ライフサイエンスコーパス: herpesvirus infection

1 d whether the HIRA chaperone complex affects herpesvirus infection.

2 ence of efficient front line defense against herpesvirus infection.

3 e establishment and control of chronic gamma-herpesvirus infection.

4 ong viral persistence is a hallmark of human herpesvirus infection.

5 new insights into this fundamental stage of herpesvirus infection.

6 viridae family and is required for effective herpesvirus infection.

7 ablishment of latency, a hallmark of chronic herpesvirus infection.

8 ding of the CD4 T cell response during gamma-herpesvirus infection.

9 investigate the effect of PML or PML NBs on herpesvirus infection.

10 critical for the control of persistent gamma-herpesvirus infection.

11 atural target of Kaposi's sarcoma-associated herpesvirus infection.

12 PEL and KS are associated with KS-associated herpesvirus infection.

13 CD8 T cell memory during a persistent gamma-herpesvirus infection.

14 he role of this chemokine during respiratory herpesvirus infection.

15 tant for immune control of EBV-related gamma-herpesvirus infection.

16 e latent genes should lead to eradication of herpesvirus infection.

17 ession makes toward immunity against a gamma-herpesvirus infection.

18 n could be used to design new treatments for herpesvirus infections.

19 the contributions made by clinically silent herpesvirus infections.

20 nal design of new drugs for the treatment of herpesvirus infections.

21 derstanding and intelligently intervening in herpesvirus infections.

22 alter parameters of highly prevalent chronic herpesvirus infections.

23 f PML-NB proteins is important for efficient herpesvirus infections.

24 dditional therapeutic options to treat human herpesvirus infections.

25 te system impacts on the latent reservoir of herpesvirus infections.

26 tent phase, a characteristic feature of many herpesvirus infections.

27 ture model as a useful model to study ocular herpesvirus infections.

28 dditional therapeutic options to treat human herpesvirus infections.

29 s a virus-natural-host model to study ocular herpesvirus infections.

30 ombination with other antivirals in treating herpesvirus infections.

31 n and are potential drug targets for curbing herpesvirus infections.

32 bute to those individuals' susceptibility to herpesvirus infections.

33 portant for control of infections, including herpesvirus infections.

34 atory-confirmed central nervous system (CNS) herpesvirus infections.

35 l DNA genome is replicated, is a hallmark of herpesvirus infections.

36 ifying enzymes as a strategy for controlling herpesvirus infections.

37 sistent viral infections, particularly gamma-herpesvirus infections.

38 ity and improve immune interventions against herpesvirus infections.

39 Thus, chronic herpesvirus infection, a component of the mammalian viro

40 Typically in permissive herpesvirus infection, abundant virus production results

41 recognized to enhance reactivation of latent herpesvirus infections, act through the GRE in oriL to s

42 ey on the incidence and clinical features of herpesviruses infections after HSCT has not yet been con

43 Latent herpesvirus infections alter immune homeostasis.

44 e may offer a novel strategy for controlling herpesvirus infection and associated disease pathogenesi

45 ndamental to understanding the mechanisms of herpesvirus infection and developing drugs and vaccines

46 G, and improved protection against recurrent herpesvirus infection and disease in CXCL10(-/-) deficie

47 CD8(+) T cell responses to recurrent ocular herpesvirus infection and disease using a well-establish

48 ociated with an increase in recurrent ocular herpesvirus infection and disease.

49 th strong protective immunity against ocular herpesvirus infection and disease.

50 CD8(+) T cell responses to recurrent ocular herpesvirus infection and disease.

51 th strong protective immunity against ocular herpesvirus infection and disease.

52 ed tissues, which protects against recurrent herpesvirus infection and disease.IMPORTANCE We determin

53 sociated with an increased susceptibility to herpesvirus infection and hematologic malignancy as well

54 ivation from latency are critical aspects of herpesvirus infection and pathogenesis.

55 mplement is a key host defense against gamma-herpesvirus infection and that gamma-herpesviruses have

56 ant roles during latent and persistent gamma-herpesvirus infection and that herpesviruses encode gene

57 sions induced injury in 293 cells typical of herpesvirus infection and was associated with apoptotic

58 which aspects of XLP disease are specific to herpesvirus infection and which reflect general immunolo

59 In the past, herpesvirus infections and acute intestinal graft-versus

60 y assays for the diagnosis and monitoring of herpesvirus infections and antiviral agents with improve

61 iatric patients with recurrent and/or severe herpesvirus infections and compared them to a healthy co

62 These are unique observations among in vitro herpesvirus infections and may have important implicatio

63 nd may provide an effective therapy for some herpesvirus infections and potentially for progressive m

64 rimase inhibitors for the treatment of acute herpesvirus infections and provide new lead compounds fo

65 individuals to more significant or frequent herpesvirus infections and reactivations.

66 he association between serologic evidence of herpesviruses infection and cognitive functioning by uni

67 ressed in latent Kaposi's sarcoma-associated herpesvirus infection, and yet it is also induced during

68 ified serological evidence of past and acute herpesvirus infection as dichotomous variables.

