ライフサイエンスコーパス: herpes virus

1 ovirus (HCMV) is the prototypical human beta-herpes virus.

2 s agents like Mycobacterium tuberculosis and herpes virus.

3 be an effective strategy for controlling koi herpes virus.

4 HSATII RNA in human cells infected with two herpes viruses.

5 ction is the high association with oncogenic herpes viruses.

6 onent of the complex cell-entry machinery of herpes viruses.

7 Static latency is the hallmark of all herpes viruses.

8 of activity that also covers hepatitis B and herpes viruses.

9 rate differences were found against 4 other herpes viruses.

10 the seroconversion rates against four other herpes viruses.

11 ivo human tonsillar tissue system) and human herpes viruses.

12 rly all adults are infected with one or more herpes viruses.

13 so silences the lytic phase of EBV and other herpes viruses.

14 precede reactivation and viremia of various herpes viruses.

15 erpes peptide-expressing cells and releasing herpes viruses.

16 of S. purpurea extracts against both pox and herpes viruses.

17 n a nuclear egress mechanism akin to that of herpes viruses.

18 cute infection in mucosal epithelium, bovine herpes virus 1 (BHV-1) establishes lifelong latency in s

19 We used the bovine herpes virus 1 (BHV-1) latency-related (LR) gene, which

20 Murine herpes virus 1 (HSV-1 KOS) infection triggers T cell-dep

21 RPP30) and a viral spike-in control (Phocine Herpes Virus 1 [PhHV-1]), which monitor sample quality a

22 stress and increased episodes of human alpha-herpes virus 1 reactivation from latency.

23 bitors: herpes simplex virus 2 ICP47, bovine herpes virus 1 UL49.5, or rhesus cytomegalovirus Rh185.

24 sequences of common pathogens, such as human herpes virus 1, can be demonstrated.

25 nsactivator VP16 and its homolog from bovine herpes-virus 1 (BHV-1) can each recruit the human homeod

26 Using the model pathogen Bovine Herpes Virus-1 (BHV-1) this study employs an extended-ga

27 nd is missing in the vFLIP encoded by equine herpes virus 2 that lacks this activity.

28 iated with smaller MS-HLA effect, with human herpes virus 3 (HHV3), JC human polyoma virus (JCV), HHV

29 implicated in breast cancer, including human herpes virus 4 (HHV4), human herpes virus 5 (HHV5), huma

30 including human herpes virus 4 (HHV4), human herpes virus 5 (HHV5), human papilloma virus (HPV), huma

31 V and MCMV), Epstein-Barr virus (EBV), human herpes virus 6 (HHV-6), varicella zoster virus (VZV), an

32 irus (OR, 2.67; 95% CI, 1.75-4.36) and human herpes virus 6 (OR, 3.50; 95% CI, 1.15-10.63) were detec

33 Subject 2 had respiratory failure, human herpes virus 6 infection, cytopenias, and no circulating

34 es comprised of genomic lambda-DNA and human herpes virus 6 type B (HHV-6B) DNA, we have used our lab

35 parechovirus, herpes simplex virus 2, human herpes virus 6, and varicella zoster virus-were >90.0%,

36 ndidate, such as Epstein-Barr virus or human herpes virus 6.

37 creasing evidence that the neurotropic human herpes viruses 6 and 7 (HHV-6, HHV-7) comprise a signifi

38 nce identity to positional homologs in human herpes viruses 6 and 7.

39 II), varicella-zoster virus (VZV), and human herpes virus-6 (HHV-6) nucleic acid sequences.

40 e 1/2 unspecified, cytomegalovirus and human herpes virus-6 measured by serum IgM, high titre IgG or

41 HSV-2), varicella-zoster virus (VZV), human herpes virus-6, 7, and 8 (HHV-6, HHV-7, and HHV-8), and

42 own CD8 T-cell epitopes from the mouse gamma-herpes virus 68.

