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1 e from dealing effectively with a pathogenic gamma-herpesvirus.
2 aintain long-term control of this persistent gamma-herpesvirus.
3 oma-associated herpesvirus (KSHV) is a human gamma-herpesvirus.
4 d NK cell-mediated immune control of a human gamma-herpesvirus.
5 re conserved in the EBNA1 orthologs of other gamma herpesviruses.
6 sequences were distributed more uniformly in gamma-herpesviruses.
7 esviruses but not in members of the beta- or gamma-herpesviruses.
8 activated differently in alpha- compared to gamma-herpesviruses.
9 DNA features differed in alpha- compared to gamma-herpesviruses.
10 the beta-subfamily and absent in alpha- and gamma-herpesviruses.
11 monstrate a novel mechanism where the murine gamma herpesvirus 68 (gammaHV68) latency-associated, ant
12 oma-associated herpesvirus (KSHV) and murine gamma herpesvirus 68 (MHV-68), plays a critical role in
14 llowing intragastric inoculation with murine gamma-herpesvirus 68 (gamma HV-68), expression of substa
15 after respiratory challenge with the murine gamma-herpesvirus 68 (gammaHV-68), then develop symptoms
16 model of gamma-herpesvirus infection, murine gamma-herpesvirus 68 (gammaHV-68), we were surprised to
17 Infection of medial smooth muscle cells with gamma-herpesvirus 68 (gammaHV68) causes severe chronic v
19 s are generated and maintained during murine gamma-herpesvirus 68 (gammaHV68) persistent infection de
20 e we demonstrate that infection of mice with gamma-herpesvirus 68 (gammaHV68) provides a novel model
21 of complement factor C3 (C3) and the murine gamma-herpesvirus 68 (gammaHV68) RCA protein in viral pa
22 ins of mice with a murine gamma-herpesvirus, gamma-herpesvirus 68 (gammaHV68), is providing insights
23 ths after respiratory exposure to the murine gamma-herpesvirus 68 (gammaHV68), then succumb with symp
24 ct effector mechanisms of CD4 T cells during gamma-herpesvirus 68 (gammaHV68)-persistent infection ar
28 d the differentiation and function of murine gamma-herpesvirus 68 (MHV-68)-specific CD4(+) T cells us
30 we report that the miRNAs encoded by murine gamma-herpesvirus 68 (MHV68) are also generated via atyp
31 T-I CTL function and the clearance of murine gamma-herpesvirus 68 and lymphocytic choriomeningitis cl
34 istinct from host protein synthesis shutoff, gamma-herpesvirus 68 down-regulates surface MHC class I
38 for the generation and maintenance of murine gamma-herpesvirus 68-specific CD8(+) set now have been a
47 a murine MHC class II-restricted epitope in gamma-herpesvirus-68 gp150 (gp150(67-83)I-A(b)) that eli
53 mune evasion strategy shared by at least two gamma-herpesviruses allows continued lytic infection in
55 of infection and protective immunity for the gamma-herpesviruses and demonstrate the utility of repli
56 cal and structural similarities to the human gamma-herpesviruses, and provides an important in vivo e
61 r pathology induced by gammaHV68 and suggest gamma-herpesviruses as candidate etiologic agents for hu
62 oma-associated herpesvirus (KSHV) is a human gamma-herpesvirus associated with several human malignan
