ライフサイエンスコーパス: HRSV

1 in combination with the NS1 gene (DeltaNS1/2 HRSV), the magnitude of the pulmonary CTL response was s

2 (92%) were positive by RT-PCR, including 66 HRSV, 2 HPIV2, 5 HPIV3, 3 influenza A virus, and 10 infl

3 Phylogenetic analysis revealed that 5-7 HRSV genotypes, including 1 or 2 predominant strains, ci

4 These 705 HRSV sequences, together with 766 HRSV sequences downloa

5 These 705 HRSV sequences, together with 766 HRSV sequences downloaded from GenBank, were analyzed to

6 The mechanism of action of ribavirin against HRSV is not well understood, although it is thought to i

7 etermine which strains predominate during an HRSV season.

8 pressed as the only viral glycoprotein in an HRSV genome, had the opposite effects: the number of inf

9 er measured by binding of CD8(+) cells to an HRSV-specific major histocompatibility complex class I t

10 e analog, although the mechanism of its anti-HRSV activity is unknown.

11 ry 2008 and February 2015 were identified as HRSV-positive and were subsequently sequenced.

12 The G(0)/G(1) phase arrest in both HRSV-infected primary cells and A549 cells was confirmed

13 This pattern of inhibition by HRSV NS1 and NS2 also extended to the newly described an

14 In contrast, HRSVs lacking the F gene or a functional replacement the

15 ely, were compared to a previously described HRSV expressing GFP in place of SH but still containing

16 t transitions and transversions occur during HRSV replication and that these changes occur in hot spo

17 stability, when expressed from an engineered HRSV genome.

18 In addition, engineered HRSVs that lacked all homologous glycoprotein genes (SH,

19 +) cells was not significantly different for HRSV lacking the NS2 gene, suggesting that the increase

20 Thus, GP64 and a GP64/HRSV F chimeric protein were functional and efficiently

21 ctivity than HRSVs containing the homologous HRSV G and F proteins.

22 spiratory syncytial virus (RSV) from humans (HRSV) and bovines (BRSV) is presented.

23 ion frequency and viral mRNA accumulation in HRSV-infected cells that were left untreated or treated

24 ed a proviral role for protein chaperones in HRSV replication and demonstrates that the function of c

25 reases the sensitivity of virus detection in HRSV pathogenesis studies.

26 f positively selected sites, particularly in HRSV B, and should be considered whenever retrospective

27 n protein abundance and/or relocalization in HRSV-infected cells; taken together, they were predicted

28 tool for the study of the role of individual HRSV transmembrane glycoproteins in virus assembly, morp

29 irst report of the recovery of an infectious HRSV lacking a fusion protein of the Paramyxoviridae fam

30 When infectious HRSV or APV was used as helper virus, replication could

31 4/F) proteins were shown to incorporate into HRSV-induced filaments at the cell surface.

32 F protein (GP(64/F)) can efficiently mediate HRSV infectivity and improve its stability, when express

33 the NS2 gene sharply reduced the ability of HRSV to induce activation of NF-kappaB.

34 s study, targeted transcriptomic analysis of HRSV-infected primary airway epithelial cells revealed a

35 re identified in both group A and group B of HRSV, although only one site was common between them, wh

36 phobic SH, attachment G, and F) in a cDNA of HRSV.

37 rveillance and molecular characterization of HRSV should be conducted to monitor the evolution of HRS

38 conducted to investigate the circulation of HRSV subgroup B (HRSVB) in China in recent years.

39 udy we addressed the more chronic effects of HRSV infection on airway function in young ferrets durin

40 uld be conducted to monitor the evolution of HRSV in China.

41 rin significantly increases the frequency of HRSV-specific RNA mutations, suggesting a direct influen

42 we investigated whether the glycoproteins of HRSV were involved in its directional targeting and rele

43 the NS1 and/or NS2 gene on the induction of HRSV-specific pulmonary cytotoxic T lymphocytes (CTL) in

44 ormation may be applied to the inhibition of HRSV.

45 Existing in vitro and in vivo models of HRSV focus almost exclusively on subgroup A viruses.

46 nderstand the recent circulation patterns of HRSV in China.

47 To characterize the circulation patterns of HRSV strains, nucleotide sequencing of the C-terminal re

48 Thus, the NS2 protein of HRSV suppresses the CTL component of the adaptive immune

49 out the processes of assembly and release of HRSV and which viral gene products are involved in the d

50 rphology, we used the prototype A2 strain of HRSV to generate a series of cDNAs from which (i) the SH

51 tern indistinguishable from the A2 strain of HRSV.

52 proposed to be involved in the synthesis of HRSV RNA by associating with the polymerase complex, the

53 Animals 1 wk old received HRSV or uninfected cell culture medium intranasally.

54 However, recombinant HRSV lacking the NS1 and NS2 genes (Delta NS1/2) induced

55 Since recombinant HRSVs from which the NS1 or NS2 genes have been deleted

56 In the absence of ribavirin, HRSV-specific transcripts accounted for up to one-third

57 censed vaccines against HPIVs and human RSV (HRSV), important respiratory pathogens of infants and ch

58 time points analyzed, the abundances of some HRSV mRNAs do not reflect the order in which the mRNAs a

59 roach for the development of safe and stable HRSV vaccine candidates.

60 icantly higher stability of infectivity than HRSVs containing the homologous HRSV G and F proteins.