43 cting these mice with EGFP-expressing murine herpes virus-68 (MHV68-EGFP) caused occasional transient

44 We detected human herpes virus 6B and 7, Epstein-Barr virus, and parvoviru

45 However, the patient had evidence of human herpes virus-6B infection.

46 e as they relate to viral factors-both human herpes virus 8 (HHV-8) and human immunodeficiency virus

47 Human herpes virus 8 (HHV-8) is a geographically limited virus

48 Human herpes virus 8 (HHV-8) or Kaposi sarcoma-associated herp

49 Human herpes virus 8 (HHV-8), also known as Kaposi's sarcoma a

50 Kaposi sarcoma (KS), a human herpes virus 8 (HHV-8; also called KSHV)-induced endothe

51 sarcoma-associated herpes virus (KSHV)/human herpes virus 8 (HHV8) DNA sequences have been demonstrat

52 Infection with human herpes virus 8 (HHV8) has been associated with Kaposi's

53 The human herpes virus 8 (HHV8)-encoded viral FLICE (Fas-associati

54 The human herpes virus 8 (HHV8)-encoded viral FLICE inhibitory pro

55 ed herpesvirus, which is also known as human herpes virus 8 (KSHV/ HHV8), has not been reported in va

56 Human T-cell leukemia virus 1 and human herpes virus 8 genomes are also found in tumor cells in

57 tivity; 14.9% (95% CI: 12.4-17.4%) for human herpes virus 8 infection.

58 sarcoma (KS)-associated herpesvirus or human herpes virus 8 is considered the etiological agent of KS

59 sarcoma-associated herpes virus (KSHV)/human herpes virus 8 is oncogenic and stimulates angiogenesis

60 The KS-associated herpesvirus/human herpes virus 8 open reading frame 74 encodes a constitut

61 Kaposi sarcoma-associated herpesvirus/human herpes virus 8 replication and uptake of the ORF45 tegum

62 e at increased risk for development of human herpes virus 8(HHV-8)-associated Kaposi's sarcoma (KS).

63 remains uncertain, a new herpes virus, human herpes virus 8, has been identified in the rare subset o

64 chemokine homologue that is encoded by human herpes virus 8.

65 Kaposi sarcoma-associated herpesvirus/human herpes virus 8.

66 Human herpes virus-8 (HHV-8) drives the hypercytokinemia in al

67 hese interactions were disrupted by an human herpes virus-8 (HHV-8)-coded oncoprotein, vIRF1, and con

68 Human herpes virus-8 (HHV8) maintains infection, in part, by e

69 is divided into idiopathic MCD (iMCD), human herpes virus-8 (HHV8)-associated MCD (HHV8-MCD), and pol

70 Human herpes virus-8 and angiogenesis, both involved in the pa

71 happen following reciprocal actions of human herpes virus-8 infection, immunosuppression, and chemica

72 Herpes viruses account for 7% of all scleritis cases and

73 ch would otherwise be resistant to oncolytic herpes virus alone.

74 which are infected with KSHV (Kaposi sarcoma herpes virus, also named HHV-8).

75 e synaptic vesicle, we have used a defective herpes virus amplicon expression system to study the tar

76 Thus, we have tested whether herpes virus amplicon vectors expressing CAT or GPX stil

77 nity, vaccine-antibody production, and human herpes virus amplify this effect.

78 Prophylaxis for herpes virus and Pneumocystis carinii is standard with t

79 Retention of human herpes virus and tumor-associated antigen (TAA)-specific

80 ocess, conserved among dsDNA viruses such as herpes viruses and bacteriophages, is key to forming inf

81 for serologic studies of IgE and IgG to four herpes viruses and constitutive specimens for genotyping

82 unds 2 and 5-9, but 4 was active against two herpes viruses and cytotoxic in the micromolar range.

83 cyclovir is a potent, selective inhibitor of herpes viruses and it is indicated for the treatment and

84 gation for treatment of infections caused by herpes viruses and orthopoxviruses.

85 mune responses to clinically important human herpes viruses and to the TAA WT1.

86 cancer), viral (e.g., human papillomavirus, herpes virus) and bacterial (e.g., Helicobacter pylori,

87 eloped viruses, including influenza viruses, herpes viruses, and coronaviruses.

