ライフサイエンスコーパス: HCMV

1 HCMV has evolved many mechanisms to evade the immune res

2 HCMV infection is ubiquitous in most populations; it is

3 HCMV infection of human foreskin fibroblasts induced NOD

4 HCMV infection relies on the recognition of cell-specifi

5 HCMV replication in the allograft causes an intrapulmona

6 HCMV replication in the allograft was associated with a

7 HCMV-specific memory T cells were investigated in the se

8 HCMV-specific strategies include using hexon channels to

9 om different anatomical compartments from 20 HCMV-infected patients (renal transplant recipients, ste

10 patients (PHIP) were enrolled, as well as 26 HCMV-seronegative and 39 HCMV-seropositive healthy contr

11 Each of 36 HCMV-seronegative men received 1 subcutaneous dose of 10

12 lled, as well as 26 HCMV-seronegative and 39 HCMV-seropositive healthy controls.

13 a) and interleukin-10 (IL-10) responses to 6 HCMV peptide pools (pp65, pp71, IE1, IE2, gB, and US3, s

14 A HCMV vaccine (Towne) protects transplant recipients.

15 Here we report a HCMV atomic structure consisting of the herpesvirus-cons

16 tments during the symptomatic stage of acute HCMV infection.

17 jects vaccinated with two fibroblast-adapted HCMV vaccines.

18 m rational design of countermeasures against HCMV, other herpesviruses, and even HIV/AIDS.

19 We argue that the EGFR allows HCMV to regulate the cellular functions of these replica

20 Although HCMV immune correlates of protection are only poorly def

21 An HCMV BACmid with the second Py mutated failed to produce

22 how that the product of the UL116 gene is an HCMV envelope glycoprotein that forms a novel gH-based c

23 Direct sequencing of an HCMV open reading frame UL56 region that included amino

24 ich plays an important role during HSV-1 and HCMV infection.

25 y enzyme-linked immunosorbent assay for anti-HCMV immunoglobulin G and immunoglobulin M and for cIL-1

26 les from 10 controls who did not display any HCMV replication episode during the follow-up.

27 De novo-assembled HCMV genome sequences were obtained for 57 of 68 sequenc

28 lls to control virus spread differed between HCMV viral strains, and this phenomenon was dependent on

29 Additionally, both HCMV specific IgM and IgG B-cell responses with the abil

30 However, in ACSS2-KO human fibroblasts both HCMV-induced lipogenesis from glucose and viral growth w

31 DNA damage response, a pathway activated by HCMV and implicated in ligand regulation.

32 show that the viral signalosome activated by HCMV binding to its entry receptor, EGFR, in CD34(+) HPC

33 Vgamma9Vdelta2 cytotoxicity was decreased by HCMV infection of targets whereas anti-IFN-gamma and ant

34 ponse caused by immune escape established by HCMV strains.

35 for successful infection of CD34(+) HPCs by HCMV.IMPORTANCE HCMV establishes lifelong persistence wi

36 tomegalovirus (HCMV) infection is limited by HCMV-specific antibody functions.

37 r our results show that antagonism of PKR by HCMV pTRS1 and pIRS1 is critical for viral protein expre

38 e unique regulation of Rb family proteins by HCMV UL97 and IE1 attests to the importance of modulatin

39 in uninfected cells, and this was reduced by HCMV IE1 expression.

40 Healthy adults who had chronic HCMV infection or were recently immunized with tetanus t

41 CD4(+) T cells specific for human CMV (HCMV) are elevated in HIV(+) HCMV(+) subjects.

42 th a fibroblast-adapted mutant of human CMV (HCMV).

43 Analysis of longitudinal or compartmental HCMV diversity revealed various patterns: no major diffe

44 re involved in protection against congenital HCMV infection.IMPORTANCE Neutralizing antibodies (NAb)

45 tion between maternal viremia and congenital HCMV infection.

46 dation to microcephaly, caused by congenital HCMV infection can be sufficiently explained in terms of

47 )/gL/pUL128-131 for prevention of congenital HCMV infection.

48 Several characteristics of congenital HCMV infections suggest that the efficacy of vaccines de

49 ine formulation to interfere with congenital HCMV infection.

50 ase PKR plays a critical role in controlling HCMV replication.

51 lta2(-) gammadelta T cells, and conventional HCMV-specific CD8(+) T cells.

