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 oded by members of the Rhadinovirus genus of gammaherpesviruses.

4 replication and is conserved among all known gammaherpesviruses.

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

6 c switch proteins and the gene expression of gammaherpesviruses.

7 regulated has not been well characterized in gammaherpesviruses.

8 reactivation between related human oncogenic gammaherpesviruses.

9 first is unique for EBV and closely related gammaherpesviruses.

10 vation is imperative for latent infection of gammaherpesviruses.

11 ing late gene expression are conserved among gammaherpesviruses.

12 7, UL91, and UL95) conserved among beta- and gammaherpesviruses.

13 ene 50, is conserved among all characterized gammaherpesviruses.

14 ng RNAs has only recently been identified in gammaherpesviruses.

15 ized for inducing oncogenesis by these human gammaherpesviruses.

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

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

18 ty against herpes simplex virus 1 (HSV-1) or gammaherpesvirus 68 (gammaHV68) infection.

19 ed heterozygous STING N153S mice with murine gammaherpesvirus 68 (gammaHV68).

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

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

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

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

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

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

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

27 Using murine gammaherpesvirus 68 (MHV68) as a small-animal model to d

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

29 Murine gammaherpesvirus 68 (MHV68) infection is characterized b

30 Murine gammaherpesvirus 68 (MHV68) is a small-animal model suit

31 t specific, and therefore the homolog murine gammaherpesvirus 68 (MHV68) is a widely used model to ob

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

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

34 Remarkably, using a murine gammaherpesvirus 68 (MHV68) reporter virus, we discovere

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

36 -1 is capable of trans-activating the murine gammaherpesvirus 68 (MHV68) RTA promoter in vitro, consi

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

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

39 sociated herpesvirus (KSHV), muSOX in murine gammaherpesvirus 68 (MHV68), BGLF5 in Epstein-Barr virus

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

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

42 or 1 (IRF-1) selectively promotes the murine gammaherpesvirus 68 (MHV68)-driven germinal center respo

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

44 with DNA viruses, including the model murine gammaherpesvirus 68 (MHV68).

45 ication of diverse viruses, including murine gammaherpesvirus 68 (MHV68).

46 ma-associated herpesvirus (KSHV), and murine gammaherpesvirus 68 (MHV68, gammaHV68, MuHV-4) establish

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

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

49 nditions, on infection of mice with a murine gammaherpesvirus 68 chimera expressing LANA, where the v

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

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

52 d upon macrophage cell infection with murine gammaherpesvirus 68.

53 Murine gammaherpesvirus-68 (MHV-68) intraperitoneal infection i

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

55 In the beta- and gammaherpesviruses, a specialized complex of viral trans

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

57 Gammaherpesviruses also target histone deacetylases (HDA

58 coma-associated herpesvirus (KSHV) are human gammaherpesviruses and are important in a variety of mal

59 Work investigating gammaherpesviruses and bacterial pathogens indicates tha

60 0 (Orf50), is well conserved among all known gammaherpesviruses and is essential for both virus repli

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

62 Lymphocryptovirus and Rhadinovirus genera of gammaherpesviruses and provide evolutionary support for

63 ights into the interaction between these two gammaherpesviruses and their host.

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

65 Gammaherpesviruses are associated with multiple diseases

66 Gammaherpesviruses are associated with the development o

67 Gammaherpesviruses are closely associated with lymphoid

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

69 of gammaherpesvirus pathogenesis.IMPORTANCE Gammaherpesviruses are ubiquitous cancer-associated path

70 As gammaherpesviruses are ubiquitous oncogenic agents, LXRs

71 Gammaherpesviruses are ubiquitous pathogens that are ass

72 Gammaherpesviruses are ubiquitous pathogens that are ass

73 Gammaherpesviruses are ubiquitous pathogens that are ass

74 Gammaherpesviruses are ubiquitous pathogens that are ass

75 Gammaherpesviruses are ubiquitous pathogens that establi

76 Gammaherpesviruses are ubiquitous pathogens that establi

77 Gammaherpesviruses are ubiquitous pathogens that establi

78 Gammaherpesviruses are ubiquitous pathogens that establi

79 Gammaherpesviruses are ubiquitous viruses that establish

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

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

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

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

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

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

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

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

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

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

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

91 A unique feature of early gammaherpesvirus chronic infection is a robust different

92 ery in this species has been confined to one gammaherpesvirus (dasyurid herpesvirus 2 [DaHV-2]), for