88 among the bZIPs and among proteins from five herpes viruses, and determining relative protein duplica

89 among the members of the alpha subfamily of herpes viruses, and the US9 gene product lacks lysines.

90 sue, Allan et al. conclude that transport of herpes-virus antigens to lymph nodes by dendritic cells

91 gesia and demonstrate the use of recombinant herpes viruses as tools for studying gene function in sp

92 lation levels on antibodies to common latent herpes viruses, as well as to glycoprotein 120 in indivi

93 phosphorylation and its deubiquitination by Herpes virus associated ubiquitin-specific protease (Hau

94 stein-Barr virus (EBV) is an oncogenic gamma-herpes virus associated with malignancies that develop i

95 bacteria (mostly mycobacteria) and viruses (herpes viruses at least), due principally to the impairm

96 A recombinant herpes virus carrying human preproENK cDNA was used to m

97 eption, a recombinant, replication-defective herpes virus carrying the human preproenkephalin cDNA wa

98 Human CMV (HCMV), a highly prevalent herpes virus causing lifelong, usually latent, infection

99 r-bearing mice better than control oncolytic herpes virus combined with topical aCD47-IgG1.

100 The neurotrophic herpes virus cytomegalovirus is a known cause of neuropa

101 G207 is an oncolytic herpes virus deficient in RR, a rate-limiting enzyme for

102 anscription PCR were performed to screen for herpes virus DNA.

103 obes that cause persistent infections (e.g., herpes viruses) do so by switching from fast-growing lyt

104 We found that herpes viruses (e.g., subtypes HHV4, HHV5, and HHV6) tha

105 ily member LIGHT and the TNF family receptor herpes virus entry mediator (HVEM) co-stimulates T cells

106 an HEp-2 cells or porcine cells that express herpes virus entry mediator (HVEM) for virus and recepto

107 The immune modulatory protein herpes virus entry mediator (HVEM) is one of several cel

108 Deficiency of either BTLA or its ligand herpes virus entry mediator (HVEM) resulted in reduced n

109 ber expressed by activated T cells, binds to herpes virus entry mediator (HVEM) which is constitutive

110 abnormal in 40% of FL patients, encodes the herpes virus entry mediator (HVEM) which limits T-cell a

111 The herpes virus entry mediator (HVEM), a member of the tumo

112 cells and dependent on the LIGHT receptors, herpes virus entry mediator (HVEM), and lymphotoxin-beta

113 In addition, BTLA's ligand, herpes virus entry mediator (HVEM), was found constituti

114 cifically binds two cellular ligands, LIGHT (herpes virus entry mediator (HVEM)-L) and Fas ligand (Fa

115 ng respiratory virus infection, we show that herpes virus entry mediator (HVEM; TNFRSF14), a member o

116 imulated CD8(+) T and NK cells through HVEM (herpes virus entry mediator A).

117 On binding to its receptors, herpes virus entry mediator and lymphotoxin beta recepto

118 y, we demonstrate that a cellular ligand for herpes virus entry mediator and lymphotoxin receptor (LI

119 y reported that LIGHT (a cellular ligand for herpes virus entry mediator and lymphotoxin receptor), a

120 Inhibition of LIGHT (a cellular ligand for herpes virus entry mediator and lymphotoxin receptor)/he

121 entry mediator, blocks the immunoinhibitory herpes virus entry mediator B and T lymphocyte attenuato

122 ymphotoxin beta receptor-deficient mice, and herpes virus entry mediator on donor T cells is required

123 that competes for glycoprotein D binding to herpes virus entry mediator on T cells (TNFSF14)) activa

124 locks immunoinhibitory signaling through the herpes virus entry mediator pathway.

125 sis factor receptor superfamily member HVEM (herpes virus entry mediator).

