunodeficiency v

252 as, B cell-intrinsic SHP1 expression plays a proviral role during the establishment of chronic infect

253 To address a proviral role for N(pro) in RNP granules, we investigate

254 as a model system to investigate a potential proviral role for polyamines using a forward screen.

255 This indicated a proviral role for protein chaperones in HRSV replication

256 The proviral role of ATM is also evident in vivo, as myeloid

257 In this investigation of the proviral role of autophagy, we found evidence for an int

258 Thus, our study defines a proviral role of B cell-specific ATM expression during c

259 The aim of this study was to demonstrate the proviral role of PLK1 in HBV biosynthesis and validate P

260 A proviral role to subvert RNA silencing through binding o

261 study suggested that RelA might also play a proviral role.

262 core protein seems to be dispensable for its proviral role.

263 Altogether, Sac1 and PI(4)P play important proviral roles during TBSV replication.IMPORTANCE Replic

264 to the viral replicase, which otherwise play proviral roles in replication.

265 his study, we have identified both anti- and proviral roles of autophagy in the compatible interactio

266 of two functional components referred to as proviral segments and nudivirus-like genes.

267 udies established that the DNA domains where proviral segments reside are amplified during replicatio

268 Although some proviral sequence evolution was demonstrable in >50% of

269 early, we sought to detect and characterize proviral sequences after 6 to 9 years on suppressive ART

270 to a proviral endpoint to obtain full-length proviral sequences and their corresponding sites of inte

271 We found that identical proviral sequences can result from both cellular expansi

272 controller, we were unable to detect intact proviral sequences despite analysing more than 1.5 billi

273 ltiple sets of independent, near-full-length proviral sequences from cART-treated individuals that we

274 al clusters of identical intact or defective proviral sequences from distinct compartments and CD4 T-

275 Moreover, the integration sites of intact proviral sequences from elite controllers showed an incr

276 ith long-term antiretroviral therapy, intact proviral sequences from elite controllers were integrate

277 as9-mediated targeted insertion of analogous proviral sequences into the LMO2 gene and then measuring

278 eighbour-joining trees to identify identical proviral sequences that might result from T-cell prolife

279 minor variations between the frequencies of proviral sequences within individual CD4 T-cell subsets

280 clonal to near-monoclonal clusters of intact proviral sequences.

281 y to link integration sites to their cognate proviral sequences.

282 Here, we used matched integration site and proviral sequencing (MIP-Seq), an experimental approach

283 tudy, we used single-genome near-full-length proviral sequencing to evaluate intact and defective pro

284 Using single-proviral sequencing, we isolated intracellular HIV-1 gen

285 at HCMV modulates the EV pathway to transfer proviral signals to uninfected cells that prime the cell

286 -wide atlas of functional nodes that mediate proviral silencing in ESCs and illuminates the comprehen

287 e editing construct designed for eliminating proviral SIV DNA, leads to broad distribution of editing

288 ple displacement amplification of individual proviral species, followed by near-full-length HIV-1 nex

289 ith the later stages that ultimately lead to proviral transcription and the production of progeny vir

290 ectivity-which in turn detrimentally affects proviral transcription and virus propagation.

291 These data support a kinetic model for proviral transcription based on continuous replacement o

292 nit, a condition that induced high levels of proviral transcription in latently infected Jurkat T cel

293 l Tat protein utilizes Cyclin T1 to activate proviral transcription, and regulation of Cyclin T1 leve

294 Since HIV-1 utilizes NF-kappaB to promote proviral transcription, the BCA2-mediated inhibition of

295 m-loop malformations predicted to inactivate proviral transcription, which was confirmed by reduced v

296 super elongation complex required for HIV-1 proviral transcription.

297 bility of ELL2 to promote HIV-1 Tat-mediated proviral transcription.

298 gher levels of HIV-1 genomic integration and proviral transcription.

299 man superelongation complex (SEC) to promote proviral transcription.

300 tly, selective piRNA processing of unspliced proviral transcripts is conserved from insects to placen