ライフサイエンスコーパス: gammaherpesvirus

1 he antiviral CD8 T cell response to a latent gammaherpesvirus.

2 unt a type I interferon response to incoming gammaherpesvirus.

3 regulated has not been well characterized in gammaherpesviruses.

4 reactivation between related human oncogenic gammaherpesviruses.

5 first is unique for EBV and closely related gammaherpesviruses.

6 vation is imperative for latent infection of gammaherpesviruses.

7 ing late gene expression are conserved among gammaherpesviruses.

8 7, UL91, and UL95) conserved among beta- and gammaherpesviruses.

9 ene 50, is conserved among all characterized gammaherpesviruses.

10 pparently conserved in betaherpesviruses and gammaherpesviruses.

11 the study of mechanisms of immune evasion by gammaherpesviruses.

12 oded by members of the Rhadinovirus genus of gammaherpesviruses.

13 anisms of immune control of the latent human gammaherpesviruses.

14 replication and is conserved among all known gammaherpesviruses.

15 ncept is extended to include a member of the gammaherpesviruses.

16 c switch proteins and the gene expression of gammaherpesviruses.

17 68) are members of the Rhadinovirus genus of gammaherpesviruses.

18 ns from cells lytically infected with murine gammaherpesvirus 68 (gammaHV68) in order to define in de

19 We have previously shown that murine gammaherpesvirus 68 (gammaHV68) induces the degradation

20 like most cell types, ECs survive productive gammaherpesvirus 68 (gammaHV68) infection and achieve an

21 f gammaherpesvirus infection, such as murine gammaherpesvirus 68 (gammaHV68) infection, are important

22 cally important for immune control of murine gammaherpesvirus 68 (gammaHV68) infection.

23 Murine gammaherpesvirus 68 (gammaHV68) provides an important ex

24 that BMT mice are more susceptible to acute gammaherpesvirus 68 (MHV-68) replication at day 7 after

25 erpes simplex virus 1 (HSV-1), and/or murine gammaherpesvirus 68 (MHV-68) with influenza virus, West

26 ons and, in agreement with studies on murine gammaherpesvirus 68 (MHV-68), complete tegumentation and

27 n during de novo lytic infection with murine gammaherpesvirus 68 (MHV-68).

28 ion in vivo is infection of mice with murine gammaherpesvirus 68 (MHV-68).

29 characterized rhadinovirus related to murine gammaherpesvirus 68 (MHV68) and Kaposi's sarcoma-associa

30 nfected caspase-1-deficient mice with murine gammaherpesvirus 68 (MHV68) and observed no impact on ac

31 oma-associated herpesvirus (KSHV) and murine gammaherpesvirus 68 (MHV68) are members of the Rhadinovi

32 tudy, we investigate the detection of murine gammaherpesvirus 68 (MHV68) by TLR9.

33 Studies using murine gammaherpesvirus 68 (MHV68) demonstrated that LANA is im

34 Murine gammaherpesvirus 68 (MHV68) infection is characterized b

35 and ATM-deficient mice in response to mouse gammaherpesvirus 68 (MHV68) infection, the generation of

36 otein present in late stages of lytic murine gammaherpesvirus 68 (MHV68) infection.

37 Analyses of a recombinant murine gammaherpesvirus 68 (MHV68) lacking both of the known ge

38 The murine gammaherpesvirus 68 (MHV68) LANA (mLANA) is critical for

39 Murine gammaherpesvirus 68 (MHV68) ORF73 (mLANA) has sequence h

40 a custom tiled microarray to examine murine gammaherpesvirus 68 (MHV68) polyadenylated transcript ex

41 The secreted M1 protein of murine gammaherpesvirus 68 (MHV68) promotes effector Vbeta4(+)

42 The ORF75c tegument protein of murine gammaherpesvirus 68 (MHV68) promotes the degradation of

43 rst, we demonstrated that the vUNG of murine gammaherpesvirus 68 (MHV68) retains the enzymatic functi

