ライフサイエンスコーパス: HCMV

1 HCMV can result in severe direct and indirect pathologie

2 HCMV disease is a direct consequence of monocyte-mediate

3 HCMV IgG level, a surrogate marker of viral activity, wa

4 HCMV infection is generally asymptomatic, but can cause

5 HCMV positive (HCMV+) and HCMV negative (HCMV-) groups w

6 HCMV then activates cellular autophagy as a countermeasu

7 HCMV uses a similar pentaloop, an interesting example of

8 HCMV-induced signaling initiated during viral entry stim

9 resenting an unexpectedly broad panel of 123 HCMV antigens.

10 Early after HCMV infection of human foreskin fibroblasts vimentin le

11 drial network undergoes fission events after HCMV infection.

12 viral and antiproliferative activity against HCMV and glioblastoma cell line (GBM6), respectively.

13 eactivity was important for activity against HCMV.

14 ential to act as antiviral compounds against HCMV via direct engagement of virions.IMPORTANCE Human c

15 vasion of humoral responses directed against HCMV virions.

16 antiviral defense effector molecule against HCMV infection and identifies it as a potential clinical

17 e been proposed to confer protection against HCMV infection, and the virion envelope glycoprotein B (

18 may have elicited partial protection against HCMV viruses with antigenically similar gB sequences.

19 erefore, we analyzed the AB-response against HCMV glycoprotein B (gB) and the pentameric complex (PC)

20 elopment of antibody-based therapies against HCMV.

21 ins gB and gH work in concert to initiate an HCMV-specific signalosome responsible for the atypical a

22 it was unknown whether skin could support an HCMV infection.

23 Thus, an HCMV vaccine represents a priority for both governmental

24 dge governing virion maturation, we analysed HCMV virions using proteomics, and identified a signific

25 ly significant association between HSV-1 and HCMV was found in hemodialysis patients and severe perio

26 st to that of KSHV's close relatives EBV and HCMV, KSHV lytic replication occurs while the APC/C is a

27 In contrast to those of EBV and HCMV, the KSHV lytic cycle occurs while the APC/C is act

28 In SOC, VZV infected the epidermis and HCMV infected the dermis.

29 ciation between gray matter volume (GMV) and HCMV has never been examined in major depressive disorde

30 otein D (gD), EBV glycoprotein 42 (gp42) and HCMV gH-gL-gO trimer and gH-gL-UL128-UL130-UL131A pentam

31 TAIL-seq on HBV and HCMV RNAs revealed that TENT4A and TENT4B are responsibl

32 driven by differences between the HCMV+ and HCMV- MDD subgroups.

33 HCMV positive (HCMV+) and HCMV negative (HCMV-) groups within each sample were bal

34 stem in modeling host-virus interactions and HCMV-induced birth defects.IMPORTANCE Human cytomegalovi

35 pstein-Barr virus, herpes simplex virus, and HCMV-specific immunoglobulin G (IgG), serum markers of i

36 d an adult human skin model to study VZV and HCMV in culture and in vivo While VZV is known to grow i

37 Previously, VZV and HCMV models used fetal tissue; here, we developed an adu

38 VZV and HCMV mouse models were developed by subcutaneous transpl

39 idespread infection was observed for VZV and HCMV.

40 Notably, we detected VZV- and HCMV-infected cells in the contralateral, uninoculated x

41 refractory to TGF-beta signaling as another HCMV miRNA, miR-UL22A, downregulates SMAD3, which is req

42 d have the capacity to be developed for anti-HCMV activity.

43 therapies has fueled the search for new anti-HCMV agents.

44 will focus on optimization of these new anti-HCMV compounds along with mechanistic studies.

45 ortant step to the development of novel anti-HCMV drugs that prevent the spread of infected monocytes

46 is important to develop a new class of anti-HCMV drugs that could target and prevent spread of the v

47 ment of the physiological repertoire of anti-HCMV T cell specificities in seropositive individuals.

48 e individuals indicate that physiologic anti-HCMV T cell responses are directed against a broad range

49 In vimentin-deficient fibroblasts, the anti-HCMV activity of artesunate is reduced compared with con

50 There is no approved HCMV vaccine, and vaccine development strategies are com

51 s the mechanisms underlying the link between HCMV infection and the induction of SLE.