52 Current HCMV therapeutics target lytic replication, but not the

53 strate micromolar antihuman cytomegalovirus (HCMV) potency.

54 Human cytomegalovirus (HCMV) acquires its membrane in an intracellular compartm

55 Human cytomegalovirus (HCMV) activation is associated with decreased renal graf

56 f DNA viruses such as human cytomegalovirus (HCMV) are devoid of histones within virions but are chro

57 nt step for efficient human cytomegalovirus (HCMV) assembly.

58 udies have shown that human cytomegalovirus (HCMV) can induce a robust increase in lipid synthesis wh

59 vous system caused by human cytomegalovirus (HCMV) congenital infection, the mechanism of HCMV neurop

60 nt recipients (LTRs), human cytomegalovirus (HCMV) DNA detection in the bronchoalveolar lavage fluid

61 n clinical strains of human cytomegalovirus (HCMV) encodes proteins required for latency and reactiva

62 s (NAb) targeting the human cytomegalovirus (HCMV) envelope pentamer complex (PC) are thought to be i

63 ed demonstrating that human cytomegalovirus (HCMV) gB depends on the S-palmitoylation of its endodoma

64 pecies specificity of Human Cytomegalovirus (HCMV) has impeded our understanding of antiviral adaptiv

65 Reactivation of human cytomegalovirus (HCMV) in transplant recipients can cause life-threatenin

66 sRNA) produced during human cytomegalovirus (HCMV) infection activate the antiviral kinase protein ki

67 Human cytomegalovirus (HCMV) infection and periodic reactivation are generally

68 Human cytomegalovirus (HCMV) infection causes disease in newborns and transplan

69 Human cytomegalovirus (HCMV) infection causes severe disease and mortality in i

70 Primary human cytomegalovirus (HCMV) infection during pregnancy is the major cause of c

71 Congenital human cytomegalovirus (HCMV) infection is a significant cause of abnormal neuro

72 antiviral.IMPORTANCE Human cytomegalovirus (HCMV) infection is carried for a lifetime and in healthy

73 Human cytomegalovirus (HCMV) infection is limited by HCMV-specific antibody fun

74 IMPORTANCE Congenital human cytomegalovirus (HCMV) infection is the most common viral infection of th

75 Human cytomegalovirus (HCMV) infection of myeloid cells is closely linked with

76 Primary human cytomegalovirus (HCMV) infection usually goes unnoticed, causing mild or

77 scriptome analyses of human cytomegalovirus (HCMV) infection.

78 dies (DB) produced by human cytomegalovirus (HCMV) infections, we evaluated scalable culture, isolati

79 Human cytomegalovirus (HCMV) infects over half of the population and is the mos

80 Human cytomegalovirus (HCMV) infects peripheral blood monocytes and triggers bi

81 Human cytomegalovirus (HCMV) is a herpesvirus with both lytic and latent life c

82 Human cytomegalovirus (HCMV) is a large, double-stranded DNA virus that causes

83 Human cytomegalovirus (HCMV) is a major human pathogen, causing serious disease

84 The human cytomegalovirus (HCMV) is a ubiquitous, human pathogenic herpesvirus.

85 Human cytomegalovirus (HCMV) is an enveloped double-stranded DNA virus that cau

86 35-kilobase genome of human cytomegalovirus (HCMV) is by far the largest of any herpesvirus, yet it h

87 Human cytomegalovirus (HCMV) is the leading cause of congenital viral infection

88 Human Cytomegalovirus (HCMV) is the most common cause of childhood hearing loss

89 As human cytomegalovirus (HCMV) is the most common infectious cause of fetal anoma

90 Human cytomegalovirus (HCMV) is the most common viral infection acquired by the

91 Human cytomegalovirus (HCMV) is the prototypical human beta-herpes virus.

92 The establishment of human cytomegalovirus (HCMV) latency and persistence relies on the successful i

93 factors required for human cytomegalovirus (HCMV) replication.

94 Clinical human cytomegalovirus (HCMV) strains invariably mutate when propagatedin vitro

95 Human cytomegalovirus (HCMV) strains that have been passaged in vitro rapidly a

96 The human cytomegalovirus (HCMV) terminase complex consists of several components a

97 The human cytomegalovirus (HCMV) US12 family consists of ten sequentially arranged

98 d 240 mg/day) against human cytomegalovirus (HCMV) was evaluated in a recent phase 2b dose-range-find

99 microRNAs encoded by human cytomegalovirus (HCMV) were readily detected in human serum and can inter

100 the entire genome of human cytomegalovirus (HCMV), a significant pathogen for immunocompromised indi

101 ny viruses, including human cytomegalovirus (HCMV), blunt host antiviral defenses by limiting ISG exp

102 ny viruses, including human cytomegalovirus (HCMV), evade host defenses.

