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1 hway, resulted in only a slight reduction in HSV infection.
2 estions in the context of a murine cutaneous HSV infection.
3 n of T cells increased their permissivity to HSV infection.
4 t was not a measurement of the prevalence of HSV infection.
5 cted viruses in studying the early events in HSV infection.
6 otein ICP0 is a multifunctional regulator of HSV infection.
7 nt a new therapeutic strategy for inhibiting HSV infection.
8 ased risk of HIV infection in the setting of HSV infection.
9 ty-four adults had confirmed primary genital HSV infection.
10 ts a promising new class of vaccines against HSV infection.
11 inducible protein-10 (IP-10, CXCL10) during HSV infection.
12 this Ag resulting in protective immunity to HSV infection.
13 nding are stimulated during the course of an HSV infection.
14 6) and human beta-defensin (hBD) 3 inhibited HSV infection.
15 ial component of the immune response against HSV infection.
16 nitiates the postattachment (entry) phase of HSV infection.
17 sociation of the gD receptor is required for HSV infection.
18 cle in which mice are susceptible to vaginal HSV infection.
19 tical in determining the outcome of neonatal HSV infection.
20 dy and subsequent neonatal susceptibility to HSV infection.
21 induction of humoral responses to peripheral HSV infection.
22 regulate transcription of type I IFNs during HSV infection.
23 r, but it could indicate resistance to overt HSV infection.
24 occurs in the corneal stroma in response to HSV infection.
25 ression of VP5 is a requirement for a normal HSV infection.
26 d mucous membranes, is the primary target of HSV infection.
27 d DNA replication, even with the presence of HSV infection.
28 association of the occurrence of EM with an HSV infection.
29 giogenesis and the severity of lesions after HSV infection.
30 a role, albeit probably a different role, in HSV infection.
31 ctions during intermediate to late stages of HSV infection.
32 elopment of immune modulatory treatments for HSV infection.
33 of plasmid DNA encoding CCR7 ligands before HSV infection.
34 paralysis-free survival during primary acute HSV infection.
35 ellular gene expression so characteristic of HSV infection.
36 cts had no clinical or virologic evidence of HSV infection.
37 role for vhs in modulating host responses to HSV infection.
38 ve sites and replication compartments during HSV infection.
39 underestimate overall prevalence of genital HSV infection.
40 oorly as shown by ELISA, and failed to block HSV infection.
41 yclovir, were tested in a mouse eye model of HSV infection.
42 for clinical investigation and diagnosis of HSV infection.
43 s for clinical and serologic evidence of new HSV infection.
44 ration which is targeted by VP16 to regulate HSV infection.
45 SV) is important in the control of recurrent HSV infection.
46 ficant change in Th subset balance following HSV infection.
47 ntibodies are relatively ineffective against HSV infection.
48 r the inability of this form of gDt to block HSV infection.
49 fic CTL response and provide protection from HSV infection.
50 otentially curative approach to treat latent HSV infection.
51 m that may contribute to the pathogenesis of HSV infection.
52 tabolite produced by Serratia marcescens, on HSV infection.
53 cephalitis, including 17 with disease due to HSV infection.
54 omatic relief from outbreaks but do not cure HSV infection.
55 perties, we investigated how it might affect HSV infection.
56 ents are, and tree shrews are susceptible to HSV infection.
57 e control of local manifestations of primary HSV infection.
58 2, to investigate telomerase activity during HSV infection.
59 o date, there is no licensed vaccine against HSV infection.
60 study, we investigate role of telomerase in HSV infection.
61 d thus has pleiotropic inhibitory effects on HSV infection.
62 sible, and may offer a pathway to a cure for HSV infection.
63 a highly prevalent chronic disease caused by HSV infection.
64 effort to induce greater protection against HSV infection.
65 rotected from behavioral pathology following HSV infection.
66 to generate a more effective vaccine against HSV infection.
67 cantly lower levels of corneal miR-132 after HSV infection.
68 ifferent mechanisms during various phases of HSV infection.