44 -1 is capable of trans-activating the murine gammaherpesvirus 68 (MHV68) RTA promoter in vitro, consi

45 Mice were first infected with murine gammaherpesvirus 68 (MHV68), a model of Epstein-Barr vir

46 of reactivation during infection with murine gammaherpesvirus 68 (MHV68), a murine gammaherpesvirus m

47 In this article, we report that murine gammaherpesvirus 68 (MHV68), in contrast to alpha- and b

48 loyed by gammaherpesviruses, including mouse gammaherpesvirus 68 (MHV68), in order to negotiate a chr

49 n wild-type and PML(-)/(-) mice using murine gammaherpesvirus 68 (MHV68), which encodes a tegument pr

50 Mouse gammaherpesvirus 68 (MHV68)-encoded protein kinase orf36

51 oma-associated herpesvirus (KSHV) and murine gammaherpesvirus 68 (MHV68).

52 earch on Epstein-Barr virus (EBV) and murine gammaherpesvirus 68 (MHV68/gammaHV68/MHV4) has revealed

53 HV-8]), Epstein-Barr virus (EBV), and murine gammaherpesvirus 68 (MHV68; also known as gammaherpesvir

54 ne gammaherpesvirus 68 (MHV68; also known as gammaherpesvirus 68 [gammaHV68] or murine herpesvirus 4

55 rs, or brains of mice latently infected with gammaherpesvirus 68 and found that distinct sets of gene

56 B cells from mice acutely infected with gammaherpesvirus 68 are defective in BCR- and CXCR4-medi

57 Using murine gammaherpesvirus 68 expressing ovalbumin (OVA), we exami

58 us, rather than promoting loss of tolerance, gammaherpesvirus 68 infection induces an immunosuppresse

59 Gammaherpesvirus 68 infection of adult mice (an EBV mode

60 contributed to increased resistance to mouse gammaherpesvirus 68 replication, suggesting that the coo

61 fection with either gammaherpesvirus (murine gammaherpesvirus 68) or betaherpesvirus (murine cytomega

62 ucose, (ii) with an irrelevant virus (murine gammaherpesvirus 68), and (iii) without either virus do

63 iruses, in replication and latency of murine gammaherpesvirus 68.

64 d upon macrophage cell infection with murine gammaherpesvirus 68.

65 Previously, we reported that murine gammaherpesvirus-68 (M1-MHV-68) induces pulmonary artery

66 by which IRF-1 attenuates the replication of gammaherpesviruses, a mechanism that is likely to be app

67 Infection with gammaherpesviruses, alphaherpesviruses, and betacoronavi

68 Moreover, ORF52 homologs in other gammaherpesviruses also inhibit cGAS activity and simila

69 Gammaherpesviruses also target histone deacetylases (HDA

70 Work investigating gammaherpesviruses and bacterial pathogens indicates tha

71 0 (Orf50), is well conserved among all known gammaherpesviruses and is essential for both virus repli

72 The second is conserved across the beta- and gammaherpesviruses and is positioned to stabilize a puta

73 ur findings reveal a mechanism through which gammaherpesviruses antagonize host cGAS DNA sensing.

74 lbumin (OVA), we examined the stability of a gammaherpesvirus antigenic locus under strong CD8 T cell

75 Gammaherpesviruses are associated with multiple diseases

76 Gammaherpesviruses are associated with the development o

77 Gammaherpesviruses are closely associated with lymphoid

78 Gammaherpesviruses are important oncogenic pathogens tha

79 Gammaherpesviruses are lymphotropic viruses that are ass

80 As the human gammaherpesviruses are strictly species specific, small

81 tagenic stage of B cell differentiation that gammaherpesviruses are thought to target for transformat

82 Gammaherpesviruses are ubiquitious pathogens that establ

83 Gammaherpesviruses are ubiquitous pathogens that are ass

84 Gammaherpesviruses are ubiquitous pathogens that are ass

85 Gammaherpesviruses are ubiquitous pathogens that establi

86 Gammaherpesviruses are ubiquitous pathogens that establi

87 aque rhadinovirus (RRV), two closely related gammaherpesviruses, are unique in their expression of vi

