ライフサイエンスコーパス: herpesvirus

1 l and tracheal swabs might be used to detect herpesvirus.

2 ruses infection, Kaposi's sarcoma-associated herpesvirus.

3 rus (HCMV) is a ubiquitous, human pathogenic herpesvirus.

4 ce to Marek's disease caused by an oncogenic herpesvirus.

5 ell-mediated immune control of a human gamma-herpesvirus.

6 e complete genome sequence of a novel murine herpesvirus.

7 esus monkey rhadinovirus (RRV), a persisting herpesvirus.

8 so a helper virus such as an adenovirus or a herpesvirus.

9 ne proteins play key roles in the biology of herpesviruses.

10 rt explained by age and infection with other herpesviruses.

11 elope protein that is highly conserved among herpesviruses.

12 nd pUL51, which have homologues in all other herpesviruses.

13 small genomic region, as seen in other human herpesviruses.

14 r viruses, including ZIKV, alphaviruses, and herpesviruses.

15 UL16 of HSV-1 but also its homologs in other herpesviruses.

16 se subunit that is partially conserved among herpesviruses.

17 re may be common among tailed DNA phages and herpesviruses.

18 n in PNS neurons is a hallmark of most alpha herpesviruses.

19 eta-subfamily and absent in alpha- and gamma-herpesviruses.

20 of Ca-SP against infections caused by other herpesviruses.

21 M and homologous essential proteins in other herpesviruses.

22 the absence of gL syncytial mutants in other herpesviruses.

23 of large double-stranded DNA viruses such as herpesviruses.

24 is conserved among all three subfamilies of herpesviruses.

25 irculating diversity of all classes of human herpesviruses.

26 Alphaherpesvirinae subfamily members, bovine herpesvirus 1 (BoHV-1) expresses an abundant transcript

27 e latency-related (LR) RNA encoded by bovine herpesvirus 1 (BoHV-1) is abundantly expressed in latent

28 Bovine herpesvirus 1 (BoHV-1) is an important pathogen of cattl

29 Bovine herpesvirus 1 (BoHV-1) is an important pathogen of domes

30 ollowing stressful stimuli.IMPORTANCE Bovine herpesvirus 1 (BoHV-1) is an important viral pathogen th

31 le.IMPORTANCE The lifelong latency of bovine herpesvirus 1 (BoHV-1) requires that significant numbers

32 Bovine herpesvirus 1 (BoHV-1), an important bovine pathogen, es

33 ion remains the best option to combat equine herpesvirus 1 (EHV-1) infection, and several different s

34 Equine herpesvirus 1 (EHV-1) is a major pathogen affecting equi

35 Two extrinsic controls (phocine herpesvirus 1 and bacteriophage MS2) were included to en

36 MDP treatment before or after infection with herpesvirus 1 did not inhibit its replication.

37 B virus (Macacine herpesvirus 1) can cause deadly zoonotic disease in huma

38 Ovine herpesvirus 2 (OvHV-2) is a gammaherpesvirus in the genu

39 Entry of ovine herpesvirus 2 (OvHV-2), the causative agent of sheep ass

40 Cyprinid herpesvirus 3 (CyHV-3) is the archetype of fish alloherp

41 Cyprinid herpesvirus 3 (CyHV-3) is the archetype of fish alloherp

42 cella-zoster virus (VZV; also known as human herpesvirus 3 [HHV-3]).

43 ever in the common carp infected by cyprinid herpesvirus 3, a native carp pathogen.

44 e of marine turtles associated with chelonid herpesvirus 5 (ChHV5), which has historically been refra

45 One example is chelonid herpesvirus 5 (ChHV5), which is associated with fibropap

46 Human herpesvirus 6 (HHV-6) species have a unique ability to i

47 virus (CMV), Epstein-Barr virus (EBV), human herpesvirus 6 (HHV-6), herpes simplex virus types 1 (HSV

48 megalovirus (CMV), BK virus (BKV), and human herpesvirus 6 (HHV-6).