126 with herpes simplex virus glycoprotein D for herpes virus entry mediator, a receptor expressed by T l

127 on, and competes with HSV glycoprotein D for herpes virus entry mediator, a receptor expressed by T l

128 n, and competing with HSV glycoprotein D for herpes virus entry mediator, a receptor expressed by T l

129 n, and competing with HSV glycoprotein D for herpes virus entry mediator, a receptor expressed by T l

130 ing receptors, lymphotoxin beta receptor and herpes virus entry mediator, because LIGHT Tg mesenteric

131 glycoprotein D, which through binding to the herpes virus entry mediator, blocks the immunoinhibitory

132 CD160 and BTLA both bind to herpes virus entry mediator.

133 lymphotoxin-beta receptor (LTbetaR) but not herpes virus entry mediator.

134 rotein that competes with glycoprotein D for herpes virus entry on T cells) is a tumor necrosis facto

135 Lytic replication of the human gamma herpes virus Epstein-Barr virus (EBV) is an essential pr

136 onal control of glioblastoma by an oncolytic herpes virus expressing a full-length anti(a)-human CD47

137 of members of the enveloped filo, alpha, and herpes virus families but not the flavivirus group and n

138 Members of the herpes virus family and hepatitis B virus (HBV) have bee

139 f viruses, especially those belonging to the herpes virus family and most importantly in varicella zo

140 uman cytomegalovirus (HCMV), a member of the herpes virus family, may play a role in the development

141 t defense against pathogenic viruses such as herpes viruses, flaviviruses, retroviruses, and coronavi

142 The Kaposi's sarcoma-associated herpes virus gene product K3 (KK3) subverts the MHC clas

143 A recognizes the same surface on HVEM as gD (herpes virus glycoprotein D) and utilizes a similar bind

144 I IEk, the nonclassical MHC T10/T22, and the Herpes virus glycoprotein gI-indicates that gamma delta

145 V-8, also called Kaposi's sarcoma-associated herpes virus) has been linked to Kaposi's sarcoma and pr

146 Many enveloped viruses, including herpes viruses, hepatitis B virus (HBV), and hepatitis C

147 the glycolytic activation induced by another herpes virus, herpes simplex virus type 1 (HSV-1).

148 ein and kinesin-1 with adenovirus, the alpha herpes viruses: herpes simplex virus (HSV1) and pseudora

149 Sequential human herpes virus (HHV) reactivation is well known in drug re

150 a-associated lymphoid tissue lymphoma, human herpes virus (HHV)-6, HHV-7, chlamydia, Epstein-Barr vir

151 Human herpes viruses (HHV) are ubiquitous and have been implic

152 ned possible pathogen(s) for detecting human herpes virus (HHV1-HHV7), HEV, or Mycoplasma pneumoniae

153 1*02:01) to > 10,000 antigens of the 9 Human Herpes Viruses (HHV1, HHV2, HHV3, HHV4, HHV5, HHV6A, HHV

154 Several viruses including human herpes viruses (HHVs), human polyomavirus JCV, and human

155 Epstein-Barr virus remains uncertain, a new herpes virus, human herpes virus 8, has been identified

156 carcinoma in other organs or any history of herpes virus, human papilloma virus, or human immunodefi

157 In addition to adeno- and herpes viruses, human papillomavirus (HPV) can serve as

158 Cells expressing herpes virus ICP-47 block the generation of this epitope

159 tify BAG3, a co-chaperone, as a regulator of herpes virus immediate early gene expression.

160 The Kaposi's sarcoma-associated herpes virus immediate-early lytic cycle trigger protein

161 dynamically regulated upon infection with a herpes virus in a manner that impacts virus replication.

162 ascular endothelial cells with KS-associated herpes virus in vitro results in a lymphatic reprogrammi

163 of latent pathogens such as Epstein-Barr and herpes viruses in COVID-19 immune-dysregulated tissue en

164 hat is used in the treatment of a variety of herpes viruses in immunocompromised patients and in a ge

165 Human herpes virus infection was similar between HEU and HU in

166 ty-five (74.4%) of these were diagnosed with herpes virus infection, 5 (10.6%) with tuberculosis, and

167 th scleritis, 35 of whom were diagnosed with herpes virus infection, seen at 2 tertiary referral cent

168 eaths from disseminated histoplasmosis and a herpes virus infection.

169 fter treatment of preexisting drug-resistant herpes virus infection.