52 ytic subunit, found to be important for both HCMV-mediated glycolytic activation and high titer infec

53 dergo apoptosis, which is rapidly blocked by HCMV to ensure the survival and dissemination of infecte

54 The broad array of organ diseases caused by HCMV is directly linked to the systematic spread of the

55 ucidation of multiple strategies employed by HCMV to effectively block NK cell targeting of virus-inf

56 a new layer of host manipulation induced by HCMV infection that leads to enhanced virus spread.

57 Of the many cell types infected by HCMV in the host, myeloid cells, such as monocytes, are

58 and the modulation of the immune response by HCMV, which is understudied in the context of endogenous

59 ts a mechanism of immune evasion utilized by HCMV to decrease the expression of MHC class II in a rel

60 Because monocytes are short-lived cells, HCMV must subvert the natural short life-span of these b

61 riguingly, in vimentin-overexpressing cells, HCMV infection is reduced compared with control cells.

62 Acute infection with human CMV (HCMV) induces the development of adaptive NKG2C(+) NK ce

63 mentin, depending on the stage of human CMV (HCMV) replication.

64 ct research aimed at developing a human CMV (HCMV) vaccine.

65 Conceivably, HCMV infection may be a treatable source of neuropatholo

66 cts may confer protection against congenital HCMV.

67 V infections is the occurrence of congenital HCMV infections (cCMV) in women with existing immunity t

68 al design of a vaccine to prevent congenital HCMV.

69 Conversely, HCMV downregulated the expression of nasal epithelial ce

70 Of the human herpesviruses, cytomegalovirus (HCMV) and Epstein-Barr virus (EBV) both impair the activ

71 aliva and 39% in GCF; human cytomegalovirus (HCMV) 11% in GCF; varicella zoster virus 6% in saliva an

72 rus 1 (HSV-1), HSV-2, human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV) entry glycoproteins h

73 for activity against human cytomegalovirus (HCMV) and identified the voltage-gated chloride ion chan

74 t evidence highlights human cytomegalovirus (HCMV) and immune activation as risk factors for tubercul

75 n (vICA) conserved in human cytomegalovirus (HCMV) and murine CMV (MCMV) prevents the activation of c

76 oster virus (VZV) and human cytomegalovirus (HCMV) are endemic to humans.

77 clinical isolates of human cytomegalovirus (HCMV) are highly cell associated, and mutations affectin

78 Human cytomegalovirus (HCMV) causes a lifelong infection through establishment

79 Human cytomegalovirus (HCMV) causes severe disease in infants and immunocomprom

80 infections.IMPORTANCE Human cytomegalovirus (HCMV) continues to cause serious and often life-threaten

81 ternal acquisition of human cytomegalovirus (HCMV) during pregnancy is a primary strategy to reduce t

82 The human cytomegalovirus (HCMV) endoplasmic reticulum (ER)-resident glycoprotein U

83 port that GA inhibits human cytomegalovirus (HCMV) genome replication and Zika virus (ZIKV) infection

84 Human cytomegalovirus (HCMV) glycoproteins H and L (gH/gL) can be bound by eith

85 Human cytomegalovirus (HCMV) has been linked to the triggering of systemic lupu

86 iral activity against Human Cytomegalovirus (HCMV) in our previous work, could restrict ZIKV infectio

87 Congenital human cytomegalovirus (HCMV) infection causes a broad spectrum of central and p

88 tical consequences of human cytomegalovirus (HCMV) infection in the transplant population and in cong

89 Human cytomegalovirus (HCMV) infection is associated with neuropathology in pat

90 control of persistent human cytomegalovirus (HCMV) infection is effectively mediated by virus-specifi

91 ersistence.IMPORTANCE Human cytomegalovirus (HCMV) infection is endemic throughout the world regardle

92 n the host.IMPORTANCE Human cytomegalovirus (HCMV) infection is endemic throughout the world, with a

93 Human Cytomegalovirus (HCMV) infection modulates cellular metabolism to support

94 Human cytomegalovirus (HCMV) infection remains an important cause of neurodevel

95 sed susceptibility to human cytomegalovirus (HCMV) infection.