49 BK virus (BKV), adenovirus (ADV), and human herpesvirus 6 (HHV6) were evaluated to determine overall

50 f interest were VR of adenovirus, EBV, human herpesvirus 6 (HHV6), cytomegalovirus (CMV), and BK viru

51 CMV, herpes simplex virus type 1, and human herpesvirus 6 infection were independently associated wi

52 BK virus, cytomegalovirus, adenovirus, human herpesvirus 6, and Epstein-Barr virus.

53 rovirus, herpes simplex virus 1 and 2, human herpesvirus 6, human parechovirus, varicella-zoster viru

54 pesviruses herpes simplex virus 1 and murine herpesvirus 68 and the parvovirus minute virus of mice (

55 The genomes of human herpesvirus 6A (HHV-6A) and HHV-6B have the capacity to

56 Human herpesvirus 6A (HHV-6A), HHV-6B, and HHV-7 are classifie

57 The human roseoloviruses human herpesvirus 6A (HHV-6A), HHV-6B, and HHV-7 comprise the

58 closely related to the roseoloviruses, human herpesviruses 6A, 6B, and 7.

59 Human herpesviruses 6A/B (HHV-6A/B) can integrate their viral

60 for cytomegalovirus, BK polyomavirus, human herpesvirus 6B, HHV-6A, adenovirus, and Epstein-Barr vir

61 e have provisionally named Macaca nemestrina herpesvirus 7 (MneHV7).

62 , parvovirus B19, cytomegalovirus, and human herpesvirus 7).

63 sized that they could be infected with human herpesvirus 8 (HHV-8) (Kaposi's sarcoma [KS]-associated

64 Human herpesvirus 8 (HHV-8) infection occurs in early childhoo

65 Viral interleukin-6 (vIL-6) encoded by human herpesvirus 8 (HHV-8) is believed to contribute via mito

66 Human herpesvirus 8 (HHV-8) is the causative agent of Kaposi s

67 Kaposi sarcoma is the most common human herpesvirus 8 (HHV-8)-related disease described after so

68 virus (EBOV), Tacaribe arenavirus, and human herpesvirus 8 (HHV-8).

69 Human herpesvirus 8 (HHV8) causes multicentric Castleman's dis

70 l Italy and a surveillance program for human herpesvirus 8 (HHV8) infection after transplant, aiming

71 roved survival and reduced the risk of human herpesvirus 8 (HHV8)-associated lymphoma.

72 aposi's sarcoma-associated herpesvirus/human herpesvirus 8 (KSHV/HHV8), exploit microtubule (MT)-base

73 increased KS risk, likely due to high human herpesvirus 8 coinfection rates.

74 Human herpesvirus 8 seroprevalence was 4% (10/249) in donors a

75 ), herpes simplex virus types 1 and 2, human herpesvirus 8) using multiplex serology on blood samples

76 ated herpesvirus (KSHV), also known as human herpesvirus 8, is the etiologic agent underlying Kaposi

77 Human herpesvirus 8, which causes Kaposi sarcoma, expresses th

78 Human herpesvirus 8-DNA was detected in 6.8% and 2.9% of HHV8-

79 on lymphomas (PEL) are associated with human herpesvirus-8 (HHV-8) and usually occur in immunocomprom

80 ly, VZV is among the most genetically stable herpesviruses, a notion supported by more than 60 comple

81 Each of the three subfamilies of herpesviruses (alpha, beta, and gamma) encode unique teg

82 CMV is a ubiquitous herpesvirus and a significant cause of disease and death

83 IAS4 in the cellular-mediated restriction of herpesviruses and establish a new functional role for th

84 x double-stranded DNA viruses, including the herpesviruses and many bacteriophages.

85 ses, with key insights drawn from veterinary herpesviruses and other large DNA virus families.