69 er was not tested, and those not at risk for HSV infection.
70 teraction of gamma(1)34.5 with TBK1 dictates HSV infection.
71 tected in IL-17 receptor knockout mice after HSV infection.
72 nce of neurons and other cells in the CNS to HSV infection.
73 s, were major producers of IL-17 early after HSV infection.
74 nd disease in mouse and guinea pig models of HSV infections.
75 timulation was shown in both influenza A and HSV infections.
76 ising drug candidate for treatment of ocular HSV infections.
77 this technology for laboratory diagnosis of HSV infections.
78 tosis may be factors in the immunobiology of HSV infections.
79 and sensitivity to Vhs cleavage during lytic HSV infections.
80 of viral tropism and damage during visceral HSV infections.
81 munity have significant problems controlling HSV infections.
82 fective for the majority of clinical VZV and HSV infections.
83 nt of severe and particularly drug-resistant HSV infections.
84 omen were followed for 20 months for primary HSV infections.
85 the innate reaction to herpes simplex virus (HSV) infection.
86 of immune responses to herpes simplex virus (HSV) infection.
87 modifies experimental herpes simplex virus (HSV) infection.
88 oped EM secondary to a herpes simplex viral (HSV) infection.
89 which is triggered by herpes simplex virus (HSV) infection.
90 eonates with perinatal herpes simplex virus (HSV) infection.
91 flammatory response to herpes simplex virus (HSV) infection.
92 a very early event in herpes simplex virus (HSV) infection.
93 nd plays a key role in herpes simplex virus (HSV) infection.
94 nd in animal models of herpes simplex virus (HSV) infection.
95 ciency virus (HIV) and herpes simplex virus (HSV) infections.
96 identify 3 subject cohorts: 1 with no prior HSV infections, 1 with HSV-2 antibodies but no recognize
99 ave addressed the question of whether latent HSV infection affects neuronal gene expression by using
100 ion that could be exploited to better manage HSV infection, aid in vaccine design, or allow targeted
103 sed the severity of ocular lesions caused by HSV infection, although no effects on this immunoinflamm
104 ere are marked differences in the outcome of HSV infection among the different neuronal populations i
105 d with reduced odds of herpes simplex virus (HSV) infection among MSM overall (0.84, 0.75-0.95; k=5;
107 in protection of mice against neuroinvasive HSV infection and do so largely by mechanisms other than
108 beled murine sensory ganglia for evidence of HSV infection and for the sensory neuron marker A5 or KH
109 teen subjects were identified with an active HSV infection and had pre-outbreak, acute-phase, and pos
110 lain the lack of nerve damage from recurrent HSV infection and may provide insight to understanding a
111 s with these pharmacological agents inhibits HSV infection and prevents focal adhesion kinase (FAK) p
113 een, develop dysfunctional CD8+ T cells upon HSV infection and readily succumb to herpes encephalitis
114 phorylation of both serines was induced upon HSV infection and required functional ICP4 and ICP27.