103 (AD169 and Towne) of human cytomegalovirus (HCMV), which are known to use cell membrane fusion rathe

104 The human cytomegalovirus (HCMV)-encoded viral cyclin-dependent kinase (v-CDK) UL97

105 The role of human cytomegalovirus (HCMV)-specific T-cell responses in breast milk of HCMV-s

106 og of both human and rhesus cytomegalovirus (HCMV and RhCMV, respectively) suppresses the functionali

107 te and adaptive immune responses with a deep HCMV imprint, revealed mainly by the expansion of NKG2C(

108 te and adaptive immune responses with a deep HCMV imprint.

109 increases plaque formation by pp71-deficient HCMV.

110 The viral spreading of US28-deficient HCMV, via culture medium or cell-to-cell transmission, w

111 t protein-tagged wild type or US28-deficient HCMV.

112 nt functions and help to prevent deleterious HCMV disease in healthy older people.

113 higher in 8 LTRs who additionally developed HCMV disease, as compared with the other 52 patients in

114 sttransplant follow-up, these LTRs displayed HCMV DNA detection in the BALF by PCR, whereas other inf

115 ties against a panel of genetically distinct HCMV clinical isolates.

116 w that STAT1 is required for efficient early HCMV-induced enhanced monocyte motility and later for HC

117 l for viral protein expression and efficient HCMV replication.

118 e is paramount to controlling or eliminating HCMV infection.

119 latency and reactivation as well as evaluate HCMV vaccines and immune responses in the context of a f

120 Also, US28 facilitates HCMV spreading in VSMCs in vitro.

121 expression of B7-H6 is upregulated following HCMV infection and that HCMV uses two of its genes: US18

122 we have shown that ACLY is not essential for HCMV growth and virally induced lipogenesis.

123 esults show that this motif is essential for HCMV replication and could be a target for development o

124 interaction site of critical importance for HCMV neutralization.

125 the PC at a site of critical importance for HCMV neutralization.

126 ced enhanced monocyte motility and later for HCMV-induced monocyte-to-macrophage differentiation and

127 positive, and 207 (86.6%) were negative for HCMV DNA.

128 ive and 42 (20.3%) with negative results for HCMV DNAemia (P = .006; odds ratio, 3.06; 95% confidence

129 on was diagnosed based on seroconversion for HCMV and/or HCMV immunoglobulin M-positive and low or mo

130 d US28 was detected in renal allografts from HCMV-positive donors independent of viremia and serostat

131 8 in 31 of 34 renal transplant biopsies from HCMV-seropositive donors.

132 for human CMV (HCMV) are elevated in HIV(+) HCMV(+) subjects.

133 subjects compared with those from an HIV(-) HCMV(+) HLA-DR7(+) cohort or with HLA-DR7-restricted CD4

134 ngs may highlight a unique mechanism for how HCMV avoids the antiviral response during infection by h

135 The mechanism of how HCMV enters cells is controversial.

136 his study furthered our understanding of how HCMV evades inhibition by PKR and identified new strateg

137 The aim of our study was to ascertain if HCMV DNA in the peripheral blood of pregnant women with

138 infection of CD34(+) HPCs by HCMV.IMPORTANCE HCMV establishes lifelong persistence within the majorit

139 on in immunocompetent individuals.IMPORTANCE HCMV-specific immune responses have been extensively doc

140 olarization of infected monocytes.IMPORTANCE HCMV promotes multiple functional changes in infected mo

141 rodevelopmental HCMV pathogenesis.IMPORTANCE HCMV brain pathogenesis has been studied in limited expe

142 genetically diverse field strains.IMPORTANCE HCMV is the leading cause of congenital viral infection,

143 topoietic cytokine interleukin 12 (IL-12) in HCMV-infected cells but not in mock-infected cells.

144 3B5 binding site is universally conserved in HCMV, contains a previously described UL128/gL interacti

145 scovered a high transcriptional diversity in HCMV, with many transcripts only slightly differing from

146 to study a post-entry role of endocytosis in HCMV life cycle.