170 The role of FTO during (herpes) virus infection remains largely unexplored.

171 virus 8 (HHV-8) or Kaposi sarcoma-associated herpes virus is the etiologic agent of Kaposi sarcoma, p

172 Epstein-Barr virus (EBV), a human herpes virus, is associated with a variety of malignanci

173 Varicella-zoster virus (VZV), an alpha-herpes virus, is the causative agent of chickenpox, shin

174 osely associated with the lymphotropic gamma herpes virus Kaposi's sarcoma-associated herpes virus (K

175 evidence suggests an association with a new herpes virus, Kaposi's sarcoma-associated herpes virus (

176 Koi herpes virus (KHV), a highly virulent disease affecting

177 quantitation of Kaposi's sarcoma-associated herpes virus (KSHV or human herpesvirus 8) DNA was evalu

178 tein-Barr virus or Kaposi sarcoma-associated herpes virus (KSHV) are exquisitely sensitive to this co

179 Kaposi sarcoma-associated herpes virus (KSHV) contains a gene that has functional

180 Kaposi's sarcoma-associated herpes virus (KSHV) contributes to the pathogenesis of K

181 Kaposi sarcoma-associated herpes virus (KSHV) encodes a D-like cyclin (K-cyclin) t

182 The Kaposi's Sarcoma associated Herpes virus (KSHV) encodes two genes with the potential

183 Virus (EBV), and Kaposi's Sarcoma-associated Herpes Virus (KSHV) in a fingerprick volume (50 microL)

184 Kaposi's sarcoma-associated herpes virus (KSHV) infects B cells and microvascular en

185 Kaposi's sarcoma-associated herpes virus (KSHV) is a human oncovirus.

186 Kaposi's sarcoma-associated herpes virus (KSHV) is a recently identified human gamma

187 Kaposi's sarcoma-associated herpes virus (KSHV) is implicated in the pathogenesis of

188 Kaposi's sarcoma-associated herpes virus (KSHV) is the causative agent of PEL.

189 he latent phase, Kaposi's sarcoma-associated herpes virus (KSHV) maintains itself inside the host by

190 Kaposi's sarcoma-associated herpes virus (KSHV) polyadenylated nuclear (PAN) RNA fac

191 miRNA encoded by Kaposi's-sarcoma-associated herpes virus (KSHV) shows significant homology to cellul

192 mma herpes virus Kaposi's sarcoma-associated herpes virus (KSHV), also called human herpesvirus 8.

193 A human oncogenic virus, Kaposi's sarcoma herpes virus (KSHV), can regulate both processes in orde

194 d by the oncogenic Kaposi sarcoma-associated herpes virus (KSHV), constitutively activates the canoni

195 ransformation mediated by the Kaposi sarcoma herpes virus (KSHV)-encoded G-protein-coupled receptor (

196 associated with Kaposi's sarcoma-associated herpes virus (KSHV).

197 ith infection by Kaposi's sarcoma-associated herpes virus (KSHV).

198 with infection by Kaposi sarcoma-associated herpes virus (KSHV).

199 Kaposi's sarcoma-associated herpes virus (KSHV)/human herpes virus 8 (HHV8) DNA sequ

200 ) encoded by the Kaposi's sarcoma-associated herpes virus (KSHV)/human herpes virus 8 is oncogenic an

201 y discovered the Kaposi's sarcoma-associated herpes virus (KSHV/HHV-8) in an uncommon and unusual sub

202 ew herpes virus, Kaposi's sarcoma-associated herpes virus (KSHV/HHV-8), and primary effusion lymphoma

203 roliferation that requires infection with KS herpes virus (KSHV/HHV-8).