88 Epstein-Barr virus (EBV) is a ubiquitous gammaherpesvirus associated with both B cell and epithel

89 KS)-associated herpesvirus (KSHV) is a human gammaherpesvirus associated with several human malignanc

90 ng viral replication in apoptosis-resistant, gammaherpesvirus-associated B lymphoma cells, suggesting

91 The nonapoptotic function of CD95 in gammaherpesvirus-associated lymphomas is largely unknown

92 Gammaherpesvirus-associated neoplasms include tumors of

93 There are few large-animal models for gammaherpesvirus-associated pathogenesis.

94 However, studies of gammaherpesvirus-associated VLVs have been largely restr

95 the productive infection of tumor-associated gammaherpesviruses, both virions and VLVs are produced a

96 organization with gammaHV68 and the primate gammaherpesviruses but is phylogenetically distinct from

97 g animal models in which the pathogenesis of gammaherpesviruses can be characterized.

98 t, like alpha- and betaherpesviruses, EBV, a gammaherpesvirus, can mediate cell fusion if gB and gHgL

99 Alcelaphine herpesvirus 1 (AlHV-1) is a gammaherpesvirus carried asymptomatically by wildebeest.

100 oma-associated herpesvirus (KSHV) is a human gammaherpesvirus casually linked to Kaposi's sarcoma (KS

101 hat type I IFNs function to enhance the anti-gammaherpesvirus CD8(+) T cell response.

102 Rhesus rhadinovirus (RRV) is a gammaherpesvirus closely related to Kaposi's sarcoma-ass

103 DNA sequence analysis reveals that JMRV is a gammaherpesvirus closely related to rhesus macaque rhadi

104 Gammaherpesviruses coevolved with the vertebrate immune

105 Site-directed mutagenesis of gammaherpesvirus conserved residues revealed functional

106 uence and characterization of a novel rodent gammaherpesvirus, designated rodent herpesvirus Peru (RH

107 viral antigen and facilitating an effective gammaherpesvirus-directed CD8(+) T cell response.

108 Gammaherpesviruses display tropism for B cells and, like

109 e E3 ligase activity of mLANA contributes to gammaherpesvirus-driven GC B cell proliferation.

110 We found that this gammaherpesvirus-driven germinal center expansion was ex

111 vide insight into the potential mechanism of gammaherpesvirus-driven lymphomagenesis.

112 ivity may allow strategies to interfere with gammaherpesvirus-driven lymphoproliferation and associat

113 box motifs is a putative strategy to control gammaherpesvirus-driven lymphoproliferation and associat

114 pha- and betaherpesvirus, gB and gHgL of the gammaherpesvirus EBV can mediate fusion and entry when e

115 is known for its neuroinvasion, whereas the gammaherpesvirus EBV is associated with cancer of epithe

116 irus pseudorabies virus (PrV) with gH of the gammaherpesvirus EBV to identify functionally equivalent

117 The prototypic human gammaherpesvirus EBV, which is associated with infectiou

118 lation becomes infected early in life by the gammaherpesvirus EBV.

119 ch has severely limited studies on the human gammaherpesviruses EBV and Kaposi's sarcoma-associated h

120 Gammaherpesviruses employ multiple mechanisms to transie

121 All gammaherpesviruses encode a conserved protein kinase tha

122 Collectively, our results demonstrate that gammaherpesviruses encode inhibitors that block cGAS-STI

123 Gammaherpesviruses encode numerous immunomodulatory mole

124 genome, like the genomes of other beta- and gammaherpesviruses, encodes G protein-coupled receptors

125 hnique to rescue the replication of a murine gammaherpesvirus engineered with a mutation in the major

126 h genetic and biologic homology to the human gammaherpesvirus Epstein-Barr virus (EBV), which infects

127 The human gammaherpesviruses Epstein-Barr virus (EBV) and Kaposi's

128 The gammaherpesviruses Epstein-Barr virus (EBV) and Kaposi's

129 However, studies of the human gammaherpesvirus, Epstein-Barr virus, have found viral i

130 on from latency of another related oncogenic gammaherpesvirus, Epstein-Barr virus.