116 cose metabolism changed during the course of HSV infection and that modulating glucose levels can inf
117 ew revelations about these guardians against HSV infection and the consequences of the alarms raised
119 t reductions in the symptoms associated with HSV infection and the symptomatic and asymptomatic shedd
121 protein plays a role in the pathogenesis of HSV infections and that changing the expression kinetics
122 nt to the link between herpes simplex virus (HSV) infection and multifocal CNS demyelination in human
125 ust to variation in test cost, prevalence of HSV infection, and random variation to study assumptions
126 ulted from nonneurologic causes unrelated to HSV infection, and three animals were sacrificed for his
127 of herpes labialis; 1 subject had a primary HSV infection; and 1 subject without baseline serology i
128 mportant manifestations and complications of HSV infection are considered here in a neuroanatomic con
138 lls, were 16- to 50-fold more susceptible to HSV infection at the apical surface than at the basolate
140 r early in the productive phase of wild-type HSV infection, but rather during establishment of a quie
141 rugs are used to treat herpes simplex virus (HSV) infection, but they cannot stop viral shedding and
142 PRO 2000 gel significantly inhibited HIV and HSV infection by at least 1000-fold, compared with CVL s
145 may shed light on the incomplete control of HSV infections by the immune system and may allow more r
147 imulation molecules expressed at the site of HSV infection can enhance vaccine efficacy even in a ful
148 otent antiviral therapy during early primary HSV infection can reduce the magnitude of the latent inf
149 This work thus shows that (i) quiescent HSV infections can be maintained in PC12 cells in vitro,
151 effect of splicing on gene expression during HSV infection, cells were transfected with plasmids harb
153 and weaknesses of each method for diagnosing HSV infection, cite performance characteristics, and rev
154 ion of VZV-specific T-helper cell responses, HSV infections, CMV disease, chronic graft-versus-host d
157 cific T-cell immunity, herpes simplex virus (HSV) infection, cytomegalovirus (CMV) disease, survival,
158 were recorded regarding clinical evidence of HSV infection, degree of immune suppression, length of i
159 harged from the hospital with a diagnosis of HSV infection did not change over this time period despi
160 our understanding of host responses against HSV infection, discuss past clinical vaccine trials, and
162 tory of recurrent oral herpes simplex virus (HSV) infections following dental treatment and antiviral
163 t identifies and types herpes simplex virus (HSV) infections for use in routine clinical settings.
164 sole receptor capable of enabling spread of HSV infection from the vaginal epithelium to the PNS and
167 erall, and children and mothers with chronic HSV infection had lower shedding rates than children wit
170 of regulation of NF-kappaB activation during HSV infection, highlighting the important role that NF-k
171 prone to disseminated herpes simplex virus (HSV) infection (ie, atopic dermatitis with a history of
172 mory CTL response to provide protection from HSV infection, immunized mice were challenged with a let
173 inst routine serologic screening for genital HSV infection in asymptomatic adolescents and adults, in
174 benefits of serologic screening for genital HSV infection in asymptomatic adolescents and adults, in
175 ing and preventive interventions for genital HSV infection in asymptomatic adults and adolescents to
176 w clear differences in the outcome of ocular HSV infection in CXCR2-/- compared with control BALB/c m
180 owever, some cellular mechanisms involved in HSV infection in rodents are different from those in hum
181 at IFN-gamma significantly attenuates latent HSV infection in the mouse model of ocular infection but
185 antly, BILS 179 BS was orally active against HSV infections in murine models of HSV-1 and HSV-2 disea
187 l is quite different from the mouse model of HSV infection, in that the virus exhibited only a mild a
189 roscopy of fluorescent viruses, we show that HSV infection induces the polarized migration of skin ce
190 hat ocular neovascularization resulting from HSV infection involves a change in the balance between V
192 understanding of the evolutionary aspects of HSV infection is crucial to the design of effective ther
195 Importance: Genital herpes simplex virus (HSV) infection is a prevalent sexually transmitted infec
202 utine serodiagnosis of herpes simplex virus (HSV) infections is currently performed using recombinant
203 a role in the protection of mice from lethal HSV infection, it does not substantively influence HSV r
204 Findings: Based on the natural history of HSV infection, its epidemiology, and the available evide
205 ting BBB permeability; and, in patients with HSV infection, magnetic resonance imaging-based temporal
206 pheral and central nervous systems following HSV infection may be important for resistance to reinfec
207 tory interactions for the control of primary HSV infection may represent a more widespread paradigm f
210 the time of labor, 10 (5%) had neonates with HSV infection (odds ratio [OR], 346; 95% confidence inte
212 ence as the heptad repeat alpha-helix blocks HSV infection of B5-expressing porcine cells and human H
214 ttern of electrophysiological changes during HSV infection of DRG neurons, which may have implication
221 the role of CD8(+) T cells in the control of HSV infection of the central nervous system and suggest
224 at Robo4 receptors are upregulated following HSV infection of the eye on the majority of the new bloo
226 that (i) either HVEM or nectin-1 can permit HSV infection of the vaginal epithelium in mice and (ii)
229 case of herpesviruses, herpes simplex virus (HSV) infection of epithelial cells results in a lytic in
231 t, we demonstrate that herpes simplex virus (HSV) infection of the cornea results in the upregulation
237 effect of a concurrent herpes simplex virus (HSV) infection on human immunodeficiency virus type 1 (H
238 -L were transiently upregulated after ocular HSV infection, on antigen-specific T cells and antigen-p
241 iver therapeutic cargos for the treatment of HSV infections or of dysfunctions of sensory ganglia.