204 atently infected Kaposi's sarcoma-associated herpes-virus (KSHV)-associated tumor cells have both end

205 s ks-vFLIP (produced by the Kaposi's sarcoma herpes virus [KSHV]), which associates with IKKgamma, an

206 G207 is an oncolytic herpes virus lacking UL39, the gene encoding RR.

207 ptors and the associated signal molecules in herpes virus latency and uncover a novel paradigm that s

208 The restriction of herpes virus latency to mammalian sensory ganglia has le

209 liferation response to HIV and opportunistic herpes viruses may lead to resistance to central nervous

210 , which likely do not replicate, and certain herpes viruses, may also play a role in disease pathogen

211 sease (MD), caused by the oncogenic MD avian herpes virus (MDV), is a major source of economic losses

212 T-cell repertoires supports the notion that herpes virus-mediated continuously de novo priming of ne

213 ved control of infection with a recombinant -herpes virus, MHV-68, engineered to express SIINFEKL pep

214 c infections such as HIV, hepatitis C virus, herpes viruses, mycobacteria, and fungal and parasitic i

215 erine protease from cytomegalovirus (CMV), a herpes virus of the beta subfamily.

216 Oncolytic herpes virus (oHSV) initiates direct tumor debulking by

217 who were injected with CAN-3110-an oncolytic herpes virus (oHSV)(3).

218 cases cannot be attributed to infection with herpes viruses or HBV.

219 , infection of macrophages lacking TRAM with herpes viruses or the bacterium Staphylococcus aureus le

220 hymidine kinase (HSV-1 TK) is the major anti-herpes virus pharmacological target, and it is being uti

221 ntibody responses to SARS-CoV-2, but also to herpes viruses, pointing to a general suppression of vir

222 (the ENE of the Kaposi's sarcoma-associated herpes virus polyadenylated nuclear RNA) are not efficie

223 ty, viral infections (cytomegalovirus, other herpes viruses) predominate and may coexist with bacteri

224 MV protease, offering a structural basis for herpes virus protease ligand specificity.

225 further evidence to support the finding that herpes virus proteases have a fold and active site disti

226 Recent evidence that a herpes virus protein lacking a classical secretory signa

227 sion in intestinal epithelial cells of M3, a herpes virus protein that binds and inhibits multiple ch

228 The activation domain from the herpes virus protein VP16 restored the ability of the ba

229 The alpha-herpes virus (pseudorabies, PRV) was used to observe cen

230 Daily suppression of this herpes virus reduces plasma HIV-1 concentrations, but wh

231 Most tailed bacteriophages and herpes viruses replicate genome as a concatemer which is

232 Most recently, I have been studying herpes virus replication and inadvertently wandered into

233 se inhibitors, and its inhibitory effects on herpes virus replication are compelling reasons to pursu

234 A better understanding of herpes virus replication will help the development of ne

235 aging reactions of tailed bacteriophages and herpes viruses require the activity of a terminase enzym

236 rtance of the B locus in the response to the herpes virus responsible for Marek's diseases.

237 Furthermore, infection with the KS herpes virus results in up-regulation of VEGF and trigge

238 tion of these compounds for activity against herpes viruses revealed that the new compounds were less

239 ins, and shells of tailed bacteriophages and herpes viruses show conserved features.

240 Oncolytic herpes viruses show promise for cancer treatment.

241 Both cases were negative for EBV, herpes virus simplex, and cytomegalovirus (CMV).

242 rpes simplex virus type 1 (HSV-1), and human herpes virus six (HHV-6) and for cytotoxicity.

243 e DRESS, which coincidentally activates many herpes virus-specific T cells.

244 ment strategies against infections caused by herpes viruses such as cytomegalovirus, Epstein-Barr vir

245 ansplantation may extend beyond CMV to other herpes viruses, such as varicella zoster virus and possi

246 neurons following CAmy or PLH injection of a herpes virus that expresses red fluorescent protein foll

247 Epstein-Barr virus (EBV) is a human herpes virus that infects >90% of individuals.

248 Epstein-Barr virus (EBV), a ubiquitous herpes virus that infects 90% of humans by adulthood, is

249 Epstein-Barr virus (EBV) is a herpes virus that is associated with several human cance

250 galovirus (HCMV) is a clinically significant herpes virus that maintains a lifelong infection in the

251 Cytomegalovirus (CMV) is a ubiquitous herpes virus that persists in the host in a latent state

252 galovirus (CMV) is a globally endemic latent herpes virus that profoundly impacts T cell immunity.

