ライフサイエンスコーパス: KSHV

1 KSHV achieves this by tethering its epigenome to the hos

2 KSHV DNA was detected in the CNS from 4 of 11 HIV-positi

3 KSHV encodes 12 pre-microRNAs (pre-miRNAs), which are pr

4 KSHV encodes 12 pre-microRNAs that yield 25 mature micro

5 KSHV episomes are known to possess bivalent chromatin do

6 KSHV establishes a latent reservoir within B lymphocytes

7 KSHV establishes lifelong infections using its latency-a

8 KSHV induction of TLR4 was mediated by multiple viral mi

9 KSHV infection has been shown to upregulate several host

10 KSHV infection induces and requires multiple metabolic p

11 KSHV infection of neurons was confirmed by in vitro infe

12 KSHV is linked to primary effusion lymphoma (PEL), and 9

13 KSHV is the etiologic agent of PEL-an aggressive lymphom

14 KSHV latent infection induces 5' untranslated region (UT

15 KSHV lytic replication induces dynamic reprogramming of

16 KSHV miR-K9 also decreased the protein levels of cleaved

17 KSHV miR-K9 protected primary endothelial cells from apo

18 KSHV miRNAs also repressed the induction of antiviral in

19 KSHV miRNAs maintain KSHV latency, enhance angiogenesis

20 KSHV miRNAs suppressed STAT3 and STAT5 activation and in

21 KSHV persisted in EBV-transformed B cells and was associ

22 KSHV transcripts contain abundant m(6)A/m modifications

23 KSHV was detected in the human central nervous system (C

24 KSHV-encoded miR-K12-6 (miR-K6) can generate two mature

25 KSHV-mediated alterations in miRNA biogenesis represent

26 -associated herpesvirus/human herpesvirus 8 (KSHV/HHV8), exploit microtubule (MT)-based retrograde tr

27 r, these results identify the host AMPK as a KSHV restriction factor that can serve as a potential th

28 vation, we successfully isolated VLVs from a KSHV mutant defective in the small capsid protein.

29 Recently a KSHV-associated inflammatory cytokine syndrome (KICS) di

30 Lack of miR-K6 abrogated KSHV suppression of CD82 resulting in compromised KSHV a

31 pecific for LANA, a protein expressed in all KSHV-infected cells and malignanciesin vivo, showed that

32 induced by the p53 activator, Nutlin-3, and KSHV miRNA-K9 inhibits this induction.

33 P1 in KSHV-infected cells increased IL-6 and KSHV miRNA expression, supporting a role for MCPIP1 in I

34 on, supporting a role for MCPIP1 in IL-6 and KSHV miRNA regulation.

35 ate the association between high glucose and KSHV replication, we xeno-grafted telomerase-immortalize

36 Upon reactivation from latency, WT KSHV- and KSHV-K1REV-infected cells displayed activated Akt kinase

37 gical agent of three human malignancies, and KSHV K1 is a signaling protein that has been shown to be

38 omised KSHV activation of c-Met pathway, and KSHV induction of cell invasion and angiogenesis.

39 turnover by K-Rta is a strategy employed by KSHV to favor the transition from latency to lytic repli

40 ation and transcription activator encoded by KSHV (ORF50), can function as an E3 ligase to degrade HL

41 ular protein whose expression is enhanced by KSHV RTA with the ability to inhibit KSHV reactivation.

42 t coinfection of HIV-positive individuals by KSHV, we sought to determine whether the central nervous

43 tral nervous system (CNS) can be infected by KSHV in HIV-positive Zambian individuals.

44 transcription 3 (STAT3) that is targeted by KSHV miRNAs.

45 ying cellular networks that were targeted by KSHV-miRNAs and employed network building strategies usi

46 findings uncover (i) a mechanism utilized by KSHV to maintain latent infection, (ii) a latency-lytic

47 lusion, our data show that by reducing CD82, KSHV miR-K6-5p expedites cell invasion and angiogenesis

48 suppression of CD82 resulting in compromised KSHV activation of c-Met pathway, and KSHV induction of

49 dle cells, the main tumor cells, all contain KSHV, mostly in the latent state, during which there is

50 pression and thereby significantly dampening KSHV infection.