147 vIL-10 was evident in HCMV+ donors (n = 19 of 26), at levels ranging 31-547 pg

148 of modulating Rb family protein function in HCMV-infected cells.

149 ated to host and viral proteins, increase in HCMV-infected cells.

150 standing in detail the processes involved in HCMV replication is important for developing novel treat

151 Therefore, to identify proteins involved in HCMV replication, we developed a methodology to conduct

152 esented here implicate endocytic pathways in HCMV maturation and egress.

153 unctional human adaptive immune responses in HCMV latently-infected huBLT (humanized Bone marrow-Live

154 SG15 monomer and protein conjugates rises in HCMV-infected cells.

155 L131 (Pentamer) complexes play a key role in HCMV cell entry and tropism.

156 s, we determined whether THY-1 has a role in HCMV entry by macropinocytosis.

157 se class II alpha (PI3K-C2A), as its role in HCMV replication was unknown.

158 early 2 (IE2) protein may play a key role in HCMV-caused neurodevelopmental disorders.

159 Instead, we found that in HCMV-infected cells glucose carbon can be used for lipid

160 nduced in cells infected with UV-inactivated HCMV, it was subsequently reduced, but not eliminated, b

161 ronchoalveolar lavage fluid (BALF) indicates HCMV replication in the pulmonary compartment.

162 asymptomatic in immunocompetent individuals, HCMV is a significant cause of morbidity and mortality i

163 ther the ISG15 polypeptide itself influences HCMV infection biology remain unknown.

164 and whether the ISG15 polypeptide influences HCMV replication remain unknown.

165 T antigen (TAg) and oncogenic H-Ras, inhibit HCMV infection.

166 bsets have differential abilities to inhibit HCMV growth and dissemination.

167 multiplicity (MOI = 0.1 PFU/cell) inhibited HCMV in a dose-dependent manner and further induced phos

168 0 T antigen-mediated transformation inhibits HCMV infection at multiple points in the viral life cycl

169 Instead, HCMV-induced ISG15 monomer and protein conjugate accumul

170 re, we investigated LTRs with intrapulmonary HCMV replication for the chemokines CCL-18 and CCL-20.

171 the clinical outcomes following intrauterine HCMV infection.

172 might be restored during infection to limit HCMV disease.

173 ection may be a successful strategy to limit HCMV disease.

174 Such local HCMV replication episodes may remain asymptomatic or may

175 ental samples, whereas a switch of the major HCMV population was observed in 6 individuals with seque

176 ongoing, the unique epidemiology of maternal HCMV infections appears discordant with strategies for v

177 Mechanistically, HCMV upregulated two specific cellular antiapoptotic pro

178 e represent promising targets for mitigating HCMV persistence.

179 mmunoglobulin M-positive and low or moderate HCMV immunoglobulin G avidity.

180 from three healthy human donors with natural HCMV infection or a vaccinated animal, we mapped eight s

181 ther our understanding of neurodevelopmental HCMV pathogenesis.IMPORTANCE HCMV brain pathogenesis has

182 Surprisingly, IE2, but not HCMV IE1 or murine CMV ie3, interferes pleiotropically w

183 n represent targets for development of novel HCMV antivirals.

184 ls associated with the long-term carriage of HCMV has been linked with poor responses to new pathogen

185 iffer in their capacity of direct control of HCMV-infected cells remains unclear.

186 hat is important in the replication cycle of HCMV, we identified a novel target that can be pursued f

187 d susceptibility for the full lytic cycle of HCMV.

188 likely serves as an important determinant of HCMV tropism for select subsets of hematopoietic cells.

189 Determination of HCMV-specific T cells by cultured ELISPOT, in pregnant w

190 pted to utilize THY-1 to facilitate entry of HCMV into macropinosomes in certain cell types.

191 ed cohort that were specific for epitopes of HCMV phosphoprotein-65, tetanus toxoid precursor, EBV nu

192 A prominent feature of HCMV is the wide range of viral gene products that it en

193 Mcl-1 and HSP27 is a distinctive feature of HCMV-induced monocyte survival.

194 Expression was independent of HCMV viremia or IgG serostatus.

195 Further knowledge about the mechanism of HCMV entry into cells may facilitate the development of

196 HCMV) congenital infection, the mechanism of HCMV neuropathogenesis and the roles of individual viral

197 -specific T-cell responses in breast milk of HCMV-seropositive mothers is not well defined.

