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1  CD8 T cell memory during a persistent gamma-herpesvirus infection.
2 he role of this chemokine during respiratory herpesvirus infection.
3 tant for immune control of EBV-related gamma-herpesvirus infection.
4  preformed capsids is a critical step during herpesvirus infection.
5 e latent genes should lead to eradication of herpesvirus infection.
6 ession makes toward immunity against a gamma-herpesvirus infection.
7 ence of efficient front line defense against herpesvirus infection.
8 e establishment and control of chronic gamma-herpesvirus infection.
9 ong viral persistence is a hallmark of human herpesvirus infection.
10 und reduced viral titers in a mouse model of herpesvirus infection.
11 data will be important for future studies of herpesvirus infection.
12 r, it is unknown if TDP-43 has a role during herpesvirus infection.
13 ally in malignant tumor patients with common herpesvirus infection.
14 ) postpartum, and a fatal course of neonatal herpesvirus infection.
15 K functions as a missing link in immunity to herpesvirus infection.
16 d whether the HIRA chaperone complex affects herpesvirus infection.
17  of iNKT cell subsets in asymptomatic ocular herpesvirus infection.
18  new insights into this fundamental stage of herpesvirus infection.
19 viridae family and is required for effective herpesvirus infection.
20 ablishment of latency, a hallmark of chronic herpesvirus infection.
21 ding of the CD4 T cell response during gamma-herpesvirus infection.
22  investigate the effect of PML or PML NBs on herpesvirus infection.
23 nding of cellular factors that contribute to herpesvirus infection.
24 critical for the control of persistent gamma-herpesvirus infection.
25 atural target of Kaposi's sarcoma-associated herpesvirus infection.
26 PEL and KS are associated with KS-associated herpesvirus infection.
27 ity and improve immune interventions against herpesvirus infections.
28  the contributions made by clinically silent herpesvirus infections.
29  as well as with increased susceptibility to herpesvirus infections.
30 nal design of new drugs for the treatment of herpesvirus infections.
31 p us better understand the complexity behind herpesvirus infections.
32  memory responses have been described during herpesvirus infections.
33 to novel strategies for combating persistent herpesvirus infections.
34 pment of next-generation antivirals to treat herpesvirus infections.
35 2 in 2 families with severe and/or recurrent herpesvirus infections.
36  associated in humans with susceptibility to herpesvirus infections.
37 ed with symptomatic and asymptomatic corneal herpesvirus infections.
38 n could be used to design new treatments for herpesvirus infections.
39 derstanding and intelligently intervening in herpesvirus infections.
40 alter parameters of highly prevalent chronic herpesvirus infections.
41 f PML-NB proteins is important for efficient herpesvirus infections.
42 dditional therapeutic options to treat human herpesvirus infections.
43 te system impacts on the latent reservoir of herpesvirus infections.
44 tent phase, a characteristic feature of many herpesvirus infections.
45 ture model as a useful model to study ocular herpesvirus infections.
46 dditional therapeutic options to treat human herpesvirus infections.
47 s a virus-natural-host model to study ocular herpesvirus infections.
48 ombination with other antivirals in treating herpesvirus infections.
49 n and are potential drug targets for curbing herpesvirus infections.
50 bute to those individuals' susceptibility to herpesvirus infections.
51 portant for control of infections, including herpesvirus infections.
52 atory-confirmed central nervous system (CNS) herpesvirus infections.
53 l DNA genome is replicated, is a hallmark of herpesvirus infections.
54 ifying enzymes as a strategy for controlling herpesvirus infections.
55 sistent viral infections, particularly gamma-herpesvirus infections.
56                                Thus, chronic herpesvirus infection, a component of the mammalian viro
57                      Typically in permissive herpesvirus infection, abundant virus production results
58 recognized to enhance reactivation of latent herpesvirus infections, act through the GRE in oriL to s
59 ey on the incidence and clinical features of herpesviruses infections after HSCT has not yet been con
60                                       Latent herpesvirus infections alter immune homeostasis.
61            HSV-1 may be one such modifier as herpesvirus infection amplifies DUX4 expression in SMCHD
62 e may offer a novel strategy for controlling herpesvirus infection and associated disease pathogenesi
63 ndamental to understanding the mechanisms of herpesvirus infection and developing drugs and vaccines
64 G, and improved protection against recurrent herpesvirus infection and disease in CXCL10(-/-) deficie
65  CD8(+) T cell responses to recurrent ocular herpesvirus infection and disease using a well-establish
66     HSV-specific CD8(+) T cells protect from herpesvirus infection and disease.
67 ociated with an increase in recurrent ocular herpesvirus infection and disease.