96 Human Cytomegalovirus (HCMV) infects over half the world's population, is a lea

97 infection.IMPORTANCE Human cytomegalovirus (HCMV) is a common pathogen that asymptomatically infects

98 tic target.IMPORTANCE Human cytomegalovirus (HCMV) is a herpesvirus present in up to 85% of some popu

99 rus spread.IMPORTANCE Human cytomegalovirus (HCMV) is a herpesvirus that leads to serious health cons

100 Human cytomegalovirus (HCMV) is a large DNA herpesvirus that is highly prevalen

101 th defects.IMPORTANCE Human cytomegalovirus (HCMV) is a leading cause of central nervous system birth

102 Human cytomegalovirus (HCMV) is a major cause of morbidity and mortality among

103 Human cytomegalovirus (HCMV) is a ubiquitous pathogen that can cause severe cli

104 Human cytomegalovirus (HCMV) is a ubiquitous pathogen that encodes many protein

105 Human Cytomegalovirus (HCMV) is a ubiquitous pathogen that has coevolved with i

106 Human cytomegalovirus (HCMV) is a ubiquitous pathogen that latently infects hem

107 Human cytomegalovirus (HCMV) is an important human pathogen and a paradigm of i

108 or (CIITA).IMPORTANCE Human cytomegalovirus (HCMV) is an opportunistic herpesvirus that is asymptomat

109 of virions.IMPORTANCE Human cytomegalovirus (HCMV) is major pathogen of nonimmunocompetent individual

110 emination strategy of human cytomegalovirus (HCMV) is the induction of monocyte survival, where monoc

111 Human cytomegalovirus (HCMV) is the most common infectious cause of infant birt

112 cal models.IMPORTANCE Human cytomegalovirus (HCMV) is the most common infectious cause of infant birt

113 cells (HPCs) support human cytomegalovirus (HCMV) latency, and their differentiation along the myelo

114 Human cytomegalovirus (HCMV) manipulates cellular processes associated with sec

115 Human cytomegalovirus (HCMV) may cause severe infections in lung transplant rec

116 angstrom structure of human cytomegalovirus (HCMV) pUL50-pUL53.

117 Infection with human cytomegalovirus (HCMV) remains a significant cause of morbidity and morta

118 le is known about the human cytomegalovirus (HCMV) tegument protein UL88.

119 e the activity of the human cytomegalovirus (HCMV) transactivator immediate early 2 (IE2).

120 cted viruses, such as human cytomegalovirus (HCMV), a leading cause of congenital infection and a maj

121 tis B virus (HBV) and human cytomegalovirus (HCMV), generated via a similar mechanism exploiting the

122 colon cancer, and in human cytomegalovirus (HCMV)-infected fibroblasts, where the RNA facilitates vi

123 with the herpesvirus, human cytomegalovirus (HCMV).

124 sites in alternative MIE promoters decreased HCMV IE gene expression upon reactivation and significan

125 tivity of a novel HCMV inhibitor that drives HCMV infection to occur independently of HSPGs and the g

126 aling to the unique activation of Akt during HCMV infection.

127 The early induction of autophagy during HCMV infection was distinctly required for the survival

128 roteins targeted for degradation late during HCMV infection.

129 nctional changes to host mitochondria during HCMV infection.

130 tivation of alternative MIE promoters during HCMV reactivation, as mutating FOXO binding sites in alt

131 spho-Thr-315 cyclin H is up-regulated during HCMV replication.

132 A key step during HCMV reactivation in latently infected HPCs is reexpress

133 mbinant strains have been transmitted during HCMV evolution, and some have apparently survived for th

134 tic proteins specifically upregulated during HCMV infection but not during growth factor treatment.

135 We used TB40/E HCMV and POka VZV strains to evaluate virus tropism in s

136 tein vaccine (gB/MF59), the most efficacious HCMV vaccine evaluated in a clinical trial, via targeted

137 ediated signaling is important for efficient HCMV gene expression, DNA synthesis, and the production

138 re, we present a novel approach that employs HCMV deletion mutant viruses lacking HLA class I immunoe

139 Our data argue that experimental HCMV latency is much more similar than it is different i

140 Here, we demonstrate that latently expressed HCMV miR-US5-2 downregulates the transcriptional repress

141 We now show AP-1 is a critical component for HCMV reactivation.

142 For example, CaMKK1 is important for HCMV infection at a low multiplicity of infection, but i

143 at the host exosome pathway is intrinsic for HCMV maturation, and reveal new host regulators involved

144 ch-needed preclinical small-animal model for HCMV and VZV and, potentially, other human-restricted vi

145 d infants, the limited treatment options for HCMV, and the rise of resistant mutants toward existing

146 dentify host genes specifically required for HCMV infection of epithelial cells.