86 ing that different APOBEC3 proteins restrict herpesviruses and parvoviruses, among others, but whethe

87 mplex virus 1 (HSV-1) is conserved among all herpesviruses and plays many roles during replication.

88 Herpesviruses and poxviruses also encode chemokines, cop

89 Given the neurotropism exhibited by other herpesviruses and the frequent coinfection of HIV-positi

90 8 (HHV-8) (Kaposi's sarcoma [KS]-associated herpesvirus) and have an important role in the developme

91 at of ET domain recognition of NSD3, LANA of herpesvirus, and integrase of MLV, which involves format

92 esign of countermeasures against HCMV, other herpesviruses, and even HIV/AIDS.

93 ponding to anelloviruses, human pegivirus 1, herpesviruses, and papillomaviruses were detected in RNA

94 Herpesviruses are a large order of animal enveloped viru

95 zoster virus, Rubella, Cytomegalovirus, and Herpesviruses are a major cause of morbidity and mortali

96 Herpesviruses are among the most complex and widespread

97 Human herpesviruses are among the most prevalent pathogens and

98 nst Epstein-Barr virus (EBV) and other human herpesviruses are limited to those targeting viral DNA r

99 Alpha herpesviruses are neuroinvasive viruses that infect the

100 Human herpesviruses are responsible for a range of debilitatin

101 erscore the potential utility of recombinant herpesviruses as vaccine vectors.

102 Tailed bacteriophages and herpesviruses assemble infectious particles via an empty

103 of infection to determine that IFITM3 limits herpesvirus-associated pathogenesis without directly pre

104 The regulation of latency is central to herpesvirus biology.

105 Herpesviruses can infect a wide range of animal species.

106 Fluorescent protein fusions to herpesvirus capsids have proven to be a valuable method

107 HHV-8 is a B-lymphotropic gamma-herpesvirus closely related to the Epstein-Barr virus (E

108 is study examined the association of 4 human herpesviruses (CMV, herpes simplex virus type 1, human h

109 rt a HCMV atomic structure consisting of the herpesvirus-conserved capsid proteins MCP, Tri1, Tri2, a

110 ating master circuits in HIV-1 and the human herpesvirus cytomegalovirus along with potential circuit

111 Moreover, herpesviruses differentially target components of the mo

112 Monomeric herpesvirus DNA is cleaved from concatemers and inserted

113 rent treatments are limited to targeting the herpesvirus DNA polymerases, but with emerging viral res

114 Like other herpesviruses, EBV has diversified through both coevolut

115 Our results show VZV, like other human herpesviruses, encodes several sncRNAs and miRNAs, and s

116 Viral latency is a central strategy by which herpesviruses ensure their lifelong persistence.

117 cing role by an unknown mechanism.IMPORTANCE Herpesviruses enter cells via attachment of the virion t

118 glycoproteins gB and gH-gL are essential for herpesvirus entry and cell-cell fusion induced syncytium

119 Herpesvirus entry into cells requires the coordinated ac

120 ors for future systematic exploration of the herpesvirus entry mechanisms.

121 As its name suggests, the host receptor herpesvirus entry mediator (HVEM) facilitates herpes sim

122 olog of the TNF receptor superfamily member, herpesvirus entry mediator (HVEM; TNFRSF14).

123 irus nectin1 and Kaposi's sarcoma-associated herpesvirus EphA2), or association with nonintegrin rece

124 s activating memory T cells from the related herpesvirus Epstein-Barr virus remained undetectable.