68 th strong protective immunity against ocular herpesvirus infection and disease.
69  CD8(+) T cell responses to recurrent ocular herpesvirus infection and disease.
70 th strong protective immunity against ocular herpesvirus infection and disease.
71 cell subsets using the mouse model of ocular herpesvirus infection and disease.
72 ed tissues, which protects against recurrent herpesvirus infection and disease.IMPORTANCE We determin
73 sociated with an increased susceptibility to herpesvirus infection and hematologic malignancy as well
74 ivation from latency are critical aspects of herpesvirus infection and pathogenesis.
75 mplement is a key host defense against gamma-herpesvirus infection and that gamma-herpesviruses have
76 ant roles during latent and persistent gamma-herpesvirus infection and that herpesviruses encode gene
77 S impaired interferon response during murine herpesvirus infection and that the inhibition occurred d
78 sions induced injury in 293 cells typical of herpesvirus infection and was associated with apoptotic
79 which aspects of XLP disease are specific to herpesvirus infection and which reflect general immunolo
80                                 In the past, herpesvirus infections and acute intestinal graft-versus
81 y assays for the diagnosis and monitoring of herpesvirus infections and antiviral agents with improve
82 iatric patients with recurrent and/or severe herpesvirus infections and compared them to a healthy co
83 These are unique observations among in vitro herpesvirus infections and may have important implicatio
84 nd may provide an effective therapy for some herpesvirus infections and potentially for progressive m
85 rimase inhibitors for the treatment of acute herpesvirus infections and provide new lead compounds fo
86  individuals to more significant or frequent herpesvirus infections and reactivations.
87 he association between serologic evidence of herpesviruses infection and cognitive functioning by uni
88 iciency, autoinflammation, susceptibility to herpesvirus infection, and natural killer cell dysfuncti
89 ressed in latent Kaposi's sarcoma-associated herpesvirus infection, and yet it is also induced during
90 piratory tract infections, susceptibility to herpesvirus infections, and impaired antibody responses.
91  Thus, endogenous HSATII RNA synthesis after herpesvirus infections appears to have functionally impo
92                                   Widespread herpesvirus infections are associated with various disea
93 ified serological evidence of past and acute herpesvirus infection as dichotomous variables.
94 viruses and its profound upregulation during herpesvirus infection as part of a germline-specific tra
95  patients receiving fingolimod were nonfatal herpesvirus infections, bradycardia and atrioventricular
96                                              Herpesvirus infections can cause devastating cancers and
97 mined CD8 T cell responses to two persistent herpesvirus infections, CMV and EBV, and to a recurrent
98 sociated with more major infections and more herpesvirus infections compared with chlorambucil (P =.0
99 nt fludarabine had more major infections and herpesvirus infections compared with chlorambucil-treate
100      The immunologic and cellular effects of herpesvirus infections contribute to risk for opportunis
101 he findings suggest that early during ocular herpesvirus infection, cornea-resident IFN-gamma-produci
102 mily members, alternate methods of combating herpesvirus infection could include blocking viral repli
103       However, serological evidence of acute herpesvirus infection doubled the odds of childhood AIS,
104     Disease associated with persistent gamma-herpesvirus infection (EBV, HHV-8) is a significant prob
105     Disease associated with persistent gamma-herpesvirus infection (EBV, human herpesvirus 8) is a si
106                                       During herpesvirus infection, egress of nascent viral capsids f
107              In contrast to other permissive herpesvirus infections, expression of EBV transforming p
108 okines and cytokines produced in response to herpesvirus infection, glial cells orchestrate a cascade
109 svirus 8 (HHV-8)/Kaposi's sarcoma-associated herpesvirus infection goes through lytic and latent phas
110 y in studies with high incidence of clinical herpesvirus infections (> or = 25% per year).
111  respond to SARS-CoV-2, even if the original herpesvirus infection happened before the COVID-19 pande
112                  Pharmacologic treatment for herpesvirus infections has targeted the virus-specific e
113 d samples, 85 (45%) showed evidence of acute herpesvirus infection; herpes simplex virus 1 was found
114 icular lesions characteristic of reactivated herpesvirus infections; however, the number of virions t
115                          Early during ocular herpesvirus infection (i.e., day 2), the gamma interfero
116            We found that early during ocular herpesvirus infection (i.e., on day 2 postinfection), IF
117 echanics is affected at the initial stage of herpesvirus infection-immediately after viral genomes ar
118 revious studies identified a role for latent herpesvirus infection in cross-protection against infect
119 of immune surveillance against chronic gamma-herpesvirus infection in immunosuppressed individuals.