147 activity indicated that HCK is required for HCMV reactivation.

148 g the repertoire of T cell specificities for HCMV is hampered by the immense protein coding capacity

149 portantly, the transfer of EVs purified from HCMV-infected cells enhanced virus spread.

150 Despite a large genome, HCMV relies exclusively on host cells for metabolic func

151 Like all herpesviruses, HCMV infection is for life.

152 In maternal populations with a high HCMV seroprevalence, cCMV that follows nonprimary matern

153 tuberculosis (P = .055), and those with high HCMV IgG 3.4 times more likely to have tuberculosis (P =

154 e incidence of cCMV in populations with high HCMV seroprevalence.

155 ow that the observations of high within-host HCMV nucleotide diversity are explained by the frequent

156 However, little is known about how HCMV infection alters the surrounding cellular environme

157 Deciphering how HCMV modulates the cellular pathway to induce monocyte s

158 nfection, thereby providing insight into how HCMV hijacks cellular metabolism for its replication, an

159 Understanding how HCMV controls the microenvironment of an infected cell s

160 nce of this research is in understanding how HCMV manipulates the host mitochondria to support bioene

161 e horizontal transmission of HCMV.IMPORTANCE HCMV is a ubiquitous human pathogen causing neurodevelop

162 this early step in HCMV infection.IMPORTANCE HCMV is a major global health concern, and antiviral che

163 n other variable loci.IMPORTANCE Advances in HCMV population genetics have greatly outpaced understan

164 and stable expansion of adaptive NK cells in HCMV infection.

165 e role and functions of tegument proteins in HCMV, many of which remain uncharacterized, will contrib

166 americ complex (PC) and the ADCC response in HCMV-seropositive (R+) LTRs and in seronegative recipien

167 ed by antibodies to block this early step in HCMV infection.IMPORTANCE HCMV is a major global health

168 lthough asymptomatic in healthy individuals, HCMV can cause severe multiorgan disease in immunocompro

169 mission is much lower in naturally infected (HCMV-seropositive) women, we hypothesize that a vaccine

170 synthesis, and the production of infectious HCMV progeny.

171 is dispensable for production of infectious HCMV virions in multiple HCMV strains and cell types.

172 e developmental stage in which HCMV infects, HCMV drives hematopoietic cells towards a weaker immune-

173 Indeed, survival of autophagy-inhibited HCMV-infected monocytes was rescued when MLKL and RIPK3

174 ein cargo was subsequently incorporated into HCMV virions during infection.

175 We investigated HCMV strain diversity.

176 crobe, Hancock et al., 2020 show that latent HCMV infection, and specifically miR-US5-2, induces TGF-

177 d that loss of 7/9 caused significantly less HCMV production.

178 men of child bearing age to prevent maternal HCMV acquisition during pregnancy.

179 Individuals with medium HCMV IgG were 2.8 times more likely to have tuberculosis

180 Multiple HCMV-directed specificities in the memory T cell pool of

181 ction of infectious HCMV virions in multiple HCMV strains and cell types.

182 HCMV positive (HCMV+) and HCMV negative (HCMV-) groups within each sample were balanced on up to

183 aracterize the antiviral activity of a novel HCMV inhibitor that drives HCMV infection to occur indep

184 Glycoprotein B of HCMV is an important target for neutralizing antibodies

185 cid sequence of gO influences the biology of HCMV.

186 ibute to our understanding of the biology of HCMV.

187 likely important for the natural biology of HCMV.

188 or immunotherapeutic to reduce the burden of HCMV-associated disease, yet after nearly a half-century

189 or immunotherapeutic to reduce the burden of HCMV-associated disease.

190 intaining the proper tegument composition of HCMV virions.

191 end points in turn, showing that control of HCMV likely depends on a combination of innate immune fa

192 By understanding the dependency of HCMV on the mitochondria, we could exploit these require

193 UL74(gO) is an important determinant of HCMV infectivity and one of the most diverse loci in the

194 the driving force behind the development of HCMV vaccines is to prevent congenital infection, the an

195 Currently, the effect of HCMV infection on host cell metabolism as an increase in

196 There was a main effect of HCMV serostatus but not diagnosis that replicated across

197 Posthoc tests revealed that the effect of HCMV was driven by differences between the HCMV+ and HCM

198 EV inhibitor GW4869 slowed the efficiency of HCMV spread.

199 mory T-cell subsets and lower frequencies of HCMV-specific multifunctional CD8 T cells.

