ライフサイエンスコーパス: KSHV

1 KSHV and EBV loads were quantified by PCR.

2 KSHV and RRV engage cellular receptors from the Eph fami

3 KSHV evades immune detection by maintaining the levels o

4 KSHV gene expression is modulated by binding of the host

5 KSHV latent infection decreases mitochondrial numbers, b

6 KSHV latently infects cells, and its genome persists as

7 KSHV loads did not correlate with antibody levels nor di

8 KSHV ORF61 also caused relocalization of these two enzym

9 KSHV seroprevalence did not differ by study group but wa

10 KSHV serostatus, peripheral blood KSHV-VL, and KSHV-asso

11 KSHV thymidine kinase (TK), the ORF21 gene product, can

12 KSHV thymidine kinase can phosphorylate zidovudine and g

13 KSHV vCD200 is the most extensively studied vCD200 molec

14 KSHV viral interleukin-6 (vIL-6) is a viral homolog of h

15 KSHV, like other herpesviruses, intermittently reactivat

16 KSHV-encoded viral interleukin-6 (vIL-6) is implicated i

17 KSHV-MCD is characterized by systemic inflammation cause

18 ronegative controls was detected in 24 of 68 KSHV-seropositive individuals tested.

19 y described the MC116 human B cell line as a KSHV-susceptible model to overcome the paradoxical refra

20 tion of vIL-6 from the KSHV genome abolished KSHV-induced cellular transformation and impaired angiog

21 here that XBP-1s can also directly activate KSHV ORF21, a lytic gene.

22 It can also directly activate KSHV-encoded viral interleukin-6 (vIL-6) and, thus, cont

23 tion indicates that CTCF primarily activates KSHV lytic transcription, whereas cohesin has primarily

24 ajor replication and transcription activator KSHV protein called RTA.

25 o applications of LANA-specific Cas9 against KSHV infection and KS.IMPORTANCE The ability for Kaposi'

26 f LXA4 and its therapeutic potential against KSHV.IMPORTANCE The latent-to-lytic switch in KSHV infec

27 d to be independent of HIV status, sex, age, KSHV Ab titer, and KSHV-neutralizing activity.

28 Although KSHV-EBV dual infection does not increase eBL risk, EBV

29 y objective was to investigate the HIV-1 and KSHV roles in viral nucleic acid detection, antibody res

30 n interaction between HIV type 1 (HIV-1) and KSHV, focusing on secretory proteins.

31 increasing its transactivation activity and KSHV spontaneous lytic gene expression and infectious vi

32 SHV gH that are critical for Eph binding and KSHV infection.

33 ted to epigenetic alterations of the EBV and KSHV genomes that mediate oncogenesis, but the detailed

34 interventional strategies that block EBV and KSHV infection of target epithelial cells.

35 but with different K1 open reading frame and KSHV whole-genome sequences and a different epidemiologi

36 nderlying KS pathogenesis induced by HIV and KSHV coinfection.

37 ltiplexed seroprofiles for EBV, malaria, and KSHV were generated for 266 eBL patients, 78 non-eBL can

38 relation between sphingolipid metabolism and KSHV+ tumor cell survival.

39 argets of an RNA quality control pathway and KSHV lytic gene expression, and demonstrates that NMD ca

40 ferences in these parameters between PEL and KSHV-associated multicentric Castleman disease.

41 nsynchronized initiation of reactivation and KSHV replication with diverse kinetics between individua

42 typing with K1 open reading frame Sanger and KSHV whole-genome sequencing.

43 of HIV status, sex, age, KSHV Ab titer, and KSHV-neutralizing activity.

44 HV serostatus, peripheral blood KSHV-VL, and KSHV-associated clinical correlates were evaluated.

45 This suggests that a strong anti-KSHV immune response, and potentially nonneutralizing an

46 our knowledge, the first evidence that anti-KSHV Abs are capable of mediating ADCC responses against

47 The current study aimed to assess KSHV diversity in a population of men who have sex with

48 ons for the development of a live-attenuated KSHV vaccine or vaccine vector.

49 tal, 86/124 (69.4%) mothers were found to be KSHV seropositive.

50 tudy highlights complex interactions between KSHV and EBV, in addition to distinct genetic architectu

51 eted for designing antiviral agents to block KSHV virion production.IMPORTANCE Kaposi's sarcoma (KS)-

52 KSHV serostatus, peripheral blood KSHV-VL, and KSHV-associated clinical correlates were ev

53 fied as an important entry receptor for both KSHV and EBV.