243 ngly, the expression of GADD34 stimulated by HSV infection parallels the status of eIF-2alpha phospho
244 AS to inhibit primary isolates of HIV, block HSV infection postentry, and cross cell membranes suppor
246 e clinical spectrum of herpes simplex virus (HSV) infections, ranging from asymptomatic to frequently
249 ldehyde-3-phosphate dehydrogenase, wild-type HSV infection reduced beta-actin mRNA levels to between
250 ions of sulforaphane into mice during active HSV infection reduced neuroinflammation via a decrease i
251 The generally mild medical consequences of HSV infection reflect a functional equilibrium between h
252 opment of treatments to prevent and/or treat HSV infection rely upon understanding viral and host fac
257 strategies to prevent herpes simplex virus (HSV) infection requires knowledge of cellular pathways h
259 ens from mice taken at different times after HSV infection revealed an early infiltration of plasmacy
261 scordant donors had more frequent and severe HSV infections than those with HSV type-concordant donor
262 Together, these results support a model for HSV infection that requires activation of IP3-responsive
263 tal herpes is the high proportion of genital HSV infections that are unrecognized by both patients an
264 ur results shed light on the pathogenesis of HSV infections that lead to generalized infection and ac
267 ent protein kinase (PKR) is activated during HSV infection, the gamma(1)34.5 protein inhibits the act
268 man recombinant antibody in animal models of HSV infection, the present results support the high ther
269 During productive herpes simplex virus (HSV) infection, the viral transactivator VP16 associates
272 gI accumulates in the TGN in early phases of HSV infection then moves to lateral surfaces, to cell ju
273 1 as part of any vaccination regimen against HSV infection to coax responses of macrophages toward an
275 unction through the proteasome very early in HSV infection to inhibit a cellular antiviral response i
276 58 rabbit eyes before herpes simplex virus (HSV) infection to evaluate its intraocular antiviral dur
278 ractions with commensal bacteria may inhibit HSV infection, underscoring the importance of studying t
279 T cells during acute and secondary stages of HSV infection using intracellular gamma interferon produ
281 ) mice are significantly more susceptible to HSV infection via the corneal and intracranial routes.
282 hus, expression of nectin-1 is necessary for HSV infection via the intracranial route and for encepha
283 5 treatment before or at the time of initial HSV infection was an effective means of reducing the sev
285 ate the role of neutrophils in pathogenesis, HSV infection was compared in BALB/c and mice of the sam
286 ecessary step in the disease process, ocular HSV infection was followed in Tg-RAG mice (OVA-TCR trans
287 nancies for which the time of acquisition of HSV infection was known, 30 percent of the infections oc
290 ating viral infection, herpes simplex virus (HSV) infection was assessed in mice that had the CD28/CD
291 nd foscarnet-resistant herpes simplex virus (HSV) infection was noted after lymphocyte-depleted blood
293 lts with a first clinical episode of genital HSV infection were assayed for HSV DNA by polymerase cha
295 ts suspected of having herpes simplex virus (HSV) infections were processed using two different extra
296 eins move to cell junctions at late times of HSV infection when the production of enveloped particles
297 portion of women with a diagnosis of genital HSV infection who gave birth to infants by vaginal deliv
299 become susceptible to the lethal effects of HSV infection, with the virus spreading to the brain cau
300 clinical or virological evidence of mucosal HSV infection yet possessed consistently detectable HSV-