200 We investigated the impact of HCMV infection on MHC class II in Kasumi-3 cells, a myel

201 However, the specific infectivity of HCMV virions suffers in the absence of UL88, as more gen

202 ulfonic acid (DIDS) as a potent inhibitor of HCMV replication.

203 n network is important for the initiation of HCMV replication but hinders its completion.

204 ence of a dose response between magnitude of HCMV IgG with risk of tuberculosis disease.

205 ynamics provides insights into mechanisms of HCMV infection and a resource for biological and therape

206 ere, we established a novel ex vivo model of HCMV infection in native human nasal turbinate tissues.

207 Using a nonhuman primate model of HCMV infection, we show that rhesus macaques immunized a

208 exosome proteins as important modulators of HCMV replication with antiviral potential.

209 We proposed that B cell epitope region of HCMV phosphoprotein 65 (HCMVpp65)(422-439) mimics an end

210 I complex or the unique short (US) region of HCMV, a region expressing many immunomodulatory genes.

211 rter system for high-throughput screening of HCMV inhibitors.

212 each compound inhibited a specific stage of HCMV replication.

213 The earliest stages of HCMV infection in the human host have remained elusive i

214 against all clinical outcomes and stages of HCMV infection.

215 provide insights into the earliest stages of HCMV infection.

216 Strains of HCMV vary considerably in the levels of gH/gL/gO and gH/

217 tential limitations of laboratory studies of HCMV biology that use single, isolated genotypes or stra

218 ghts from each model germane to the study of HCMV vaccines.

219 was distinctly required for the survival of HCMV-infected monocytes, as repression of autophagosome

220 iting immune responses analogous to those of HCMV-seropositive subjects may confer protection against

221 tions against the horizontal transmission of HCMV and potentially that of other viruses.

222 tions against the horizontal transmission of HCMV.IMPORTANCE HCMV is a ubiquitous human pathogen caus

223 ning disease, our molecular understanding of HCMV latency is incomplete.

224 tibody (AB)-dependent cytotoxicity (ADCC) on HCMV is still unclear.

225 sistently degraded by the minimally passaged HCMV strain Merlin but not the extensively passaged stra

226 In 23 D+R- patients, HCMV-specific ABs developed.

227 Unique to the natural history of perinatal HCMV infections is the occurrence of congenital HCMV inf

228 HCMV positive (HCMV+) and HCMV negative (HCMV-) groups within each samp

229 direct identification of naturally presented HCMV-derived HLA ligands by mass spectrometry.

230 it antiviral immune factors that can prevent HCMV-associated disease.

231 Thus, a vaccine to prevent HCMV-associated congenital disease is a public health pr

232 of vaccines or immunotherapeutics to prevent HCMV-mediated congenital and transplant disease.

233 A pp28-luciferase recombinant HCMV was used as a reporter system for high-throughput s

234 Serendipitously, the entry of DIDS-resistant HCMV also became independent of heparan sulfate proteogl

235 Although sequencing of DIDS-resistant HCMV revealed enrichment of a mutation within UL100 (enc

236 dicated that its induction does not restrict HCMV infection.

237 s a potential clinical candidate to restrict HCMV infections.IMPORTANCE Human cytomegalovirus (HCMV)

238 As a result, HCMV infections are highly problematic in individuals wi

239 on of five structurally unique and selective HCMV inhibitors, active at sub to low micromolar concent

240 Here, we deep sequence HCMV genomes recovered from single and longitudinally co

241 For the first time, we showed HCMV successfully grows in adult human skin, as does VZV

242 ncrease the activity of EV biogenesis, since HCMV-infected fibroblasts have increased vesicle release

243 Specifically, HCMV infected fibroblasts, endothelial cells, and hemato

244 r cell culture systems utilized for studying HCMV do not endogenously express MHC class II.

245 Relative to HCMV- subjects, HCMV+ subjects in sample 1 showed a significant reductio

246 ion stabilizes it and antagonizes subsequent HCMV-mediated vimentin destabilization, thus suppressing

247 ve been found to be important for successful HCMV infection.