69 patients receiving fingolimod were nonfatal herpesvirus infections, bradycardia and atrioventricular

70 mined CD8 T cell responses to two persistent herpesvirus infections, CMV and EBV, and to a recurrent

71 sociated with more major infections and more herpesvirus infections compared with chlorambucil (P =.0

72 nt fludarabine had more major infections and herpesvirus infections compared with chlorambucil-treate

73 The immunologic and cellular effects of herpesvirus infections contribute to risk for opportunis

74 However, serological evidence of acute herpesvirus infection doubled the odds of childhood AIS,

75 Disease associated with persistent gamma-herpesvirus infection (EBV, HHV-8) is a significant prob

76 Disease associated with persistent gamma-herpesvirus infection (EBV, human herpesvirus 8) is a si

77 In contrast to other permissive herpesvirus infections, expression of EBV transforming p

78 okines and cytokines produced in response to herpesvirus infection, glial cells orchestrate a cascade

79 svirus 8 (HHV-8)/Kaposi's sarcoma-associated herpesvirus infection goes through lytic and latent phas

80 y in studies with high incidence of clinical herpesvirus infections (> or = 25% per year).

81 Pharmacologic treatment for herpesvirus infections has targeted the virus-specific e

82 d samples, 85 (45%) showed evidence of acute herpesvirus infection; herpes simplex virus 1 was found

83 icular lesions characteristic of reactivated herpesvirus infections; however, the number of virions t

84 revious studies identified a role for latent herpesvirus infection in cross-protection against infect

85 of immune surveillance against chronic gamma-herpesvirus infection in immunosuppressed individuals.

86 Altogether, our results indicate that upon herpesvirus infection in mice, HS is rapidly upregulated

87 eutrophil responses that prevents pathogenic herpesvirus infection in peripheral organs.

88 ntagious, and potentially lethal respiratory herpesvirus infection in psittacine birds, while infecti

89 odel in which to study the causative role of herpesvirus infection in the development of atherosclero

90 ce understanding of the nature and impact of herpesvirus infection in the lacrimal gland; to determin

91 of IFNgamma reactivated latent murine gamma-herpesvirus infection in vivo, suggesting a "two-signal"

92 ption factor Stat6, reactivated murine gamma-herpesvirus infection in vivo.

93 We evaluated the T-cell compartment and herpesvirus infections in 6-year-old children.

94 e of CD8+ CTLs in controlling lentivirus and herpesvirus infections in humans and nonhuman primates.

95 the defective control of intercurrent gamma-herpesvirus infections in patients with AIDS not only is

96 L66H substitution) is associated with severe herpesvirus infections in rare patients.

97 Persistent herpesvirus infections including cytomegalovirus (CMV) i

98 understanding how immunity and chronic gamma-herpesvirus infection inter-relate.

99 Herpesvirus infection is a possible risk factor for athe

100 In the immune-competent population, primary herpesvirus infection is associated with higher morbidit

101 The early lytic phase of Kaposi's sarcoma herpesvirus infection is characterized by viral replicat

102 r, how NF-kappaB is activated during de novo herpesvirus infection is not fully understood.

103 However, the role of AMPK in herpesvirus infection is unclear.

104 One aspect of cellular restriction of herpesvirus infections is mediated by components of nucl

105 The realization that latent herpesvirus infection modulates immune responses in asym

106 Using the murine model of gamma-herpesvirus infection, murine gamma-herpesvirus 68 (gamm

107 her, these observations indicate that gamma2-herpesvirus infection of DCs is a mechanism of viral imm

108 013) report that Kaposi's sarcoma-associated herpesvirus infection of lymphatic endothelial cells (LE

109 eveloped to detect antibodies for a specific herpesvirus infection of marine turtles.

110 here is a causal relationship, the effect of herpesvirus infection on the development of atherosclero

111 nent during the replicative phase of a gamma-herpesvirus infection protects against subsequent challe

112 us, the immune environment created by latent herpesvirus infection provides a mechanism whereby host

113 e generation of protective memory to a gamma-herpesvirus infection remains unknown.

114 tified as potential antivirals against human herpesvirus infections resulting from human cytomegalovi

115 mo-old animals that had experienced lifelong herpesvirus infections showed impaired bacterial control

116 o known as ND10) have restrictive effects on herpesvirus infections that are countered by viral prote

117 In herpesvirus infections, the virus persists for life but

118 Chronic herpesvirus infection, therefore, significantly alters t

119 During herpesvirus infection, these antiviral proteins are inde

120 Glial cells can respond to herpesvirus infections through the production of cytokin

121 y for the first time causally links lifelong herpesvirus infection to all-cause mortality in mice and

122 Herpesvirus infection was associated with reduced naive

123 Of the adults, herpesvirus infection was present in 94% of animals that

124 herpesvirus 8 (HHV-8; Kaposi's sarcoma [KS] herpesvirus) infection was determined by IFA in 297 pers

125 mechanisms that regulate chronic and latent herpesvirus infection, we analyzed the role of interfero

126 op the tree shrew as a useful model to study herpesvirus infection, we studied the establishment of l

127 To test whether this is the case in a herpesvirus infection, we used a mutant murine gammaherp

128 Herpesviruses infections were uncommon after HSCT, excep

129 We sought to determine whether herpesvirus infections, which are potentially treatable,

130 For herpesvirus infections, which cycle between latency and

131 clusters were triggered by other neurotropic herpesviruses, infection with unrelated viruses failed t

132 f host immunity, we hypothesized that latent herpesvirus infection would arm NK cells.