51 homa (PEL), and a form of Castleman disease (KSHV-MCD).

52 nd cellular m(6)A/m epitranscriptomes during KSHV latent and lytic infection.

53 s an important role in immune evasion during KSHV primary infection, through inhibition of the host c

54 Similar results were also observed during KSHV lytic cycle induction in TREX-BCBL-1 cells with the

55 e localization of DSB repair proteins during KSHV replication, we have determined that a DNA damage r

56 s a tegument protein with vital roles during KSHV lytic replication.

57 2017) develop humanized mouse models for EBV/KSHV co-infection and identify their complementary effec

58 lytic EBV replication was also found in EBV/KSHV dually infected lymphoproliferative disorders in hu

59 a model for KSHV infection and find that EBV/KSHV dual infection enhanced KSHV persistence and tumori

60 We generated an MHV68 virus that encodes KSHV LANA (kLANA) in place of MHV68 LANA (mLANA) and eva

61 ease then risk of KSHV infection but enhance KSHV dissemination and progression to KS if infection oc

62 d find that EBV/KSHV dual infection enhanced KSHV persistence and tumorigenesis.

63 ppresses, while inhibition of AMPK enhances, KSHV lytic replication by regulating the expression of v

64 ulating host cell responses and facilitating KSHV lytic replication.IMPORTANCE Cells lytically infect

65 use of metformin as a therapeutic agent for KSHV infection and replication.

66 We show here for KSHV that transcription of the gene encoding RTA is comp

67 uman immune system components as a model for KSHV infection and find that EBV/KSHV dual infection enh

68 is, but tissue location and cell tropism for KSHV infection has not been established.

69 atory cytokine syndrome (KICS) distinct from KSHV-MCD was reported.

70 (microRNAs) expressed by a gammaherpesvirus (KSHV), which identified a gene called GADD45B as a targe

71 As a gammaherpesvirus, KSHV is able to acutely replicate, enter latency, and re

72 on of Kaposi sarcoma-associated herpesvirus (KSHV) and is characterized by uncontrolled neoangiogenes

73 from Kaposi sarcoma-associated herpesvirus (KSHV) and MHV68 exhibit considerable sequence divergence

74 TANCE Kaposi sarcoma-associated herpesvirus (KSHV) and murine gammaherpesvirus 68 (MHV68) are members

75 as Kaposi's sarcoma-associated herpesvirus (KSHV) are known to interact extensively with the DDR dur

76 rom Kaposi's sarcoma-associated herpesvirus (KSHV) as a model system, we sought to dissect a putative

77 and Kaposi's sarcoma-associated herpesvirus (KSHV) cause lifelong persistent infection and play causa

78 NCE Kaposi's sarcoma-associated herpesvirus (KSHV) causes AIDS-related malignancies, including lympho

79 Kaposi's sarcoma-associated herpesvirus (KSHV) encodes 12 pre-microRNAs during latency that are p

80 of Kaposi's sarcoma-associated herpesvirus (KSHV) enhances protein synthesis by mimicking the functi

81 Kaposi's sarcoma-associated herpesvirus (KSHV) enters human dermal microvascular endothelial cell

82 ) and Kaposi sarcoma-associated herpesvirus (KSHV) establish persistent infections in B cells.

83 the Kaposi's sarcoma-associated herpesvirus (KSHV) genome and postulated the existence of multiple vi

84 the Kaposi's sarcoma-associated herpesvirus (KSHV) genome undergo m(6)A modification.

85 und Kaposi's sarcoma-associated herpesvirus (KSHV) genomes in the host cell nucleus.