125 V, HPyV6, HPyV7, TSPyV, HPyV9, HPyV10) and 5 herpesviruses (Epstein Barr virus (EBV), cytomegalovirus

126 Herpesviruses establish life-long chronic infections tha

127 r current understanding of nuclear egress in herpesviruses, examines the experimental evidence and mo

128 Herpesviruses exploit this interaction to execute a rang

129 Many herpesviruses express small noncoding RNAs (sncRNAs), in

130 anism by which HHV-6A, a member of the human herpesvirus family, may contribute to inadequate myelin

131 ve and clinically significant members of the herpesvirus family: varicella zoster virus, human cytome

132 Current neuronal models in the herpesvirus field vary widely and have caveats, includin

133 he HSV-1 UL37 protein is conserved among all herpesviruses, functions in both retrograde and anterogr

134 In the multicomponent herpesvirus fusion machinery, glycoprotein B (gB) acts a

135 Herpesvirus gene expression is co-ordinately regulated a

136 these noncanonical defense pathways and how herpesvirus gene products counter them, highlighting the

137 , many of which were most closely related to herpesvirus genes.

138 We consider the impacts of cell culture on herpesvirus genomes and how to accurately describe the v

139 It is well established that infecting herpesvirus genomes are chromatinized upon entry into th

140 As herpesvirus genomes enter the nucleus as naked DNA, we a

141 Herpesvirus genomes exist and replicate as episomes insi

142 Annotation of herpesvirus genomes has traditionally been undertaken th

143 Herpesvirus genomes readily undergo homologous recombina

144 ture of overlapping transcription throughout herpesvirus genomes, however, poses substantial problems

145 recent data on the mechanisms that generate herpesvirus genomic diversity and underlie the evolution

146 The highly conserved herpesvirus glycoprotein complex gB/gH-gL mediates membr

147 Epstein-Barr virus, another herpesvirus, has two properties that have driven its stu

148 Unusually, herpesviruses have evolved a complex mechanism of nuclea

149 Herpesviruses have evolved multiple ways to adapt the in

150 Neuroinvasive herpesviruses have evolved to efficiently infect and est

151 sted for their ability to be infected by the herpesviruses herpes simplex virus 1 and murine herpesvi

152 have at least one actively replicating human herpesvirus (HHV) in their mucosal secretions at any one

153 Human herpesvirus (HHV) infections are common during infancy.

154 Human herpesviruses (HHV) establish lifelong latent infection

155 Asymptomatic replication of human herpesviruses (HHV) is frequent in HIV-infected men and

156 s follows: cytomegalovirus (CMV), 44%; human herpesvirus [HHV] 6, 18%; HHV8, 6%; Epstein-Barr virus,

157 Seminal HIV RNA and DNA from 7 human herpesviruses (HHVs) were measured by real-time polymera

158 of conserved aromatic amino acids through 20 herpesviruses homologues of pUL56 suggests an involvemen

159 ffects of Ca-SP on Kaposi sarcoma-associated herpesvirus/human herpes virus 8 replication and uptake

160 inhibited entry of Kaposi sarcoma-associated herpesvirus/human herpes virus 8.

161 gammaherpesvirus Kaposi's sarcoma-associated herpesvirus/human herpesvirus 8 (KSHV/HHV8), exploit mic

162 brate facing a viral disease possibly due to herpesvirus (i) whether nestlings with either low levels

163 on these findings, we hypothesize that host herpesvirus immune history may influence the pathogenesi

164 sid exemplified by tailed bacteriophages and herpesviruses.IMPORTANCE Adenovirus is a double-edged sw

165 an immunodeficiency virus type 1 (HIV-1) and herpesviruses, in large part due to viral latency and th

166 Although many herpesviruses, including herpes simplex virus 1 (HSV-1),

167 The tegument proteins of herpesviruses, including Kaposi's sarcoma-associated her

168 Herpesviruses, including rhesus monkey rhadinovirus (RRV

169 und that HDAC inhibiting proteins from human herpesviruses induce human NKG2D ligand ULBP-1.

170 G, and improved protection against recurrent herpesvirus infection and disease in CXCL10(-/-) deficie

171 CD8(+) T cell responses to recurrent ocular herpesvirus infection and disease using a well-establish

172 ociated with an increase in recurrent ocular herpesvirus infection and disease.

173 th strong protective immunity against ocular herpesvirus infection and disease.