120   Altogether, our results indicate that upon herpesvirus infection in mice, HS is rapidly upregulated
121 eutrophil responses that prevents pathogenic herpesvirus infection in peripheral organs.
122 ntagious, and potentially lethal respiratory herpesvirus infection in psittacine birds, while infecti
123 odel in which to study the causative role of herpesvirus infection in the development of atherosclero
124 ce understanding of the nature and impact of herpesvirus infection in the lacrimal gland; to determin
125  of IFNgamma reactivated latent murine gamma-herpesvirus infection in vivo, suggesting a "two-signal"
126 ption factor Stat6, reactivated murine gamma-herpesvirus infection in vivo.
127      We evaluated the T-cell compartment and herpesvirus infections in 6-year-old children.
128 e of CD8+ CTLs in controlling lentivirus and herpesvirus infections in humans and nonhuman primates.
129  the defective control of intercurrent gamma-herpesvirus infections in patients with AIDS not only is
130 L66H substitution) is associated with severe herpesvirus infections in rare patients.
131 the use of encapsidation inhibitors to treat herpesvirus infections in the clinic.
132                                   Persistent herpesvirus infections including cytomegalovirus (CMV) i
133 understanding how immunity and chronic gamma-herpesvirus infection inter-relate.
134                                              Herpesvirus infection is a possible risk factor for athe
135  In the immune-competent population, primary herpesvirus infection is associated with higher morbidit
136    The early lytic phase of Kaposi's sarcoma herpesvirus infection is characterized by viral replicat
137 r, how NF-kappaB is activated during de novo herpesvirus infection is not fully understood.
138                 However, the role of AMPK in herpesvirus infection is unclear.
139        One aspect of cellular restriction of herpesvirus infections is mediated by components of nucl
140                  The realization that latent herpesvirus infection modulates immune responses in asym
141              Using the murine model of gamma-herpesvirus infection, murine gamma-herpesvirus 68 (gamm
142 her, these observations indicate that gamma2-herpesvirus infection of DCs is a mechanism of viral imm
143 013) report that Kaposi's sarcoma-associated herpesvirus infection of lymphatic endothelial cells (LE
144 eveloped to detect antibodies for a specific herpesvirus infection of marine turtles.
145 here is a causal relationship, the effect of herpesvirus infection on the development of atherosclero
146                                       During herpesvirus infection, PML-NBs induce epigenetic silenci
147 nent during the replicative phase of a gamma-herpesvirus infection protects against subsequent challe
148 us, the immune environment created by latent herpesvirus infection provides a mechanism whereby host
149  of the innate immune network during chronic herpesvirus infection remains poorly defined.
150 e generation of protective memory to a gamma-herpesvirus infection remains unknown.
151 tified as potential antivirals against human herpesvirus infections resulting from human cytomegalovi
152 mo-old animals that had experienced lifelong herpesvirus infections showed impaired bacterial control
153 lthough most individuals effectively control herpesvirus infections, some suffer from severe and/or r
154 o known as ND10) have restrictive effects on herpesvirus infections that are countered by viral prote
155                                           In herpesvirus infections, the virus persists for life but
156                                      Chronic herpesvirus infection, therefore, significantly alters t
157                                       During herpesvirus infection, these antiviral proteins are inde
158                   Glial cells can respond to herpesvirus infections through the production of cytokin
159 y for the first time causally links lifelong herpesvirus infection to all-cause mortality in mice and
160                                              Herpesvirus infection was associated with reduced naive
161                               Of the adults, herpesvirus infection was present in 94% of animals that
162  herpesvirus 8 (HHV-8; Kaposi's sarcoma [KS] herpesvirus) infection was determined by IFA in 297 pers
163  mechanisms that regulate chronic and latent herpesvirus infection, we analyzed the role of interfero
164 op the tree shrew as a useful model to study herpesvirus infection, we studied the establishment of l
165        To test whether this is the case in a herpesvirus infection, we used a mutant murine gammaherp
166                                              Herpesviruses infections were uncommon after HSCT, excep
167               We sought to determine whether herpesvirus infections, which are potentially treatable,
168                                          For herpesvirus infections, which cycle between latency and
169 clusters were triggered by other neurotropic herpesviruses, infection with unrelated viruses failed t
170 d looping in regulating transcription during herpesvirus infection, with a specific focus on the beta
171 f host immunity, we hypothesized that latent herpesvirus infection would arm NK cells.
172  is known to play a protective role in other herpesvirus infections; yet, ADCC has never been investi

 
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