86 ith Kaposi's sarcoma-associated herpesvirus (KSHV) harbor multiple copies of the KSHV genome in the f

87 Kaposi's sarcoma-associated herpesvirus (KSHV) has a causal role in a number of human cancers, an

88 nic Kaposi's sarcoma-associated herpesvirus (KSHV) has latent and lytic replication phases that are e

89 Kaposi's sarcoma-associated herpesvirus (KSHV) has tropism for B lymphocytes, in which it establi

90 ure Kaposi's sarcoma-associated herpesvirus (KSHV) infected human B cells in 3-D using a microwell ar

91 ith Kaposi's sarcoma-associated herpesvirus (KSHV) infection.

92 of Kaposi's sarcoma-associated herpesvirus (KSHV) interacts with multiple cellular signaling pathway

93 Kaposi's sarcoma-associated herpesvirus (KSHV) is a gammaherpesvirus that has been associated wit

94 of Kaposi's sarcoma-associated herpesvirus (KSHV) is encoded by the first open reading frame (ORF) o

95 Kaposi's sarcoma-associated herpesvirus (KSHV) is etiologically associated with all forms of Kapo

96 Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent of commonly fatal malignanc

97 Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent of fatal malignancies of im

98 Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent of Kaposi sarcoma (KS), one

99 Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiologic agent of Kaposi's sarcoma (KS), a

100 Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiologic agent of Kaposi's sarcoma (KS).

101 Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiological agent of three human malignanci

102 of Kaposi's sarcoma-associated herpesvirus (KSHV) is thought to play key roles in disease, including

103 of Kaposi's sarcoma-associated herpesvirus (KSHV) latent episomes are poised to be activated by the

104 ted Kaposi's sarcoma-associated herpesvirus (KSHV) lytic replication in primary human umbilical vein

105 man Kaposi's sarcoma-associated herpesvirus (KSHV) miRNAs revealed several viral miRNA homologs.

106 how Kaposi's sarcoma-associated herpesvirus (KSHV) modulates these cellular pathways during its lytic

107 g a Kaposi's sarcoma-associated herpesvirus (KSHV) mutant that is defective in small capsid protein a

108 the Kaposi's sarcoma-associated herpesvirus (KSHV) performs a variety of functions to establish and m

109 on: Kaposi's sarcoma-associated herpesvirus (KSHV) stably clusters its genomes across generations to

110 of Kaposi's sarcoma-associated herpesvirus (KSHV), a nuclear DNA virus, inhibits mRNA export in a tr

111 of Kaposi's sarcoma-associated herpesvirus (KSHV), against influenza A virus (IAV) were investigated

112 Kaposi sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8, is the etiolog

113 rus Kaposi's sarcoma-associated herpesvirus (KSHV), by targeting the ATP-dependent formation of viral

114 as Kaposi's sarcoma associated herpesvirus (KSHV), is an oncogenic virus that can cause Kaposi's sar

115 us, Kaposi's sarcoma-associated herpesvirus (KSHV), is tightly associated with the development of Kap

116 ing Kaposi's sarcoma-associated herpesvirus (KSHV), play key roles in the viral life cycle.

117 Kaposi's sarcoma-associated herpesvirus (KSHV), the causative agent of Kaposi's sarcoma, encodes

118 and Kaposi's sarcoma-associated herpesvirus (KSHV), which are associated with a variety of diseases i

119 of Kaposi's sarcoma-associated herpesvirus (KSHV)-related malignancies, including Kaposi's sarcoma (

120 by Kaposi's sarcoma-associated herpesvirus (KSHV).

121 gically caused by KS-associated herpesvirus (KSHV).

122 nt, Kaposi's sarcoma-associated herpesvirus (KSHV; HHV8), expresses multiple microRNAs (miRNAs), but

123 Kaposi sarcoma herpesvirus (KSHV) is the cause of Kaposi sarcoma (KS), primary effus

124 us (Kaposi's sarcoma-associated herpesvirus [KSHV], Epstein-Barr virus [EBV], and herpes simplex viru

125 d albumin; higher C-reactive protein; higher KSHV VL; elevated interleukin (IL)-6 and IL-10; and an i

126 How KSHV episomes are prepared such that they maintain laten

127 This study documents how KSHV manipulates and downregulates the secretion of the

128 icroscopy were used to localize and identify KSHV-infected cells.