64 P receptors in mice results in an increased gamma-herpesvirus burden and an altered host response.
67 ng latent infection with gammaHV68, a murine gamma-herpesvirus closely related to human gamma-herpesv
70 The gL proteins of alpha herpesviruses and gamma herpesviruses do not have a significant percentage
83 ble tegument components included the EBV and gamma-herpesvirus-encoded BLRF2, BRRF2, BDLF2 and BKRF4
86 us nuclear antigen 1 (EBNA-1) of the related gamma-herpesvirus Epstein-Barr virus, specific DNA recog
87 are homology with two lymphotropic oncogenic gamma-herpesviruses, Epstein-Barr virus and Herpesvirus
88 d herpesvirus, we have used a natural rodent gamma-herpesvirus experimental infection model, gamma-he
89 Together, these observations suggested that gamma-herpesviruses exploit the B cell life cycle in the
93 tion of inbred strains of mice with a murine gamma-herpesvirus, gamma-herpesvirus 68 (gammaHV68), is
96 effective, long-term control of a persistent gamma-herpesvirus (gammaHV68) in Ig(-/-) microMT mice, s
101 ck of relevant small animal models for human gamma-herpesviruses has impeded progress in understandin
103 against gamma-herpesvirus infection and that gamma-herpesviruses have evolved an immune evasion strat
107 ided valuable new information on the role of gamma-herpesviruses in the pathogenesis of AIDS-associat
109 gammaHV68 shares latency programs with human gamma-herpesviruses - including the loci for gene 73, v-
110 ection with either influenza virus or murine gamma-herpesvirus induced the expected expression of GrB
112 ically alcelaphine herpesvirus 1 (AlHV-1), a gamma-herpesvirus inducing malignant catarrhal fever (MC
115 hat complement is a key host defense against gamma-herpesvirus infection and that gamma-herpesviruses
116 important roles during latent and persistent gamma-herpesvirus infection and that herpesviruses encod
117 ation of immune surveillance against chronic gamma-herpesvirus infection in immunosuppressed individu
118 ockade of IFNgamma reactivated latent murine gamma-herpesvirus infection in vivo, suggesting a "two-s
121 prominent during the replicative phase of a gamma-herpesvirus infection protects against subsequent
130 y that the defective control of intercurrent gamma-herpesvirus infections in patients with AIDS not o
132 butor to alterations in gene expression, and gamma-herpesviruses interface with the host RNA targetin
133 ated members of the rhadinovirus subgroup of gamma herpesviruses, K1 and STP exhibit no similarity in
137 ssecting mechanisms of CD4 immune control of gamma-herpesvirus latency and the development of therape
139 ice represents a unique system for analyzing gamma-herpesvirus latency in splenic B cells at differen
140 c viral replication is not a requirement for gamma-herpesvirus latency in vivo and suggest that viral
141 ntribution of humoral immunity to control of gamma-herpesvirus latency, and have significant implicat
143 ls are critical effectors for the control of gamma-herpesvirus latent infection, and they mediate thi
145 n excellent animal model system to study the gamma herpesvirus life cycle both in vitro and in vivo.
147 Recently, the DNA sequences of a novel human gamma-herpesvirus-like (HHV-8) agent have been detected
148 MP1 signaling.IMPORTANCE EBV is a ubiquitous gamma herpesvirus linked to malignancies such as nasopha
150 Intranasal infection of mice with the murine gamma-herpesvirus MHV-68 results in an acute lytic infec
151 us recrudescence can be modeled using murine gamma-herpesvirus (MHV)-68 in mice lacking CD4(+) T cell
158 CD8 T cell memory that is maintained during gamma-herpesvirus persistence has the capacity to surviv
161 response, Tarakanova et al. characterized a gamma-herpesvirus protein, which phosphorylates histone
162 Immune surveillance failure followed by gamma-herpesvirus recrudescence can be modeled using mur
163 Immune surveillance failure followed by gamma-herpesvirus recrudescence can be modeled using mur
164 ine lymphotropic herpesvirus-1 (PLHV-1) is a gamma-herpesvirus related to Epstein-Barr virus (EBV) an
165 svirus (KSHV) is a recently discovered human gamma herpesvirus strongly implicated in AIDS-related ne
166 e gamma-herpesvirus closely related to human gamma-herpesviruses such as EBV and Kaposi's sarcoma-ass
167 uired for malignant transformation caused by gamma-herpesviruses, such as Kaposi's sarcoma virus.
168 are encoded by Herpesvirus saimiri (HVS), a gamma Herpesvirus that causes aggressive T cell leukemia
169 Murine herpesvirus-68 (MHV-68) is a type 2 gamma herpesvirus that productively infects alveolar epi
173 Epstein-Barr virus (EBV) is a lymphotropic gamma-herpesvirus that has co-evolved with human species
175 (KSHV), or human herpervirus 8 (HHV-8), is a gamma-herpesvirus that infects human lymphocytes and is
177 Herpesvirus saimiri (HVS) is an oncogenic gamma-herpesvirus that produces microRNAs (miRNAs) by co
178 saimiri (HVS) is an oncogenic, lymphotropic, gamma-herpesvirus that transforms human and simian T cel
179 svirus (also named human herpesvirus 8) is a gamma-herpesvirus that undergoes both lytic and latent i
182 NA decay rates impact transcription and that gamma-herpesviruses use this feedback mechanism to facil
185 repeats predominated in alpha-herpesviruses, gamma-herpesviruses were enriched in short, GC-rich init
187 uman and primate lymphotropic herpesviruses (gamma-herpesviruses) with the development of lymphomas,
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