131 Infection with the human gammaherpesviruses, Epstein-Barr virus (EBV) and Kaposi'

132 IMPORTANCE Gammaherpesviruses establish chronic infection in a majo

133 Gammaherpesviruses establish chronic infection in a majo

134 Most known gammaherpesviruses establish latency in B lymphocytes.

135 Gammaherpesviruses establish lifelong infection in most

136 Gammaherpesviruses establish lifelong infections that ar

137 ssociated herpesvirus (KSHV) is an oncogenic gammaherpesvirus etiologically associated with Kaposi's

138 Thus, gammaherpesviruses evade immune activation by the cytoso

139 In general, the characterized gammaherpesviruses exhibit a very narrow host tropism, w

140 Thus, a CD8 T cell response to a gammaherpesvirus-expressed antigen that is not essential

141 Members of the alpha-, beta-, and gammaherpesvirus families all express proteins that inte

142 established observation among members of the gammaherpesvirus family is the link between viral reacti

143 ciated herpesvirus (KSHV) is a member of the gammaherpesvirus family.

144 mice with an EBV-related and rodent-specific gammaherpesvirus, gammaHV68.

145 Gammaherpesviruses (gammaHVs) have a dynamic strategy fo

146 Lymphocyte colonization by gammaherpesviruses (gammaHVs) is an important target for

147 factor can trigger expression of the murine gammaherpesvirus gene involved in driving virus reactiva

148 arently functioning with four other beta- or gammaherpesvirus gene products in a pattern that appears

149 Gammaherpesviruses (GHVs) are a diverse and rapidly expa

150 Gammaherpesviruses (GHVs) carry homologs of cellular gen

151 The gammaherpesviruses (GHVs) cause lifelong infection and c

152 Gammaherpesviruses (GHVs) establish lifelong infection i

153 ther and how such tegument proteins exist in gammaherpesviruses have been mysteries.

154 As obligate pathogens, gammaherpesviruses have evolved a plethora of mechanisms

155 pathway, it is intriguing to speculate that gammaherpesviruses have evolved to usurp the type I inte

156 Alphaherpesviruses, unlike beta- and gammaherpesviruses, have the unique ability to infect an

157 ion, are important for studying the roles of gammaherpesvirus immune evasion genes in in vivo infecti

158 V68 that have sequence similarity to primate gammaherpesvirus immunomodulatory genes or cellular gene

159 Taken together, murine gammaherpesvirus impairment of the inflammatory cytokine

160 Ovine herpesvirus 2 (OvHV-2) is a gammaherpesvirus in the genus Macavirus that is carried

161 lymphocryptovirus (rLCV) are closely related gammaherpesviruses in the lymphocryptovirus subgroup tha

162 vation, and latency establishment of several gammaherpesviruses in vitro, suggesting that ATM is prov

163 by members of the rhadinovirus subfamily of gammaherpesviruses, including Kaposi sarcoma-associated

164 Gammaherpesviruses, including Kaposi's sarcoma-associate

165 cellular pathways is a strategy employed by gammaherpesviruses, including mouse gammaherpesvirus 68

166 pe death receptor controls the life cycle of gammaherpesviruses independent of its apoptotic activity

167 we found decreased IRF-1 expression in human gammaherpesvirus-induced B cell malignancies.

168 interfering with infection in the setting of gammaherpesvirus-induced diseases.

169 risk factors that predispose the host toward gammaherpesvirus-induced malignancies are still poorly u

170 aherpesvirus infection of B cells.IMPORTANCE Gammaherpesviruses infect a majority of the human popula

171 pression is required to ensure survival of a gammaherpesvirus-infected host past the first 8 days of

172 n of IRF3 at the beta interferon promoter in gammaherpesvirus-infected primary macrophages.