54 The prevalence for both KSHV and KS are highest in sub-Saharan Africa where HIV-

55 for differences in EphA2 binding affinity by KSHV.IMPORTANCE Virus entry into target cells is the fir

56 RTANCE Viral CD200 homologues are encoded by KSHV and the closely related RRV.

57 Induction of NE genes by KSHV could also provide a potential survival advantage,

58 vasion, and growth transformation induced by KSHV.

59 an important immune evasion strategy used by KSHV for its survival and maintenance in the host.

60 e total 124 mothers, 81 had at least 1 child KSHV seroconvert during the 2 years analyzed, while the

61 ially serve as therapeutic targets to combat KSHV-associated KS.

62 In sharp contrast, KSHV-infected LECs predominantly entered lytic replicati

63 LANA mRNA could be exploited for controlling KSHV latency.

64 stress), increased cell death, and decreased KSHV gene expression.

65 , POU2F1/Oct-1 expression was induced during KSHV reactivation, and POU2F1 knockdown diminished infec

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

67 cRNA, LINC00313, which is upregulated during KSHV reactivation, interacts with HIV Tat to promote end

68 EBV/KSHV co-infection (OR = 5.71(1.58-7.12)), HIV positivity

69 n the association of mortality with elevated KSHV-VL in critically ill HIV-infected patients with sus

70 ORF21 encodes KSHV thymidine kinase (TK), which increases the pool of

71 EGFR, blocks HIV-associated exosome-enhanced KSHV infection.

72 associated exosomes contributes to enhancing KSHV infectivity through the epidermal growth factor rec

73 fractoriness of B cell lines to experimental KSHV infection.

74 At the proper time for their expression, KSHV late transcripts evade PPD through the activity of

75 provides a potential therapeutic avenue for KSHV-associated cancers.

76 IV-associated exosomes are a risk factor for KSHV infection in the HIV-infected population.

77 We investigated the risk factors for KSHV DNA detection by real-time polymerase chain reactio

78 f lymphatic development, are key factors for KSHV genome maintenance and lytic cycle in lymphatic end

79 s identified here could serve as markers for KSHV-infected cells and could potentially serve as thera

80 genes could potentially serve as markers for KSHV-infected KS lesion endothelial cells as well as nov

81 considered as potential effect modifiers for KSHV-associated cancers in sub-Saharan Africa.

82 kinase A2 (EphA2) is a cellular receptor for KSHV and EBV.

83 The oral cavity is a major route for KSHV infection and transmission.

84 analyzed, while the remaining 43 mothers had KSHV-seronegative children.

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

86 Kaposi's sarcoma-associated herpesvirus (KSHV) and Epstein-Barr Virus (EBV) establish life-long i

87 Kaposi sarcoma (KS)-associated herpesvirus (KSHV) and preventing disease development, the exact fact

88 and Kaposi's sarcoma-associated herpesvirus (KSHV) are human gammaherpesviruses and are important in

89 and Kaposi's sarcoma-associated herpesvirus (KSHV) are two of the classical oncogenic herpesviruses k

90 in Kaposi's sarcoma-associated herpesvirus (KSHV) biology helped discover that KSHV infection hijack

91 nic Kaposi's sarcoma-associated herpesvirus (KSHV) deregulates the activity of APC/C during the lytic

92 ble Kaposi's sarcoma-associated herpesvirus (KSHV) DNA in blood and increased antibody titres may ind

93 cts Kaposi's sarcoma-associated herpesvirus (KSHV) infection.

94 nic Kaposi's sarcoma-associated herpesvirus (KSHV) is a highly angiogenic and invasive vascular tumor

95 Kaposi's sarcoma-associated herpesvirus (KSHV) is a human oncogenic nuclear DNA virus that expres

96 NCE Kaposi's sarcoma-associated herpesvirus (KSHV) is an oncogenic gammaherpesvirus that causes Kapos

97 NCE Kaposi's sarcoma-associated herpesvirus (KSHV) is associated with a substantial disease burden in

98 NCE Kaposi's sarcoma-associated herpesvirus (KSHV) is causally linked to Kaposi's sarcoma and several

99 Kaposi's sarcoma-associated herpesvirus (KSHV) is etiologically associated with endothelial Kapos

100 Kaposi sarcoma-associated herpesvirus (KSHV) is necessary but not sufficient for primary effusi

101 Kaposi's sarcoma-associated herpesvirus (KSHV) is the causal agent for Kaposi's sarcoma (KS), the

102 NCE Kaposi's sarcoma-associated herpesvirus (KSHV) is the causal agent for Kaposi's sarcoma (KS), the

103 Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent for Kaposi sarcoma (KS), pr

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

105 Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent of two B-cell lymphoprolife

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

107 rus Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiological agent of Kaposi's sarcoma and p

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

109 aposi's sarcoma (KS)-associated herpesvirus (KSHV) is tightly linked with KS, primary effusion lympho

110 the Kaposi's sarcoma-associated herpesvirus (KSHV) latent and lytic gene replication.