129 We sought to determine if KSHV and MHV68 LANA homologs are functionally interchang

130 THDF2 enhanced lytic replication by impeding KSHV RNA degradation.

131 ment of PEL and related disorders.IMPORTANCE KSHV vFLIP (ks-vFLIP) has been shown to have a crucial r

132 ge in promoting lytic replication.IMPORTANCE KSHV productive lytic replication plays a pivotal role i

133 therapeutic avenues for KS tumors.IMPORTANCE KSHV is the etiologic agent of Kaposi's sarcoma, the mos

134 This observed complexity in KSHV RTA expression and function likely plays a critical

135 TLR4 pathway was activated constitutively in KSHV-transformed cells, resulting in chronic induction o

136 duction resulted in significant decreases in KSHV entry and viral gene expression.

137 This study opens up new domains in KSHV research focusing on how the virus modulates lipoxi

138 urthermore, ectopic expression of GADD45B in KSHV-infected cells promoted apoptosis.

139 the TLR4 pathway and chronic inflammation in KSHV-induced tumorigenesis, which helps explain why HIV-

140 mited data concerning the sorting of K15P in KSHV-infected cells.

141 To date, the role of m(6)A/m in KSHV replication and tumorigenesis is unclear.

142 ddition, repression with siRNAs to MCPIP1 in KSHV-infected cells increased IL-6 and KSHV miRNA expres

143 nown about the role of microRNAs (miRNAs) in KSHV entry.

144 a critical role of m(6)A/m modifications in KSHV lifecycle and provide rich resources for future inv

145 rk for understanding the roles of PAN RNA in KSHV infection.

146 pathways and is thought to play key roles in KSHV-associated endothelial cell angiogenesis, regulatio

147 ature microRNAs (miRNAs), but their roles in KSHV-induced tumor metastasis and angiogenesis remain la

148 ctor-regulated tyrosine kinase substrate) in KSHV entry into HMVEC-d by macropinocytosis.

149 he trans-Golgi network (TGN) marker TGN46 in KSHV-infected PEL cells.

150 Here, we show that TLR4 is upregulated in KSHV-infected spindle tumor cells in human Kaposi sarcom

151 ught to play key roles in disease, including KSHV-associated angiogenesis and the survival and growth

152 heterogeneity in the responses of individual KSHV episomes to stimuli within a single reactivating ce

153 cations toward more active forms and induced KSHV reactivation in naturally infected cells.

154 st cell novel miR-36 to specifically inhibit KSHV-induced expression of interferon induced transmembr

155 nced by KSHV RTA with the ability to inhibit KSHV reactivation.

156 e have shown that soluble HIV-1 Vpr inhibits KSHV lytic replication by activating NF-kappaB signaling

157 of the viral lytic activator RTA, initiating KSHV lytic gene expression.

158 ication transcription activator (RTA), a key KSHV lytic switch protein, and halted viral lytic replic

159 a cell system capable of establishing latent KSHV infection and robust reactivation, we successfully

160 H2O2, which mediates reactivation of latent KSHV through multiple mechanisms.

161 nce in capture efficiencies between latently KSHV-infected and uninfected BJAB B lymphoma cells at th

162 rate that knockdown of IFI16 in the latently KSHV-infected B-lymphoma BCBL-1 and BC-3 cell lines resu

163 and how these may differ in latent and lytic KSHV infections are poorly understood.

164 KS tumors support both latent and lytic KSHV replication.

165 r doxycycline-induced cells expressing lytic KSHV proteins.

166 ssion of lytic transcripts, and a late lytic KSHV gene product(s) targets IFI16 for degradation durin

167 number of cells permissive for primary lytic KSHV infection.

168 riety of functions to establish and maintain KSHV latency.