174 CD8(+) T cell responses to recurrent ocular herpesvirus infection and disease.

175 th strong protective immunity against ocular herpesvirus infection and disease.

176 ed tissues, which protects against recurrent herpesvirus infection and disease.IMPORTANCE We determin

177 ified serological evidence of past and acute herpesvirus infection as dichotomous variables.

178 However, the role of AMPK in herpesvirus infection is unclear.

179 d whether the HIRA chaperone complex affects herpesvirus infection.

180 d samples, 85 (45%) showed evidence of acute herpesvirus infection; herpes simplex virus 1 was found

181 clusters were triggered by other neurotropic herpesviruses, infection with unrelated viruses failed t

182 We evaluated the T-cell compartment and herpesvirus infections in 6-year-old children.

183 Persistent herpesvirus infections including cytomegalovirus (CMV) i

184 One aspect of cellular restriction of herpesvirus infections is mediated by components of nucl

185 o known as ND10) have restrictive effects on herpesvirus infections that are countered by viral prote

186 We sought to determine whether herpesvirus infections, which are potentially treatable,

187 derstanding and intelligently intervening in herpesvirus infections.

188 n could be used to design new treatments for herpesvirus infections.

189 ey on the incidence and clinical features of herpesviruses infections after HSCT has not yet been con

190 Herpesviruses infections were uncommon after HSCT, excep

191 proteins (VTPs) mediate key functions in the herpesvirus infectious cycle.

192 Whether a herpesvirus initiates a lytic infection in a host cell o

193 ve a higher particle-to-PFU ratio than other herpesviruses; instead, the cells previously used to pro

194 Kaposi's sarcoma-associated herpesvirus is a leading cause of cancers in individuals

195 The tegument of herpesviruses is a highly complex structural layer betwe

196 A hallmark of all herpesviruses is their biphasic life cycle-viral latency

197 , which is similar in size to those of other herpesviruses, is stabilized.

198 ible protein 16) recognizes nuclear episomal herpesvirus (Kaposi's sarcoma-associated herpesvirus [KS

199 ed by infection of Kaposi sarcoma-associated herpesvirus (KSHV) and is characterized by uncontrolled

200 LANA homologs from Kaposi sarcoma-associated herpesvirus (KSHV) and MHV68 exhibit considerable sequen

201 o MHV68.IMPORTANCE Kaposi sarcoma-associated herpesvirus (KSHV) and murine gammaherpesvirus 68 (MHV68

202 viruses such as Kaposi's sarcoma-associated herpesvirus (KSHV) are known to interact extensively wit

203 otease (Pr) from Kaposi's sarcoma-associated herpesvirus (KSHV) as a model system, we sought to disse

204 virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) cause lifelong persistent infection a

205 cycle.IMPORTANCE Kaposi's sarcoma-associated herpesvirus (KSHV) causes AIDS-related malignancies, inc

206 Kaposi's sarcoma-associated herpesvirus (KSHV) encodes 12 pre-microRNAs during laten

207 me 36 (ORF36) of Kaposi's sarcoma-associated herpesvirus (KSHV) enhances protein synthesis by mimicki

208 rr virus (EBV) and Kaposi sarcoma-associated herpesvirus (KSHV) establish persistent infections in B

209 entirety of the Kaposi's sarcoma-associated herpesvirus (KSHV) genome and postulated the existence o

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

211 merase II around Kaposi's sarcoma-associated herpesvirus (KSHV) genomes in the host cell nucleus.

212 ls infected with Kaposi's sarcoma-associated herpesvirus (KSHV) harbor multiple copies of the KSHV ge

213 Kaposi's sarcoma-associated herpesvirus (KSHV) has a causal role in a number of huma

214 Oncogenic Kaposi's sarcoma-associated herpesvirus (KSHV) has latent and lytic replication phas

215 Kaposi's sarcoma-associated herpesvirus (KSHV) has tropism for B lymphocytes, in whi

216 roach to culture Kaposi's sarcoma-associated herpesvirus (KSHV) infected human B cells in 3-D using a

217 associated with Kaposi's sarcoma-associated herpesvirus (KSHV) infection.