248 ated gB1, gB2, and gB4 genotype "supergroup" HCMV variants among vaccine recipients, suggesting that

249 d vimentin destabilization, thus suppressing HCMV replication.

250 In this work, we demonstrate that HCMV glycoproteins gB and gH work in tandem to reroute c

251 Here, we find that HCMV depends on two kinase isoforms to support infection

252 We find that HCMV specifically induces expression of the AMPKa2 subun

253 This study finds that HCMV manipulates this pathway to increase the efficiency

254 This study finds that HCMV modulates EV biogenesis machinery through upregulat

255 Although we found that HCMV activated RIP3K upon infection, MLKL was not activa

256 Accordingly, we found that HCMV blocked the activation of caspase 8, which was main

257 We found that HCMV glycoproteins gB and gH directly bind and activate

258 We further found that HCMV infection of epithelial cells is blocked by a synth

259 We found that HCMV rapidly induced autophagy within infected monocytes

260 Overall, our data indicate that HCMV glycoproteins gB and gH work in concert to initiate

261 Taken together, these data indicate that HCMV induces autophagy to prevent necroptotic cell death

262 Collectively, our data indicate that HCMV infection selectively induces the expression of spe

263 Our results also indicate that HCMV specifically induces the expression of the non-ubiq

264 Here, we report that HCMV infection or treatment of ARPE-19 diploid epithelia

265 Additionally, we show that HCMV infection similarly interferes with the AP-1 comple

266 early time points, we were able to show that HCMV strains can be highly specialized to either cell-fr

267 They also show that HCMV-infected cells become resistant to TGF-beta signali

268 MHC class II (HLA-DR), this study shows that HCMV decreases the expression of HLA-DR in infected cell

269 These results suggest that HCMV has evolved mechanisms to target specific metabolic

270 This suggests that HCMV modulates the EV pathway to transfer proviral signa

271 The HCMV glycoprotein UL148 retains CD58 within the ER, ther

272 The HCMV IE1 protein induces P2Y2 expression; and P2Y2-media

273 tigenic epitope vaccine ensemble against the HCMV that should elicit T and B cell responses in the en

274 f HCMV was driven by differences between the HCMV+ and HCMV- MDD subgroups.

275 Outcomes in the HCMV field have previously been measured against a varie

276 s (r = -0.19, p(uncorrected) = 0.043) in the HCMV+ group of sample 1.

277 ssays with synthetic peptides presenting the HCMV- and EBV-specific NEC hook sequences, we characteri

278 We show the HCMV receptor integrin beta 1 dissociates from extracell

279 We previously showed the HCMV-encoded G protein-coupled receptor US28 is expresse

280 Thus, HCMV strains can be highly specialized for either for ce

281 ggest that the host cell ETC is essential to HCMV replication.

282 ns (cCMV) in women with existing immunity to HCMV, infections that have been designated as nonprimary

283 -specific innate immune response patterns to HCMV, comparing infected human nasal mucosal and placent

284 Relative to HCMV- subjects, HCMV+ subjects in sample 1 showed a sign

285 s a "trap door" death pathway in response to HCMV subversion of apoptosis.

286 Humoral response to HCMV, but not Epstein-Barr or herpes simplex virus, was

287 at nasal mucosal tissues were susceptible to HCMV infection, with predominant infection of ciliated r

288 city to cause ER reorganization is unique to HCMV UL148.IMPORTANCE In myriad examples, viral gene pro

289 oforms and AMPK subunit isoforms make toward HCMV infection.

290 We identified 368 unique HCMV-derived HLA class I ligands representing an unexpec

291 Moreover, using HCMV::EBV hook domain swap constructs, computational pre

292 nd release of infectious progeny, in various HCMV strains and cell types.

293 In vitro, HCMV entry and viral progeny are reduced in vimentin-def

294 Elucidating the mechanisms by which HCMV stimulates monocyte survival is an important step t

295 gardless of the developmental stage in which HCMV infects, HCMV drives hematopoietic cells towards a

296 servations provide a mechanism through which HCMV induces global myelosuppression following HSCT whil

297 ken pox) and herpes zoster (shingles), while HCMV causes serious disease in immunocompromised patient

298 twork-wide metabolic changes associated with HCMV infection, it is important for the remodeling of a

299 kedly increased when cells are infected with HCMV or treated with zeocin.

300 Cultured cell lines infected with HCMV show induction of POLR3E expression.