169 KSHV miRNAs maintain KSHV latency, enhance angiogenesis and dissemination of

170 ll pluripotency, plays a role in maintaining KSHV latent infection in naturally infected cells.

171 olysis, and FAS are all required for maximal KSHV virus production and that these pathways appear to

172 fining the roles and mechanisms of action of KSHV miRNAs in KS development.

173 e we show that during lytic amplification of KSHV DNA, the Ku70/80 heterodimer and the MRN complex co

174 al for the dissemination and angiogenesis of KSHV-induced malignant tumors.

175 s can transcriptionally activate an array of KSHV promoters to various levels.

176 eus may be a previously unexplored aspect of KSHV gene regulation by confiscation of a limited supply

177 ms of KSHV pathogenesis, clinical aspects of KSHV-associated diseases, and current treatments for can

178 HV gene regulation through focal assembly of KSHV episomes and a molecular mechanism of late gene exp

179 Challenge of KSHV-infected B cells with CD4(+)T cells specific for LA

180 The clustering of KSHV plasmids provides it with an effective evolutionary

181 The clustering of KSHV requires the viral protein, LANA1, to bind viral ge

182 In the context of KSHV replication, we demonstrated that VLV-induced upreg

183 T cell immunity is vital for the control of KSHV infection and disease; however, few models of B lym

184 role of the K1 protein in the life cycle of KSHV, we constructed recombinant viruses that were defic

185 plays an important role in the life cycle of KSHV.

186 n essential role of Vpr in the life cycle of KSHV.

187 es that are essential for the development of KSHV-associated cancers.

188 t protects against the pathogenic effects of KSHV GPCR by facilitating its endolysosomal degradation.

189 Exploration of KSHV-directed therapy is warranted.

190 ar energy sensor, as a restriction factor of KSHV lytic replication during primary infection.

191 e of cell cycle and without any induction of KSHV lytic cycle reactivation.

192 The influence of KSHV infection on anti-inflammatory molecules is not wel

193 f IkappaBalpha and reduced Vpr inhibition of KSHV lytic replication, while overexpression of miR-942-

194 ion of miR-942-5p enhanced Vpr inhibition of KSHV lytic replication.

195 y infected with KSHV, specific inhibitors of KSHV miR-K9 led to increased GADD45B expression and apop

196 st cell miRNA to regulate internalization of KSHV, EBV, and HSV-2 in hematopoietic and endothelial ce

197 lls expressed significantly higher levels of KSHV lytic genes in hyperglycemic mice than in normal mi

198 ytic reactivation and increases in levels of KSHV lytic transcripts, proteins, and viral genome repli

199 joins PAN/nut1/T1.1 as a bona fide lncRNA of KSHV with potentially important roles in viral gene regu

200 signaling events during macropinocytosis of KSHV.

201 l event required for the macropinocytosis of KSHV.

202 may provide insight into the maintenance of KSHV latent infection and the switch to lytic replicatio

203 zed DNA into chromatin, but the mechanism of KSHV genome chromatinization post-replication is not und

204 SHV field, including molecular mechanisms of KSHV pathogenesis, clinical aspects of KSHV-associated d

205 In a model of KSHV-induced cellular transformation, KSHV upregulated e

206 ral partitioning and viral genome numbers of KSHV.

207 we observed increased lytic reactivation of KSHV from latently infected cells upon STAT3 repression

208 Here, we examined the regulation of KSHV latency by HIV-1 viral protein R (Vpr).

209 tions that occur during lytic replication of KSHV and provides a deeper insight into how the DDR is m

210 NK cell activation may decrease then risk of KSHV infection but enhance KSHV dissemination and progre

211 g VLVs but also shows the important roles of KSHV-associated VLVs in intercellular communication and

212 Our findings uncover a strategy of KSHV gene regulation through focal assembly of KSHV epis

213 , resulting in epigenetic transactivation of KSHV lytic genes.

214 G-quadruplex stabilizers in the treatment of KSHV-associated diseases.

215 ch has implications for our understanding of KSHV biology.