218 brane protein of Kaposi's sarcoma-associated herpesvirus (KSHV) interacts with multiple cellular sign

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

220 Kaposi's sarcoma-associated herpesvirus (KSHV) is etiologically associated with all

221 Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent of commonly fa

222 Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent of fatal malig

223 Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent of Kaposi sarc

224 Kaposi sarcoma herpesvirus (KSHV) is the cause of Kaposi sarcoma (KS),

225 Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiologic agent of Kaposi's sa

226 Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiologic agent of Kaposi's sa

227 K15P protein of Kaposi's sarcoma-associated herpesvirus (KSHV) is thought to play key roles in disea

228 cific regions of Kaposi's sarcoma-associated herpesvirus (KSHV) latent episomes are poised to be acti

229 ivity restricted Kaposi's sarcoma-associated herpesvirus (KSHV) lytic replication in primary human um

230 arisons to human Kaposi's sarcoma-associated herpesvirus (KSHV) miRNAs revealed several viral miRNA h

231 l concerning how Kaposi's sarcoma-associated herpesvirus (KSHV) modulates these cellular pathways dur

232 VLVs by using a Kaposi's sarcoma-associated herpesvirus (KSHV) mutant that is defective in small cap

233 en (LANA) of the Kaposi's sarcoma-associated herpesvirus (KSHV) performs a variety of functions to es

234 ral replication: Kaposi's sarcoma-associated herpesvirus (KSHV) stably clusters its genomes across ge

235 rt that ORF10 of Kaposi's sarcoma-associated herpesvirus (KSHV), a nuclear DNA virus, inhibits mRNA e

236 otein (vFLIP) of Kaposi's sarcoma-associated herpesvirus (KSHV), against influenza A virus (IAV) were

237 Kaposi sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8, i

238 ), also known as Kaposi's sarcoma associated herpesvirus (KSHV), is an oncogenic virus that can cause

239 ammaherpesvirus, Kaposi's sarcoma-associated herpesvirus (KSHV), is tightly associated with the devel

240 ruses, including Kaposi's sarcoma-associated herpesvirus (KSHV), play key roles in the viral life cyc

241 Kaposi's sarcoma-associated herpesvirus (KSHV), the causative agent of Kaposi's sarc

242 virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV), which are associated with a variety

243 essive growth of Kaposi's sarcoma-associated herpesvirus (KSHV)-related malignancies, including Kapos

244 seases caused by Kaposi's sarcoma-associated herpesvirus (KSHV).

245 ncy is etiologically caused by KS-associated herpesvirus (KSHV).

246 sponsible agent, Kaposi's sarcoma-associated herpesvirus (KSHV; HHV8), expresses multiple microRNAs (

247 mal herpesvirus (Kaposi's sarcoma-associated herpesvirus [KSHV], Epstein-Barr virus [EBV], and herpes

248 The transcriptional program associated with herpesvirus latency and the viral genes regulating entry

249 other acidic patch-binding proteins such as herpesvirus latency-associated nuclear antigen (LANA).

250 gnaling.IMPORTANCE EBV is a ubiquitous gamma herpesvirus linked to malignancies such as nasopharyngea

251 Human herpesviruses may cause severe complications after allog

252 Systemic reactivations of herpesviruses may occur in intensive care unit (ICU) pat

253 se species, and recent data now suggest that herpesviruses might also be considered candidates for po

254 NA bacteriophages, adenoviruses, poxviruses, herpesviruses, mimiviruses, megaviruses, pandoraviruses,

255 A complete understanding of herpesvirus morphogenesis requires studies of capsid ass

256 ion with a helper virus (e.g., adenovirus or herpesvirus) or treatment with genotoxic agents.