253 erpesvirus 6 (HHV-6), a newly described beta-herpes virus that shares homology with cytomegalovirus (

254 daloid pathway, was performed using an alpha-herpes virus, the Bartha strain of pseudorabies virus (P

255 ed with neurological disease caused by other herpes viruses, the clinical features of acute EBV myelo

256 for viruses as dissimilar as lambda and the herpes viruses, the model may find general utility in ou

257 In tailed bacteriophages and herpes viruses, the viral DNA is packaged through the po

258 (HCV), human papillomavirus (HPV), and human herpes viruses, this paradigm is not applicable.

259 The herpes virus thymidine kinase (HSV-tk) is a critical enz

260 In contrast, herpes virus thymidine kinase (HSV1-TK) readily activate

261 thetic Renilla luciferase (hRluc), EGFP, and Herpes virus thymidine kinase (sr39TK).

262 ing element and a kappaB motif linked to the herpes virus thymidine kinase promoter were able to medi

263 expression in the context of a heterologous (herpes virus thymidine kinase) promoter.

264 In addition, herpes virus thymidine kinases are being explored in gen

265 IITA is very similar to that mediated by the herpes virus transactivator VP16 in the ways that have b

266 ein interactions, including that between the herpes virus transcriptional activator VP16 and the mamm

267 Important examples include HIV, herpes viruses, tuberculosis, leprosy, and malaria.

268 ssion of the ICP0-related proteins of bovine herpes virus type 1 (BHV-1), equine herpesvirus type 1 (

269 Herpes virus type 1 thymidine kinase (HSV1-tk) and the m

270 eutic efficacy for hepatic CRC tumors, using herpes virus type 1 thymidine kinase (HSV1-tk) as a ther

271 uthors examined whether maternal exposure to herpes virus type 2 is associated with risk for adult sc

272 omatitis virus, bluetongue virus, and bovine herpes virus type 2.

273 ied to a clinically relevant real-time human herpes virus type 6 (HHV6) PCR assay that used a minor g

274 ia/lymphoma virus type 2 (HTLV-2), and human herpes virus type 8 (HHV-8) genomes.

275 pha (IFN-alpha) to induce apoptosis in Human Herpes Virus Type 8 (HHV-8) positive Primary Effusion Ly

276 Infection with human herpes virus type 8 (HHV8), a B cell lymphotrophic virus

277 nfections such as Helicobacter pylori, human herpes virus type 8 and cytomegalovirus.

278 f noninvasive imaging of adenoviral-mediated herpes virus type one thymidine kinase (HSV1-tk) gene tr

279 he feasibility and sensitivity of imaging of herpes virus type one thymidine kinase (HSV1-tk) gene tr

280 The viruses are bovine herpes virus types 1, 3, 4 and 5, bovine viral diarrhea

281 iquitin (Ub) ligase domains, one, designated herpes virus Ub ligase 1 (HUL-1) located in a domain enc

282 domain encoded in exon 3 and one designated herpes virus Ub ligase 2 (HUL-2) associated with the rea

283 Tailed bacteriophages and herpes viruses use powerful ATP-driven molecular motors

284 Tailed bacteriophages and herpes viruses use powerful molecular machines to packag

285 Tailed bacteriophages and herpes viruses use powerful molecular motors to transloc

286 viruses, including tailed bacteriophages and herpes viruses, use a homomeric ring ATPase to processiv

287 ations, and could inform the design of other herpes virus vaccines.

288 as well as imaging of gene delivery using a herpes virus vector.

289 d rat hippocampal neurons, using a defective herpes virus vector.

290 viral infections and the often asymptomatic herpes-virus viraemia after DRESS.

291 ignment scores for PPI networks of different herpes viruses, we reconstruct their phylogenetic relati

292 The interactions of herpes virus with vessels wall remind us of the affinity

293 lation has often centered on the neurotropic herpes viruses, with herpes simplex virus 1 (HSV1) consi

294 Cytomegalovirus (CMV) is a common beta-herpes virus worldwide with an estimated seroprevalence

295 The equine herpes virus zinc ring domain nuclear magnetic resonance

296 sses 54% sequence similarity with the equine herpes virus zinc ring domain.