61 These findings demonstrate that HRSV produces prolonged alterations of TSM function in f

62 ned, these data provide direct evidence that HRSV F is an essential viral protein required for cell-t

63 It has been shown previously that HRSV nonstructural proteins 1 and 2 (NS1 and NS2) inhibi

64 In addition, earlier work has shown that HRSV HR-C peptides, like the HIV-1 gp41 C peptides, inhi

65 The HRSV F protein, a glycoprotein essential for viral entry

66 The HRSV N/C complex was crystallized and its x-ray structur

67 t these changes occur in hot spots along the HRSV genome.

68 remarkable structural similarity between the HRSV N/C complex and the fusion protein core of other vi

69 ntic VSV G protein or a VSV G containing the HRSV F protein CT were examined.

70 es encoding SH and G can be deleted from the HRSV genome and infectious virus recovered.

71 smembrane glycoproteins, including F, in the HRSV life cycle, we generated a cell line expressing a h

72 tious viruses were recovered that lacked the HRSV SH, G, and F proteins and expressed instead the GP6

73 yxoviridae family and of manipulation of the HRSV entry pathway via incorporation of a nonparamyxovir

74 arrying the 12 C-terminal amino acids of the HRSV F protein (GP(64/F)) can efficiently mediate HRSV i

75 he N-terminal and C-terminal segments of the HRSV F protein, respectively, form a stable alpha-helica

76 ed with the 12 C-terminal amino acids of the HRSV fusion (F) protein, induced low-pH-dependent cell-c

77 ng a direct influence on the fidelity of the HRSV polymerase.

78 Together, these results show that the HRSV F protein CT plays a critical role in F protein cel

79 The results of these studies showed that the HRSV glycoproteins are not required for apical maturatio

80 We have now found that the HRSV NS2 protein strongly controls IFN induction in mous

81 to- and transmembrane domains coupled to the HRSV F cytoplasmic tail; and the F ORF was replaced with

82 In contrast, when the HRSV replication complex was supplied from cDNA plasmids

83 Two heptad-repeat regions within the HRSV F sequence were predicted by the computer program l

84 teria is of concern because - in contrast to HRSV and HMPV - S. pneumoniae can become part of the nas

85 erstanding is needed of the host response to HRSV and its attenuated vaccine derivatives.

86 At early times postinfection, wild-type HRSV and the NS1/NS2 deletion mutants were very similar

87 ace of SH but still containing the wild-type HRSV G and F proteins (RSDeltaSH).

88 moviruses human respiratory syncytial virus (HRSV) and avian pneumovirus (APV) was studied using mini

89 The human respiratory syncytial virus (HRSV) core viral RNA polymerase comprises the large poly

90 Human respiratory syncytial virus (HRSV) expresses three transmembrane glycoproteins: small

91 The human respiratory syncytial virus (HRSV) fusion (F) protein cytoplasmic tail (CT) and matri

92 cted with human respiratory syncytial virus (HRSV) has shown alteration of the cell cycle during infe

93 oteins of human respiratory syncytial virus (HRSV) have been shown to antagonize the type I interfero

94 Human respiratory syncytial virus (HRSV) is a major cause of a number of severe respiratory

95 Human respiratory syncytial virus (HRSV) is a major cause of serious lower respiratory trac

96 Human respiratory syncytial virus (HRSV) is a major cause of serious respiratory tract infe

97 Human respiratory syncytial virus (HRSV) is a major pediatric pathogen.

98 Wild-type human respiratory syncytial virus (HRSV) is a poor inducer of alpha/beta interferons (IFN-a

99 Human respiratory syncytial virus (HRSV) is released from the apical membrane of polarized

100 Human respiratory syncytial virus (HRSV) is the leading cause of serious pediatric acute re

101 Human respiratory syncytial virus (HRSV) is the most important viral cause of severe respir

102 nfectious human respiratory syncytial virus (HRSV) lacking matrix (M) protein expression (M-null viru

103 with the human respiratory syncytial virus (HRSV) leads to a significant decrease in an airway's non

104 Human respiratory syncytial virus (HRSV) nonstructural protein 1 (NS1) is a good example of

105 Human respiratory syncytial virus (HRSV) represents a major health care and economic burden

106 ts of the human respiratory syncytial virus (HRSV) SH (small hydrophobic), G (attachment), and F (fus

107 study of human respiratory syncytial virus (HRSV) was conducted to examine the distribution of its s

108 cation of human respiratory syncytial virus (HRSV) was examined by monitoring the behavior of viruses

109 nfectious Human respiratory syncytial virus (HRSV) with an aberrant RNA synthesis pattern was recover

110 nduced by human respiratory syncytial virus (HRSV), a virus with a similar genome organisation and re

111 an virus, human respiratory syncytial virus (HRSV).

112 ssays for human respiratory syncytial virus (HRSV); human parainfluenza viruses 1, 2, and 3 (HPIV1, -

113 ed that human respiratory syncytial viruses (HRSV) and human metapneumoviruses (HMPV) were involved i

114 Of these, 336 samples were HRSV subgroup A (HRSVA), 368 samples were HRSV subgroup

115 re HRSV subgroup A (HRSVA), 368 samples were HRSV subgroup B (HRSVB), and 1 sample contained both HRS

116 These findings are consistent with HRSV outbreaks' being community based in nature, althoug

117 in 8-wk-old ferrets previously infected with HRSV in the first week of life (p = 0.0001).

118 In mice infected with HRSV lacking the NS2 gene (DeltaNS2) or lacking the NS2

119 f D-type cyclins in A549 cells infected with HRSV.

120 ice in response to intranasal infection with HRSV lacking the NS1 and/or NS2 gene and subsequent chal

121 Whilst there was overlap with HRSV, there was unique commonality to the EBOV variants.

122 ed compared to that of mice infected with wt HRSV or the DeltaNS1 mutant, whether measured by binding

123 and subsequent challenge with wild-type (wt) HRSV.