216 important effectors for thein vivocontrol of KSHV-infected B lymphocytes.

217 The effect of miR-36 on KSHV infection of cells was at a post-binding stage of v

218 inhibitor had the direct opposite effect on KSHV infection of cells, allowing enhanced viral infecti

219 wing overexpression of the viral oncoprotein KSHV vFLIP (ks-vFLIP).

220 KSHVDeltaK1), stop codons within the K1 ORF (KSHV-K15xSTOP), or a revertant K1 virus (KSHV-K1REV).

221 on with RRV, a homolog of the human pathogen KSHV, led to perinuclear wrapping by acetylated MT bundl

222 Studies on persistent KSHV infection in vivo and the role of EBV co-infection

223 ne the metabolic requirements for productive KSHV infection, we induced lytic replication in the pres

224 and activation of the ATM kinase can promote KSHV replication, proteins involved in nonhomologous end

225 1 was necessary and sufficient to reactivate KSHV by activating its RTA promoter.

226 KSHV life cycle, we engineered a recombinant KSHV ORF52-null mutant virus and found that loss of ORF5

227 -1-secreted regulatory protein Vpr regulates KSHV latency and the pathogenesis of AIDS-related malign

228 during the late stage of lytic replication, KSHV selectively degrades IFI16, thus relieving transcri

229 Individual binding sites of select KSHV gene products on PAN RNA were also identified in in

230 Given that at least some KSHV latent antigens are thought to be poor targets for

231 B lymphocytes, but few models exist to study KSHV-infected B cells other than the transformed PEL cel

232 How such KSHV chromatin domains are maintained to be reactivatabl

233 the attack of the cell host's immune system, KSHV switches from the lytic to the latent phase, a phas

234 tify a new miRNA target and demonstrate that KSHV miRNAs are important for protecting infected cells

235 We recently demonstrated that KSHV induces a plethora of host cell miRNAs during the e

236 munofluorescent microscopy demonstrated that KSHV infected neurons and oligodendrocytes in parenchyma

237 We hypothesized that KSHV miRNAs target human GADD45B to protect cells from c

238 Our findings illustrate that KSHV miRNAs may be critical for the dissemination and an

239 Our findings indicate that KSHV RTA facilitates evasion of the virus from the immun

240 Our studies reveal that KSHV has evolved to utilize the innate immune sensor IFI

241 These results reveal that KSHV utilizes the innate immune nuclear DNA sensor IFI16

242 Together, we show that KSHV miRNAs suppress a network of targets associated wit

243 Our study showed that KSHV infects human CNS-resident cells, primarily neurons

244 Our data suggest that KSHV augments EBV-associated tumorigenesis via stimulati

245 Hrs during macropinocytosis and suggest that KSHV entry requires both Hrs- and ROCK1-dependent mechan

246 RTA pre-mRNA splicing but also suggest that KSHV has evolved a mechanism to manipulate the host m(6)

247 replicating viral genomic DNA suggests that KSHV assembles an "all-in-one" factory for both gene tra

248 present work reports for the first time that KSHV genome-encoded mRNAs undergo m(6)A modification, wh

249 The KSHV miRNA cluster probably targets enzyme 15-lipoxygena

250 hen lytic reactivation was stimulated by the KSHV protein replication and transcription activator (RT

251 t episomes are poised to be activated by the KSHV replication and transcription activator (K-Rta).

252 vestigate the role of the K1 gene during the KSHV life cycle, we constructed a set of recombinant vir

253 t that K1 plays an important role during the KSHV life cycle.

254 d a recombinant MHV68 virus that encodes the KSHV LANA protein in place of the MHV68 LANA homolog.

255 eview recent and ongoing developments in the KSHV field, including molecular mechanisms of KSHV patho

256 assays to distinguish all RNA species in the KSHV latency region.