198 stimulated for 12 days with peptide pools of HCMV proteins IE-1, IE-2, and pp65, and subsequently res

199 e thought to contribute to the prevention of HCMV infection.

200 The immediate early 1 (IE1) protein of HCMV also rescues p107- and p130-mediated repression of

201 Despite this, reactivation of HCMV from its latent reservoir in the bone marrow causes

202 hat ISG15 itself controls the replication of HCMV, which causes life-threatening disease among the im

203 x and DNAemia may help to assess the risk of HCMV fetal transmission.

204 re significantly associated with the risk of HCMV infection in women who were infected with HCMV duri

205 to conduct a high-throughput siRNA screen of HCMV-infected cells.

206 d their progenitors are an important site of HCMV latency, and one viral gene expressed by latently i

207 tion is conserved among different strains of HCMV and the various cell types that support infection,

208 These laboratory-adapted strains of HCMV generally exhibit restricted tropism, produce high

209 ies to cross-neutralize the field strains of HCMV, remains a challenge.

210 a feature of WT but not passaged strains of HCMV.

211 s to characterize the lytic transcriptome of HCMV strain Towne varS.

212 Here we show both are deposited on HCMV genomes during lytic and latent infections suggesti

213 osed based on seroconversion for HCMV and/or HCMV immunoglobulin M-positive and low or moderate HCMV

214 However, host immune responses or HCMV virulence in these patients has not so far been inv

215 In immunosuppressed patients, HCMV can remain relatively stable or undergo drastic gen

216 ) are thought to be important for preventing HCMV transmission from the mother to the fetus, thereby

217 ancy, development of a vaccine that prevents HCMV infection is considered a global health priority.

218 of immune mechanisms involved during primary HCMV infection in immunocompetent individuals.IMPORTANCE

219 ecific immunoglobulin G (IgG) during primary HCMV infection is associated with a limited induction of

220 , some rare severe clinical cases of primary HCMV infection have been reported in immunocompetent pat

221 mpetent adults experiencing a severe primary HCMV infection.

222 Twenty primary HCMV-infected patients (PHIP) were enrolled, as well as

223 ipheral blood of pregnant women with primary HCMV infection at the time of amniocentesis may have a p

224 ured ELISPOT, in pregnant women with primary HCMV infection, in association with avidity index and DN

225 d in a cohort of pregnant women with primary HCMV infection.

226 and pIRS1 proteins antagonize PKR to promote HCMV protein synthesis and replication; however, the mec

227 ISG15 gene product itself directly regulates HCMV replication and that its accumulation restricts pro

228 In addition to regulating HCMV entry/trafficking, EGFR signaling may also shape th

229 Transduction of IE2 largely rescued HCMV gene expression in TAg-expressing fibroblasts but d

230 interferon-stimulated gene, ISG15, restricts HCMV replication, and that IE1 is sufficient to blunt IS

231 tudy establishes that ISG15 itself restricts HCMV replication and that HCMV-induced ISG15 accumulatio

232 nclusion, our results demonstrate that serum HCMV-miR-US4-1 can serve as a novel biomarker for predic

233 In summary, HCMV-encoded US28 was detected in renal allografts from

234 trafficking factor important for supporting HCMV infection.

235 ernal-fetal medicine division with suspected HCMV infection.

236 main asymptomatic or may lead to symptomatic HCMV disease.

237 18 responses are associated with symptomatic HCMV disease, proposing that CCL-18 BALF levels could se

238 pecific proteins to apical exosomes and that HCMV exploits this pathway for virion excretion.

239 pregulated following HCMV infection and that HCMV uses two of its genes: US18 and US20, to interfere

240 5 itself restricts HCMV replication and that HCMV-induced ISG15 accumulation is triggered by host def

241 inhibited EMT and induced MET, arguing that HCMV induces an epithelium-like cellular environment dur

242 pharmacological inhibitors, we document that HCMV activation of the epidermal growth factor receptor

243 We previously identified that HCMV induces the upregulation of multiple proinflammator

244 Our data indicate that HCMV triggers these changes, in the absence of de novo v

245 Our data indicate that HCMV utilizes two phases of STAT1 activation, which we a

246 We now show that HCMV induces the enhanced expression and activation of a

247 We show that HCMV infection increases the protein level of a cellular

248 We now show that HCMV is initially retained in early endosomes and then m

249 We now show that HCMV more robustly upregulated Mcl-1 than normal myeloid

250 We now show that HCMV utilizes the traditionally IFN-associated gene prod

251 Here we show that HCMV-infected cells produce more glucose-derived pyruvat

252 Together, the results show that HCMV-specific CD4(+) T cell responses, even those from e

253 te/ApppI following ZOL treatment showed that HCMV infection boosts their accumulation.