111 uce Kaposi's sarcoma-associated herpesvirus (KSHV) lytic replication and directly activate viral inte

112 NCE Kaposi's sarcoma-associated herpesvirus (KSHV) manipulates several cellular pathways for its surv

113 of Kaposi's sarcoma-associated herpesvirus (KSHV) reactivation have been studied primarily by measur

114 Kaposi sarcoma (KS)-associated herpesvirus (KSHV) subtype depends mostly on patient origin.

115 Kaposi's sarcoma-associated herpesvirus (KSHV) transcribes a long noncoding polyadenylated nuclea

116 Kaposi's sarcoma-associated herpesvirus (KSHV) transcription is regulated by CTCF and cohesin, wi

117 le of Kaposi sarcoma-associated herpesvirus (KSHV), also endemic in Africa, has not been evaluated as

118 V), Kaposi's sarcoma-associated herpesvirus (KSHV), and human papillomavirus (HPV) share the common p

119 rus Kaposi's sarcoma-associated herpesvirus (KSHV), and the closely related rhesus macaque rhadinovir

120 Kaposi sarcoma-associated herpesvirus (KSHV), one of the human oncogenic viruses, is the princi

121 for Kaposi's sarcoma-associated herpesvirus (KSHV), the causative agent of Kaposi's sarcoma (KS), to

122 with Kaposi sarcoma-associated herpesvirus (KSHV), the maternal immune response remains largely unch

123 In Kaposi's sarcoma-associated herpesvirus (KSHV), these vTAs are encoded by ORF18, ORF24, ORF30, OR

124 the Kaposi's sarcoma-associated herpesvirus (KSHV)-encoded LANA protein enhances the ubiquitin ligase

125 The Kaposi's sarcoma-associated herpesvirus (KSHV)-encoded latency-associated nuclear antigen (LANA)

126 rs, Kaposi's sarcoma-associated herpesvirus (KSHV)-transformed cells depend on glutamine rather than

127 ed by Kaposi sarcoma-associated herpesvirus (KSHV).

128 er of Kaposi sarcoma-associated herpesvirus (KSHV).

129 with Kaposi sarcoma-associated herpesvirus (KSHV).

130 NCE Kaposi's sarcoma-associated herpesvirus (KSHV; human herpesvirus 8) is an oncogenic gammaherpesvi

131 irus (EBV) and Kaposi's sarcoma herpesvirus (KSHV) human DNA tumor viruses.

132 tumor caused by Kaposi sarcoma herpesvirus (KSHV) infection and is thought to originate from lymphat

133 (ELEFN(50-54)) motif is important for higher KSHV fusion and that EBV gH/gL does not utilize a simila

134 an lncRNA serves as a novel connector in HIV-KSHV interactions.IMPORTANCE KS is a prevalent tumor ass

135 racting lncRNA that potentially mediates HIV-KSHV interactions.

136 However, how KSHV breaches the oral epithelial barrier for spreading

137 discovery of this critical role of K8.1A in KSHV B cell tropism opens promising new avenues to unrav

138 of LXA4 and its targetable receptor, AhR, in KSHV's pathogenesis.

139 esting a potential role of integrin beta3 in KSHV pathogenesis and development of Kaposi's sarcoma.

140 is an essential component of this complex in KSHV and that its inclusion in the complex depends upon

141 e a potential target to induce cell death in KSHV-infected cells.

142 ression of the NE genes HRH1 and NSE/ENO2 in KSHV-infected KS tissue samples and KS visceral tissue m

143 g of human IL-6 (hIL-6) that is expressed in KSHV-associated malignancies.

144 identified LXA4-interacting host factors in KSHV-infected cells, which could help provide an underst

145 Our study underscores the role of LXA4 in KSHV biology and emphasizes that KSHV is strategic in do

146 he mechanism of KSHV activation of mTORC1 in KSHV-induced cancers remains unclear.