173 Chronic gammaherpesvirus infection and pathogenesis in a DNA dam

174 signaling ensures host survival during acute gammaherpesvirus infection and supports IFN gamma-mediat

175 resents a plausible host factor to attenuate gammaherpesvirus infection and tumorigenesis.

176 Available data support a model in which gammaherpesvirus infection drives B cell proliferation a

177 is both activated and subverted during human gammaherpesvirus infection in culture.

178 spondingly, in the absence of IRF-1, chronic gammaherpesvirus infection induced pathological changes

179 e role of the vUNG in a pathogenic course of gammaherpesvirus infection is not known.

180 Chronic gammaherpesvirus infection is poorly controlled in a hos

181 Here we demonstrate that chronic gammaherpesvirus infection is poorly controlled in an an

182 ting memory B cells, suggesting that chronic gammaherpesvirus infection is primarily dormant.

183 Gammaherpesvirus infection leads to severe disease in im

184 f ATM as a host factor that promotes chronic gammaherpesvirus infection of B cells.IMPORTANCE Gammahe

185 on of a type I interferon response following gammaherpesvirus infection of primary macrophages.

186 o monitor murine B2 SINE expression during a gammaherpesvirus infection revealed transcription from 2

187 Infected cells counteract gammaherpesvirus infection via innate immune signaling m

188 amage response and immune control of chronic gammaherpesvirus infection, a connection that is likely

189 a unique yet incompletely understood role in gammaherpesvirus infection, as it has both proviral and

190 ls can enhance CD8(+) T cell function during gammaherpesvirus infection, potentially through suppress

191 tly species specific, small animal models of gammaherpesvirus infection, such as murine gammaherpesvi

192 Due to the ubiquitous and chronic nature of gammaherpesvirus infection, the role of HDAC1 and -2 in

193 he complex relationship between host ATM and gammaherpesvirus infection, we depleted ATM specifically

194 replication and reactivation associated with gammaherpesvirus infection.

195 in B cells, a cell type critical for chronic gammaherpesvirus infection.

196 deficient and -proficient macrophages during gammaherpesvirus infection.

197 odulated by SINE ncRNAs, particularly during gammaherpesvirus infection.

198 zes the intrinsic cytokine production during gammaherpesvirus infection.

199 oviral and antiviral roles in the context of gammaherpesvirus infection.

200 nduction of the antiviral state during acute gammaherpesvirus infection.

201 1a, B cells display the highest frequency of gammaherpesvirus infection.

202 cell-specific ATM expression during chronic gammaherpesvirus infection.

203 n (IFN) and IRF-1 cooperate to control acute gammaherpesvirus infection.

204 order, a malignant condition associated with gammaherpesvirus infection.

205 An integral feature of gammaherpesvirus infections is the ability to establish

206 Gammaherpesvirus infections, such as those caused by EBV

207 H2AX is important for gammaherpesvirus infectivity, and its phosphorylation at

208 Kaposi sarcoma herpesvirus (KSHV), a human gammaherpesvirus, is the etiological agent for the endot

209 ) and its close homolog, the oncogenic human gammaherpesvirus Kaposi's sarcoma-associated herpesvirus

210 The human gammaherpesvirus, Kaposi's sarcoma-associated herpesviru

211 Two closely related gammaherpesviruses, Kaposi's sarcoma-associated herpesvi

212 development of improved therapeutics against gammaherpesvirus kinases.

213 s sarcoma-associated herpesvirus (KSHV) is a gammaherpesvirus known to establish lifelong latency in

214 all nucleic acids (microRNAs) expressed by a gammaherpesvirus (KSHV), which identified a gene called

215 As a gammaherpesvirus, KSHV is able to acutely replicate, ent

216 ument proteins in the prototypical member of gammaherpesviruses, KSHV.