93 Late gene transcription in the beta- and gammaherpesviruses depends on a set of virally encoded t

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

95 Gammaherpesviruses display tropism for B cells and, like

96 of interleukin-1 (IL-1) receptor attenuates gammaherpesvirus-driven B cell differentiation and viral

97 Thus, in spite of decreased SHP1 levels in gammaherpesvirus-driven B cell lymphomas, B cell-intrins

98 While risk factors for developing gammaherpesvirus-driven cancers are poorly understood, i

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

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

101 eration of hematopoietic cells, enhances the gammaherpesvirus-driven germinal center response and the

102 cell-intrinsic SHP1 expression supports the gammaherpesvirus-driven germinal center response and the

103 The gammaherpesvirus-driven germinal center response in comb

104 nd viral factors that selectively affect the gammaherpesvirus-driven germinal center response remain

105 wn to either promote or selectively restrict gammaherpesvirus-driven germinal center response, viral

106 ling promote irrelevant B cell responses and gammaherpesvirus-driven germinal center responses, with

107 he target of malignant transformation during gammaherpesvirus-driven lymphomagenesis, identification

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

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

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

111 l activation and is downregulated in several gammaherpesvirus-driven malignancies.

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

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

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

115 echanism has recently been uncovered for the gammaherpesvirus EBV, in which a subunit of the viral pr

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

117 Gammaherpesviruses employ multiple mechanisms to transie

118 To facilitate colonization of a host, gammaherpesviruses encode gene products that manipulate

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

120 Here, we show that gammaherpesvirus-encoded conserved protein kinase and ho

121 expression and the enzymatic activity of the gammaherpesvirus-encoded conserved protein kinase select

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

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

124 The human gammaherpesvirus Epstein-Barr virus (EBV) (human herpesv

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

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

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

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

129 g mechanism include papillomaviruses and the gammaherpesviruses Epstein-Barr virus and Kaposi's sarco

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

131 of MHV68 infection.IMPORTANCE The two human gammaherpesviruses, Epstein-Barr virus (EBV) and Kaposi'

132 Gammaherpesviruses establish chronic infection in a majo

133 IMPORTANCE Gammaherpesviruses establish chronic infection in a majo

134 s to facilitate host colonization.IMPORTANCE Gammaherpesviruses establish lifelong chronic infections

135 age of infection and pathogenesis.IMPORTANCE Gammaherpesviruses establish lifelong infection in a maj

136 Gammaherpesviruses establish lifelong infection in most

137 ression by non-B cell populations.IMPORTANCE Gammaherpesviruses establish lifelong infection in over

138 Gammaherpesviruses establish lifelong infections that ar

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

140 Thus, gammaherpesviruses evade immune activation by the cytoso

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 (EBV) which, similar to KSHV, belongs to the Gammaherpesvirus family.

144 R isoforms, restricts reactivation of latent gammaherpesvirus from peritoneal cells.

145 Persistent infection with gammaherpesviruses (gammaHV) can cause lymphomagenesis i

146 Gammaherpesviruses (gammaHVs) have a dynamic strategy fo

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

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

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

150 Gammaherpesviruses (GHVs) are a diverse and rapidly expa

151 Gammaherpesviruses (GHVs) are DNA tumor viruses that est

152 Gammaherpesviruses (GHVs) carry homologs of cellular gen

153 The gammaherpesviruses (GHVs) cause lifelong infection and c

154 Gammaherpesviruses (GHVs) establish lifelong infection i

155 set of orthologous genes found in beta- and gammaherpesviruses have been determined to encode a vira

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

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

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

159 Taken together, murine gammaherpesvirus impairment of the inflammatory cytokine

160 mologous genes for the cell tropism of other gammaherpesviruses.IMPORTANCE Elucidating the molecular

161 n-specific T cell responses against a common gammaherpesvirus in mice.IMPORTANCE Mechanisms of immuno

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

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

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

165 The oncogenic gammaherpesviruses, including human Epstein-Barr virus (

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

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

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

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

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

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

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

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

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

175 actor for the treatment of poorly controlled gammaherpesvirus infection and associated lymphomagenesi

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

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

178 Chronic gammaherpesvirus infection has been implicated in both l

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

180 contrast, IRF-7 expression restricted latent gammaherpesvirus infection in the peritoneal cavity unde

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

182 ingdom host-virus-microbiome interactions in gammaherpesvirus infection influences gammaherpesviral i