147 The NE gene expression observed in KSHV-infected cells was recapitulated in uninfected endo

148 nfected cells as an essential participant in KSHV genome replication and as a driver of dysregulated

149 erstand the roles of these decay pathways in KSHV gene expression.

150 RCC2 to be LXA4-interacting host proteins in KSHV-infected cells.

151 endocrine receptors having opposing roles in KSHV-infected cell proliferation.

152 SHV.IMPORTANCE The latent-to-lytic switch in KSHV infection is one of the critical events regulated b

153 pact and underlying mechanisms of HIV Tat in KSHV-infected endothelial cells undergoing viral lytic r

154 dothelial cells with live and UV-inactivated KSHV demonstrated that viral gene expression is responsi

155 d and increased antibody titres may indicate KSHV reactivation, while the transmission of KSHV occurs

156 eous, hypoxia-induced, or chemically induced KSHV lytic replication and enhances the inhibitory effec

157 During latent infection, KSHV significantly alters mitochondrial biology, leading

158 V-RTA/ORF50 nor the production of infectious KSHV virions in PEL.

159 othelial cells could be exploited to inhibit KSHV-associated tumor cells.

160 some maintenance protein (EMP), namely LANA (KSHV), EBNA1 (EBV), and E2 (HPV).

161 During latency, KSHV expresses a small subset of genes, including the la

162 As there is no direct treatment for latent KSHV, identification of host vulnerabilities in latently

163 Longitudinal KSHV titers were fairly stable over time, although seror

164 expression correlated with latent and lytic KSHV protein expression.

165 cation and sensitivity to rapamycin in lytic KSHV-infected cells.

166 e and transcriptional activation of the main KSHV transcription factor RTA, itself an NMD target.

167 anti-inflammatory LXA4 secretion to maintain KSHV latency in infected cells.

168 an acetylation-dependent mechanism mediating KSHV persistence and expand the role of acidic domain re

169 In this study, we generated a gH-null mutant KSHV and provided evidence that deficiency of gH express

170 Here, we identified LINC00313 as a novel KSHV reactivation-activated long noncoding RNA (lncRNA)

171 We found that 51% of KSHV-strains were subtype C (85% C3), and 33% were subty

172 Lastly, analysis of KSHV latency and reactivation models revealed the latenc

173 es in the pathobiological characteristics of KSHV-infected endothelial cells, including a potential m

174 eporter-KSHV and initial characterization of KSHV replication in single cells are presented.

175 as never been investigated in the context of KSHV infection.

176 specific components in the cotransfection of KSHV is unclear.

177 APC/C during the lytic replication cycle of KSHV and found that, in contrast to that of KSHV's close

178 cal inhibition of SOX18 caused a decrease of KSHV genome copy numbers.

179 (vIL-6) is implicated in the development of KSHV-induced malignancies; however, the mechanisms under

180 s (ELEFN(50-54)) in the N-terminal domain of KSHV gH that are critical for Eph binding and KSHV infec

181 omes is a risk factor for the enhancement of KSHV infection and that the inhibition of EGFR serves as

182 taneous virus production to the expansion of KSHV-infected tumor cells and the cellular factors that

183 Nuclear expression of KSHV genes results in exposure to at least two host-medi

184 treatment neither induces the expression of KSHV-RTA/ORF50 nor the production of infectious KSHV vir

185 complex affects the number and integrity of KSHV viral episomes.

186 t differed in compared to the interaction of KSHV gH/gL with EphA2.

187 Currently, the mechanism of KSHV activation of mTORC1 in KSHV-induced cancers remain

188 he well-characterized iSLK.219 cell model of KSHV infection and established a new infection model of

189 Mothers of KSHV-negative children had higher geometric mean titers

190 higher geometric mean titers than mothers of KSHV-positive children; however, there was no difference

191 ents reveal the highly heterogenic nature of KSHV replication/gene expression at individual cell leve

192 , by lytic replication and overproduction of KSHV vIL-6 in XBP-1s-expressing lymph node plasmablasts.

193 and, thus, contribute to the pathogenesis of KSHV MCD.

194 cells and contribute to the pathogenesis of KSHV multicentric Castleman disease (MCD).

195 and, thus, contribute to the pathogenesis of KSHV-MCD and the activity of zidovudine and valganciclov

196 s absolutely required for the persistence of KSHV in the host cell.

197 isk, EBV appears to suppress reactivation of KSHV while malaria exposure is associated with KSHV infe

198 s a tool to examine heterogenic responses of KSHV reactivation for a deeper understanding of KSHV rep

199 euroendocrine tumors is probably a result of KSHV infection-induced transformation of nonneuronal end

200 KSHV and found that, in contrast to that of KSHV's close relatives EBV and HCMV, KSHV lytic replicat

201 at restrict or activate the transcription of KSHV lytic genes.