217 ther, these results demonstrate that ongoing gammaherpesvirus latency affects the number and phenotyp

218 We observed that ongoing gammaherpesvirus latency affects the number and phenotyp

219 mechanisms that underlie the role of PML in gammaherpesvirus latency and may yield clues for how PML

220 Host suppression of gammaherpesvirus latency and reactivation requires both

221 sary for the establishment or maintenance of gammaherpesvirus latency but that it does affect reactiv

222 data showing that miR-155 is dispensable for gammaherpesvirus latency but that it is critical for rea

223 nt of a chronically infected host attenuates gammaherpesvirus latency in a route-of-infection-specifi

224 ral miR-155 homologs in the establishment of gammaherpesvirus latency in B cells.

225 repress the establishment or maintenance of gammaherpesvirus latency in vivo.

226 these studies was to determine the effect of gammaherpesvirus latency on T cell number and differenti

227 ls and antibody contribute to the control of gammaherpesvirus latency, reactivation, and spread.

228 s is required for efficient establishment of gammaherpesvirus latency.

229 uclear antigen (mLANA) E3 ligase activity in gammaherpesvirus latent infection.

230 WT virus contamination in an animal model of gammaherpesvirus lethality.

231 The mechanisms by which gammaherpesviruses maintain latency are unclear.

232 uses, including the papillomaviruses and the gammaherpesviruses, maintain their plasmid genomes by te

233 immunity in mice suggest that infection with gammaherpesviruses may be protective rather than patholo

234 ver, these findings suggest a model in which gammaherpesviruses may gain access to the mature B cell

235 maintenance of latency in vivo using murine gammaherpesvirus (MHV-68) infection.

236 The murine gammaherpesvirus MHV68 has both genetic and biologic hom

237 Here we demonstrate that the murine gammaherpesvirus (MHV68) homolog, encoded by gene 50, is

238 murine gammaherpesvirus 68 (MHV68), a murine gammaherpesvirus model for Epstein-Barr virus.

239 Here we used a murine gammaherpesvirus model to show that previously uninfecte

240 ittle HS and that upon infection with either gammaherpesvirus (murine gammaherpesvirus 68) or betaher

241 Rhesus macaque rhadinovirus (RRV) is a gammaherpesvirus of rhesus macaque (RM) monkeys that is

242 s (alphaherpesviruses, betaherpesviruses, or gammaherpesviruses) of Herpesviridae.

243 Unexpectedly, we found that murine gammaherpesvirus pathogenesis was not enhanced in mice l

244 Gammaherpesviruses persist for the lifetime of the host.

245 ay be the best vaccine option for preventing gammaherpesvirus persistence.

246 this study, we identify a novel function of gammaherpesvirus protein kinase as a regulator of class

247 y, we have previously shown that a conserved gammaherpesvirus protein kinase interacts with HDAC1 and

248 scription factor, XBP-1, to the induction of gammaherpesvirus reactivation, and we show here that ind

249 establish the TLKs as cellular repressors of gammaherpesvirus reactivation.

250 l gene product involved in the initiation of gammaherpesvirus replication and is conserved among all

251 The impact of the inflammasome response on gammaherpesvirus replication and latency in vivo is not

252 that regulate later stages of the productive gammaherpesvirus replication cycle are still poorly defi

253 In contrast, a brief period of active gammaherpesvirus replication during acute infection of a

254 We show that statin treatment attenuated gammaherpesvirus replication in primary immune cells and

255 into the mechanism by which IRF-1 attenuates gammaherpesvirus replication in primary immune cells, a

256 5-hydroxylase, a host enzyme that restricted gammaherpesvirus replication in primary macrophages and

257 tenuation of cholesterol synthesis decreases gammaherpesvirus replication in primary macrophages in v

258 In this study, we show that IRF-1 restricts gammaherpesvirus replication in primary macrophages, a p

259 ere we show that IRF-1 expression attenuates gammaherpesvirus replication in primary macrophages, in

260 inase interacts with HDAC1 and -2 to promote gammaherpesvirus replication in primary macrophages.