257 7) of persistent DNA viruses (anelloviruses, herpesviruses, papillomaviruses and polyomaviruses) over

258 The core virome structure included herpesviruses, papillomaviruses, polyomaviruses, adenovi

259 Herpesviruses possess a genome-pressurized capsid.

260 sults demonstrate the feasibility of imaging herpesvirus procapsids and their morphogenesis in living

261 lls lytically infected with tumor-associated herpesviruses produce a high proportion of virus-like ve

262 ta and comparative analyses of other dimeric herpesvirus proteases.

263 protein of HSV and PRV, was one of the first herpesvirus proteins to be fused to a fluorescent protei

264 es simplex virus 1 that are conserved in all herpesviruses: pUL7 and pUL51.

265 Herpesvirus reactivations were documented in 68% of sept

266 The repertoire of herpesvirus receptors consists of nonintegrin and integr

267 ayer cell cultures, in which most studies of herpesvirus replication have been performed.

268 Also, pronounced inhibition of herpesvirus replication was observed.

269 Herpesvirus saimiri, a gamma-herpesvirus that establishe

270 he incidence of infection of the eight human herpesviruses simultaneously in 1 045 peripheral blood s

271 ectron microscopy studies have revealed that herpesvirus small capsid proteins bind to capsids via th

272 lphaherpesviruses that is not found in other herpesvirus subfamilies.

273 Alpha herpesviruses, such as herpes simplex virus and pseudora

274 rug Administration approval of the oncolytic herpesvirus talimogene laherparepvec in advanced melanom

275 tify for the first time that these conserved herpesvirus tegument proteins localize to focal adhesion

276 cells in the same tumors using murine CMV, a herpesvirus that causes a persistent/latent infection, a

277 rus (PRV) is a broad host range, swine alpha herpesvirus that enters neuronal cells and utilizes intr

278 Herpesvirus saimiri, a gamma-herpesvirus that establishes latency in the T cells of N

279 scribed mouse thymic virus (MTV), a putative herpesvirus that has not been molecularly characterized.

280 re infected or not with murine CMV (MCMV), a herpesvirus that infects the salivary gland and promotes

281 simplex virus 1 (HSV-1) is one of the eight herpesviruses that can infect humans and is prevalent wo

282 ce and little efficacy against the oncogenic herpesviruses, there is an urgent need for new antiviral

283 Like all herpesviruses, they show two stages in their life cycle:

284 formatics have expanded our understanding of herpesviruses through genome-wide comparisons of sequenc

285 a regulatory mechanism that allows different herpesviruses to regulate the kinetics of terminase nucl

286 rticular genomic regions, but not individual herpesvirus transcripts.

287 Equine herpesvirus type 1 (EHV1), a well-known member of the al

288 ses (CMV, herpes simplex virus type 1, human herpesvirus type 6, and Epstein-Barr virus) with change

289 and will better enable future development of herpesvirus vaccines.

290 The neurotropic herpesvirus varicella-zoster virus (VZV) establishes a l

291 ely associated with greater LTL attrition (3 herpesviruses vs none, beta = -0.07 and P = .02; 4 infec

292 Seropositivity to more herpesviruses was additively associated with greater LTL

293 The incidences of infection for each herpesvirus were as follows: cytomegalovirus (CMV), 44%;

294 All herpesviruses were screened and quantified in plasma by

295 wild-type mice were equally infected by the herpesviruses, while APOBEC3A but not mouse APOBEC3 conf

296 Human cytomegalovirus (HCMV) is a herpesvirus with both lytic and latent life cycles.

297 We focus on human herpesviruses, with key insights drawn from veterinary h

298 This indicates that herpesviruses withstand the internal pressure that is ge

299 logy Annual Meeting (ASV), the International Herpesvirus Workshop (IHW), the Positive-Strand RNA Viru

300 alovirus (HCMV) is by far the largest of any herpesvirus, yet it has been unclear how its capsid, whi