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

184 Chronic gammaherpesvirus infection is poorly controlled in a hos

185 A unique feature of early gammaherpesvirus infection is the robust increase in dif

186 Gammaherpesvirus infection leads to severe disease in im

187 hat promote germinal center responses during gammaherpesvirus infection may offer an insight into the

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

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

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

191 ll-intrinsic SHP1 deficiency cooperated with gammaherpesvirus infection to increase the levels of dou

192 Infected cells counteract gammaherpesvirus infection via innate immune signaling m

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

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

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

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

197 of IRF-7 continues into the chronic phase of gammaherpesvirus infection, wherein IRF-7 restricts the

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

199 odulated by SINE ncRNAs, particularly during gammaherpesvirus infection.

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

201 nduction of the antiviral state during acute gammaherpesvirus infection.

202 1a, B cells display the highest frequency of gammaherpesvirus infection.

203 cell-specific ATM expression during chronic gammaherpesvirus infection.

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

205 order, a malignant condition associated with gammaherpesvirus infection.

206 replication and reactivation associated with gammaherpesvirus infection.

207 deficient and -proficient macrophages during gammaherpesvirus infection.

208 al role of IRF-7 during the chronic stage of gammaherpesvirus infection.IMPORTANCE The innate immune

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

210 The oncogenic gammaherpesvirus Kaposi sarcoma-associated herpesvirus (

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

212 by several DNA viruses, including the human gammaherpesvirus Kaposi's sarcoma-associated herpesvirus

213 mechanism is shared with the closely related gammaherpesvirus Kaposi's sarcoma-associated herpesvirus

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

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

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

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

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

219 ations with A3B to include a closely related gammaherpesvirus, KSHV, and a more distantly related alp

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

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

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

223 Host suppression of gammaherpesvirus latency and reactivation requires both

224 he precise determinants that mediate in vivo gammaherpesvirus latency and tumorigenesis remain unclea

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

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

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

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

229 ic infection by restricting establishment of gammaherpesvirus latency in the peritoneal cavity and, t

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

231 s is required for efficient establishment of gammaherpesvirus latency.

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

233 lication.IMPORTANCE Infection with oncogenic gammaherpesviruses leads to long-term viral persistence

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

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

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

237 The murine gammaherpesvirus MHV68 has both genetic and biologic hom

238 Here, we established that infection with the gammaherpesvirus MHV68 leads to a dramatic induction of

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

240 s-68 (MHV-68) intraperitoneal infection is a gammaherpesvirus model for producing severe vasculitis,

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 ction in distinct cellular subsets to direct gammaherpesvirus pathogenesis.

245 n may offer an insight into the mechanism of gammaherpesvirus pathogenesis.IMPORTANCE Gammaherpesviru

246 Gammaherpesviruses persist for the lifetime of the host.

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

248 receptor alpha isoform (LXRalpha) restricts gammaherpesvirus reactivation in an anatomic-site-specif

249 Thus, LXRalpha restricts gammaherpesvirus reactivation through a novel mechanism

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

251 tionally, the critical host defenses against gammaherpesvirus reactivation, virus-specific CD8(+) T c

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

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

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

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

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

257 5-hydroxylase, a host enzyme that restricted gammaherpesvirus replication in primary macrophages and

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

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

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

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

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

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

264 e cultures, with a corresponding increase in gammaherpesvirus replication.

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

266 nt of chronic infection, suggesting that the gammaherpesvirus-SHP1 interaction is more nuanced and is

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

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

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

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

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

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

273 ar RNA class of RNAs across 4 members of the gammaherpesvirus subfamily, and they identify orthologue

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

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

276 ssociated herpesvirus (KSHV) is an oncogenic gammaherpesvirus that causes Kaposi's sarcoma and other

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 (KSHV; human herpesvirus 8) is an oncogenic gammaherpesvirus that is the causative agent of multiple

284 an intriguing beneficial interaction between gammaherpesviruses that are presumed to profit from B ce

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

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 argely associated with the unique ability of gammaherpesviruses to usurp B cell differentiation, spec

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

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

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

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

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

295 This human gammaherpesvirus was discovered in 1994 by Drs.

296 ses, papillomaviruses, polyomaviruses, and a gammaherpesvirus, were identified, as well as known mamm

297 Epstein-Barr virus (EBV) is a ubiquitous gammaherpesvirus which asymptomatically infects the majo

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

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