257 Onset of the lytic phase in the KSHV life cycle is accompanied by the rapid, global degr

258 To characterize the roles of ORF52 in the KSHV life cycle, we engineered a recombinant KSHV ORF52-

259 ally interacts with A/T-rich elements in the KSHV origin of lytic replication (oriLyt), and this was

260 predict the presence of such elements in the KSHV pre-microRNA transcript K12-2.

261 ion and transcription activator (RTA) is the KSHV lytic switch protein due to its ability to drive th

262 ibit cGAS to promote the reactivation of the KSHV from latency.

263 early and early gene cluster regions of the KSHV genome and contributed to tethering of polycomb rep

264 esvirus (KSHV) harbor multiple copies of the KSHV genome in the form of episomes.

265 s of the cell during different stages of the KSHV life cycle.

266 the latent and the replicative stages of the KSHV life cycle.IMPORTANCE Kaposi's sarcoma-associated h

267 is well established that reactivation of the KSHV lytic cycle is associated with KS pathogenesis.

268 1-secreted proteins Tat and Nef regulate the KSHV life cycle and synergize with KSHV oncogenes to pro

269 list of cellular proteins that regulate the KSHV lytic cycle, which has implications for our underst

270 We determined that the KSHV LANA protein is capable of supporting MHV68 latency

271 Previous studies suggested that the KSHV switch from latency to lytic replication is primari

272 The results demonstrate that the KSHV-infected B cells can be grown up to 15 days in a 3-

273 lial cells that are infected with KSHV (TIVE-KSHV) into hyperglycemic and normal nude mice.

274 BC-3 cells demonstrated that IFI16 binds to KSHV gene promoters.

275 s to a more active configuration, leading to KSHV reactivation.

276 h the recruitment of DSB-sensing proteins to KSHV RCs is a consistent occurrence across multiple cell

277 del of KSHV-induced cellular transformation, KSHV upregulated expression of TLR4, its adaptor MyD88,

278 network building strategies using validated KSHV miRNA targets.

279 ed from the brain tissue specimens to verify KSHV infection.

280 Kaposi's sarcoma-associated herpes virus (KSHV) polyadenylated nuclear (PAN) RNA facilitates lytic

281 RF (KSHV-K15xSTOP), or a revertant K1 virus (KSHV-K1REV).

282 te infection of closely related DNA viruses: KSHV, Epstein-Barr virus (EBV), and herpes simplexvirus-

283 d its intracellular distribution change when KSHV switches from its latent (quiescent) phase to the l

284 n mRNA expression profiling experiments when KSHV miRNAs were introduced to uninfected cells.

285 The mechanism by which KSHV evades an attack by the immune system has not been

286 The mechanism by which KSHV evades the attack of the immune system and establis

287 genesis represent a novel mechanism by which KSHV interacts with its host and a new mechanism for the

288 human umbilical vein endothelial cells while KSHV infection did not markedly affect the endogenous AM

289 rus (HIV)-infected cohorts, including 1 with KSHV coinfection.

290 f KICS by evaluating symptomatic adults with KSHV using a prespecified definition.

291 infection in primary endothelial cells with KSHV, growth arrest DNA damage-inducible gene 45 beta (G

292 g mitogenic stimuli and then challenged with KSHV-specific CD4(+)T cells.

293 e collected from individuals coinfected with KSHV and HIV.

294 ein endothelial cells that are infected with KSHV (TIVE-KSHV) into hyperglycemic and normal nude mice

295 In B lymphocytes latently infected with KSHV, specific inhibitors of KSHV miR-K9 led to increase

296 loped a model of B lymphocyte infection with KSHV in which infected tonsillar B lymphocytes were expa

297 gy-related protein, Beclin 2, interacts with KSHV GPCR, facilitates its endolysosomal degradation, an

298 plication by kLANA, as previously shown with KSHV, is a kLANA-specific function that is transferable

299 ulate the KSHV life cycle and synergize with KSHV oncogenes to promote angiogenesis and tumorigenesis

300 Upon reactivation from latency, WT KSHV- and KSHV-K1REV-infected cells displayed activated