202 KSHV reactivation, while the transmission of KSHV occurs via viral shedding in saliva.

203 sible for much of the onward transmission of KSHV.

204 Treatment of KSHV-infected cells with LXA4 minimizes the activation o

205 vir to toxic moieties, enabling treatment of KSHV-MCD with these drugs.

206 udine and valganciclovir in the treatment of KSHV-MCD.

207 V reactivation for a deeper understanding of KSHV replication.IMPORTANCE Sensitivity and resolution o

208 similar, although less pronounced, effect on KSHV infection.

209 n have both positive and negative effects on KSHV lytic replication as well as effects on the host ce

210 ulating programmed death-ligand 1 (PD-L1) on KSHV-carrying tumor cells.

211 Studies on KSHV gene regulation at the individual cell level would

212 by K8.1/LANA or in combination with 5 other KSHV antigens (ORF59, ORF65, ORF61, ORF38, and K5) was a

213 preexposure prophylaxis (PrEP), we performed KSHV typing with K1 open reading frame Sanger and KSHV w

214 FR serves as a novel strategy for preventing KSHV infection and transmission in the oral cavity.IMPOR

215 HIV-associated exosomes promote KSHV infection, which depends on HIV trans-activation re

216 tants of HIV-1-infected T-cell lines promote KSHV infectivity in immortalized and primary human oral

217 ecreted by HIV-infected T-cell lines promote KSHV infectivity in immortalized and primary oral epithe

218 Rainbow-KSHV replicated similarly to a prototype reporter-KSHV,

219 nant reporter virus, which we named "Rainbow-KSHV," that encodes three fluorescence-tagged KSHV prote

220 We prepared a recombinant KSHV that can report on its replication stage in host ce

221 chromosome containing a complete recombinant KSHV genome and recombinant DNA technology, we inserted

222 Strategies to reduce KSHV episomal persistence in latently infected cells mig

223 n inhibitory aptamer against TAR RNA reduces KSHV infection facilitated by the synthetic TAR RNA in o

224 al cells, which can be targeted for reducing KSHV infection.

225 probably counteract each other in regulating KSHV-infected endothelial cell proliferation.

226 (LECs) infected with a lytically replicating KSHV BAC16 mutant.

227 he utilization of a newly developed reporter-KSHV and initial characterization of KSHV replication in

228 replicated similarly to a prototype reporter-KSHV, KSHVr.219, and wild-type BAC16 virus.

229 effects, with cohesin primarily restricting KSHV lytic transcription.

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

231 As a result, KSHV transcripts are subject to degradation by at least

232 Four patients with severe KSHV disease (2 with visceral KS, 1 with multicentric Ca

233 in Caucasian MSM and associated with severe KSHV disease, suggesting that subtype F could be split i

234 Significantly, KSHV LANA mutants lacking the acidic domain reader seque

235 Since KSHV and HIV infect distinct cell types, the virus-virus

236 ause of deviation from icosahedral symmetry, KSHV portal and tegument structures have largely been ob

237 SHV," that encodes three fluorescence-tagged KSHV proteins (mBFP2-ORF6, mCardinal-ORF52, and mCherry-

238 cted but not microbiologically confirmed TB, KSHV-VL and KICS criteria may guide diagnostic and thera

239 We conclude that KSHV fine-tunes the temporal expression of its genes by

240 From these studies, we conclude that KSHV uses PPD to fine-tune the temporal expression of it

241 Here, we demonstrate that KSHV infection upregulates the expression of genes relat

242 Further analysis demonstrated that KSHV latent open reading frame K12 (ORFK12) gene (kaposi

243 pesvirus (KSHV) biology helped discover that KSHV infection hijacks the proinflammatory cyclooxygenas

244 c pathways are regulated and discovered that KSHV hijacks the citrulline-nitric oxide (NO) cycle to p

245 of LXA4 in KSHV biology and emphasizes that KSHV is strategic in downregulating LXA4 secretion in th

246 aps unsurprisingly, we previously found that KSHV uses specific mechanisms to protect its transcripts

247 s human oncovirus and the host pathways that KSHV dysregulates.