261 in prenylation was responsible for decreased gammaherpesvirus replication in statin-treated primary m

262 antiviral effects of type II IFN to restrict gammaherpesvirus replication in vivo, in the lungs, and

263 ed signaling events capable of driving lytic gammaherpesvirus replication or enhancing immediate-earl

264 Late gene expression in gammaherpesviruses requires the coordination of six earl

265 importance of DNA methylation in regulating gammaherpesvirus RTA/gene 50 transcription during virus

266 we provide for the first time evidence that gammaherpesvirus sncRNAs contribute to the maintenance o

267 t role for type I IFN signaling in enhancing gammaherpesvirus-specific CD8(+) T cell cytokine product

268 s sarcoma-associated herpesvirus (KSHV) is a gammaherpesvirus-specific immediate-early tegument prote

269 We recently found that one such gammaherpesvirus-specific protein, ORF52, has an importa

270 In this report, we show that the gammaherpesvirus-specific tegument protein ORF52 is crit

271 ciated herpesvirus (KSHV) ORF52, an abundant gammaherpesvirus-specific tegument protein, subverts cyt

272 tein with homologs in the alpha-, beta-, and gammaherpesvirus subfamilies.

273 rus (KSHV) virion, a member of the oncogenic gammaherpesvirus subfamily.

274 Gammaherpesviruses, such as Epstein-Barr virus (EBV), ar

275 ong conservation of the DLD across beta- and gammaherpesviruses suggests that integrin recognition an

276 HVS is an oncogenic gammaherpesvirus that causes acute T-cell lymphomas and

277 stein-Barr virus (EBV) is a ubiquitous human gammaherpesvirus that establishes a latency reservoir in

278 s sarcoma-associated herpesvirus (KSHV) is a gammaherpesvirus that has been associated with primary e

279 Epstein-Barr virus (EBV) is an oncogenic gammaherpesvirus that infects and persists in 95% of adu

280 Epstein-Barr Virus (EBV) is a gammaherpesvirus that infects the majority of the human

281 NA1.IMPORTANCE Epstein-Barr virus is a human gammaherpesvirus that is causally associated with variou

282 Epstein-Barr virus (EBV) is a ubiquitous gammaherpesvirus that is highly prevalent in almost all

283 Epstein-Barr virus (EBV) is an oncogenic gammaherpesvirus that is implicated in several human mal

284 function and provides a novel mechanism for gammaherpesviruses that helps them to escape host immune

285 Epstein-Barr virus (EBV) are closely related gammaherpesviruses that infect and cause disease in rhes

286 h tegument proteins have been identified for gammaherpesviruses, the third herpesvirus subfamily, whi

287 production and for the antiviral response to gammaherpesvirus through two independent kinome-wide RNA

288 fatty acids stimulate the two related human gammaherpesviruses to enter the lytic cycle through diff

289 st antibody drives the majority of sensitive gammaherpesvirus-transformed B cells to undergo caspase-

290 While ATM expression did not affect gammaherpesvirus tropism for B-1 B cells, B cell-specifi

291 urprisingly, both replication and latency of gammaherpesviruses, ubiquitous cancer-associated pathoge

292 an optimal adaptive immune response against gammaherpesvirus unveils an important connection between

293 It is still unknown whether a noninfectious gammaherpesvirus vaccine is able to prevent or reduce vi

294 These data show that the gammaherpesvirus viral cyclin functions specifically to

295 Neither the beta- nor gammaherpesvirus VP1-2 motifs were identified by predict

296 This human gammaherpesvirus was discovered in 1994 by Drs.

297 In the case of gammaherpesviruses, which are associated with the develo

298 The genome of Epstein-Barr virus (EBV), a gammaherpesvirus with potent B-cell growth-transforming

299 Coevolution of gammaherpesviruses with their hosts has resulted in an i

300 ociated tegument proteins are organized in a gammaherpesvirus, with five tegument densities capping e