254 We have shown that HCMV induces a proinflammatory state in infected monocyt

255 We have previously shown that HCMV infection of human hematopoietic progenitor cells e

256 Our findings suggest that HCMV has adapted to utilize THY-1 to facilitate entry of

257 Taken together, our results suggest that HCMV reroutes the biphasic activation of a traditionally

258 Our data suggest that HCMV utilizes EGFR- and integrin-dependent (but IFN-inde

259 The HCMV pTRS1 and pIRS1 proteins antagonize PKR to promote

260 The HCMV-specific CD4(+) T cell response to pp65, IE1, IE2,

261 The HCMV-specific T-cell response may have a role in the pre

262 id proteins MCP, Tri1, Tri2, and SCP and the HCMV-specific tegument protein pp150-totaling 4000 mole

263 ivation are generally well controlled by the HCMV-specific T cell response in healthy people.

264 d with dsDNA was prevented by expressing the HCMV multifunctional IE1 transactivator.

265 ttern of infection provides insight into the HCMV transcriptome associated with latency in the host a

266 Here we perform a systems analysis of the HCMV host-cell transcriptome, using gene set enrichment

267 However, the function of the HCMV-induced interferon (IFN)-stimulated genes (ISGs) in

268 hlighting the advisability of sequencing the HCMV stocks used in experiments.

269 se to HCMV has been extensively studied, the HCMV-specific CD4(+) T cell effector response is not as

270 These results indicate that the HCMV huBLT mouse model may provide a valuable tool to st

271 We previously showed that the HCMV tegument protein pUL103 is required for cVAC biogen

272 CD4(+) T cells specific to the HCMV proteins studied were predominantly effector memory

273 tated failed to produce any virus, while the HCMV with the first Py mutated replicated with a defecti

274 Our work demonstrates that these HCMV-specific immune cells retain many important functio

275 Thus, HCMV containing a wild-type gene complement can be gener

276 a subset of immune cells (CD4(+) T cells) to HCMV proteins in healthy donors of all ages, and we demo

277 ative mechanism by which UL97 contributes to HCMV DNA synthesis.

278 IE2 is a pivotal factor that contributes to HCMV-induced abnormalities in the context of the embryon

279 vestigate the response of human monocytes to HCMV following LPS stimulation in vitro.

280 While the CD8(+) T cell response to HCMV has been extensively studied, the HCMV-specific CD4

281 ls produce effector functions in response to HCMV-infected cells and can prevent virus spread.

282 ranulate or secrete cytokines in response to HCMV-infected primary fetal extravillous trophoblasts.

283 CD4(+) T cell responses to HCMV-infected dendritic cells were sufficient to control

284 r is the current drug of choice for treating HCMV, knowing the provenance of the dNTPs incorporated i

285 nonprogressor HIV subjects with undetectable HCMV plasma viremia.

286 In contrast to US28, HCMV-encoded immediate early antigen was detected in les

287 ited experimental settings, such as in vitro HCMV infection of neural progenitor cells or in vivo mur

288 To determine whether HCMV epitope-specific CD4(+) T cell memory inflation occ

289 This novel mechanism by which HCMV may interfere with the production of neutralizing a

290 sought to investigate conditions under which HCMV can be propagated without incurring genetic defects

291 compared with the other 52 patients in whom HCMV replication remained asymptomatic (P < 0.001, Mann-

292 aft and/or the blood and are associated with HCMV disease.

293 THY-1 associated with HCMV virions on the cell surface and colocalized with vi

294 MV infection in women who were infected with HCMV during participation in a glycoprotein B vaccine tr

295 y in the context of direct interactions with HCMV-infected cells.

296 pon compartmental analysis of 1 patient with HCMV retinitis.

297 ic outcome of infants infected in utero with HCMV.

298 ted in an increase in ICP0-null HSV-1 and wt HCMV replication and plaque formation; therefore, this s

299 phenotype, we reconstructed a wild-type (WT) HCMV genome using bacterial artificial chromosome techno

300 In this study, we show that WT-HCMV produces extremely low titers of cell-free virus bu