248 Here we report that KSHV vIL-6 is able to induce the expression of ITGB3 and

249 It has been previously reported that KSHV infection of endothelial cells leads to an increase

250 bilities than RRV vCD200, and also show that KSHV vCD200 does not efficiently induce signaling via RM

251 lls (BEC and LEC, respectively) to show that KSHV-infected BECs progressively lose viral genome as th

252 (siRNA) depletion and inhibitor studies that KSHV vIL-6 can increase ITGB3 by inducing STAT3 signalin

253 This suggests that KSHV has evolved to replicate independently of the activ

254 The KSHV viral load in blood did not correlate with the vira

255 XBP-1s can activate the KSHV replication and transcription activator (RTA) and l

256 Finally, genetic deletion of vIL-6 from the KSHV genome abolished KSHV-induced cellular transformati

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

258 this study, we have further examined how the KSHV-reprogramed metabolic pathways are regulated and di

259 search tool to nondestructively identify the KSHV replication stage in an infected cell would not onl

260 erted ORF57 gene in the targeted site in the KSHV genome in one of two characterized single cell clon

261 at the KSHV ORF34 protein is involved in the KSHV life cycle by regulating the expression of HIF-1alp

262 tion, highlighting their significance in the KSHV lytic cycle.

263 and PROX1, regulated different steps of the KSHV life cycle.

264 our knowledge about the architecture of the KSHV viral preinitiation complex and suggests that it fu

265 We found that the KSHV gH (ELEFN(50-54)) motif is important for higher KSH

266 The results show that the KSHV ORF34 protein is involved in the KSHV life cycle by

267 Consistent with our recent report that the KSHV ORF57 protein increases viral transcript stability

268 Our data demonstrate that the KSHV protein viral interleukin-6 (vIL-6) can induce inte

269 iator of lytic replication, and bound to the KSHV genome in the promoter region of ORF50, increasing

270 nalyses revealed that cohesin binding to the KSHV genome is highly CTCF dependent, whereas CTCF bindi

271 ell proteins CTCF and cohesin complex to the KSHV genome.

272 ependence of CTCF and cohesin binding to the KSHV genome.

273 r, especially SMARCB1, which upregulates the KSHV ORF50 promoter.

274 hile CTCF is required for cohesin binding to KSHV, they have very distinct effects, with cohesin prim

275 This suggests that malaria may lead to KSHV reactivation, thereby increasing the transmission a

276 nstrate that HACE1 facilitates resistance to KSHV infection-induced oxidative stress by promoting Nrf

277 cterize the longitudinal humoral response to KSHV in a cohort of HIV-infected Zambian mothers without

278 t render the lymphatic environment unique to KSHV life cycle.

279 ic basis for targeting this pathway to treat KSHV-associated cancers.

280 l hydrocarbon receptor (AhR) in LXA4-treated KSHV-infected cells than in untreated KSHV-infected cell

281 )-S6 kinase-dependent manner in LXA4-treated KSHV-infected cells.

282 host hedgehog (hh) signaling in LXA4-treated KSHV-infected cells.

283 EC fate in the regulation of the tumorigenic KSHV life cycle.

284 reated KSHV-infected cells than in untreated KSHV-infected cells, which probably facilitates the affi

285 tegrin beta3 (ITGB3) subunit is induced upon KSHV infection.

286 Thus, XBP-1s may directly upregulate KSHV ORF21 and, thus, contribute to the pathogenesis of

287 e, Kaposi's sarcoma-associated herpes virus (KSHV) maintains itself inside the host by escaping the h

288 n by Kaposi sarcoma-associated herpes virus (KSHV).

289 d with infections with two distinct viruses, KSHV and HIV.

290 Therefore, our study identified another way KSHV can modulate cellular gene expression.IMPORTANCE E3

291 e novel findings define a mechanism by which KSHV inhibits the CAV1 pathway and establish the scienti

292 While KSHV establishes latency in virtually all susceptible ce

293 R, and is more robust than RRV vCD200, while KSHV vCD200 does not appear to induce efficient signalin

294 HV while malaria exposure is associated with KSHV infection and/or reactivation.

295 GWAS reveals associations with KSHV antibody response in the HLA-B/C region (p = 6.64 x

296 ares this conserved inhibitory function with KSHV ORF57.

297 hat endothelial cells latently infected with KSHV express several neuronal and NE genes.

298 ur results suggest that SIRT6 interacts with KSHV ori-Lyt and ORF50 promoters.

299 pression in the lymph nodes of patients with KSHV-MCD is predominantly found in cells with XBP-1.

300 ein HIV Tat has been found to synergize with KSHV lytic proteins to induce angiogenesis.