ライフサイエンスコーパス: ASLV

1 ASLV weakly favored integration in active transcription

2 ASLV(A) envelope glycoproteins that contain the C9,45S a

3 ASLV-A env (EnvA) exists on the viral surface as a trime

4 el directly, we have now followed subgroup A ASLV (ASLV-A) virions entering cells via either the tran

5 The cellular receptor for subgroup A ASLV, Tva, utilizes a 40-residue, acidic, cysteine-rich

6 Avian sarcoma and leukosis virus subgroup A (ASLV-A) entry is mediated by interactions between the vi

7 avian sarcoma and leukosis virus subgroup A (ASLV-A) TM subunit of the envelope protein were characte

8 For ASLV subgroup A (ASLV-A), association with its receptor (Tva) at neutral

9 ) of avian sarcoma/leukosis virus subtype A (ASLV-A) binds to liposomes at neutral pH following incub

10 the avian sarcoma/leukosis virus subtype A (ASLV-A) Env (EnvA) are important for infectivity and cel

11 for avian sarcoma/leukosis virus subtype A (ASLV-A), Tva, is the simplest member of the low density

12 A-MLV), avian sarcoma/leukosis virus type A (ASLV-A), and influenza A virus.

13 eplication-competent ASLV mutant subgroup A [ASLV(A)] variants with these cysteine residues mutated w

14 ntial to act as a restriction factor against ASLV.

15 icient ASLV receptors to demonstrate that an ASLV CPE can be uncoupled from the death-promoting funct

16 were fully susceptible to infection with an ASLV-A vector.

17 ffector cells expressing Env from ASLV-A and ASLV-B and target cells expressing cognate receptors.

18 pseudotyped on HIV-1 virions, the A-MLV and ASLV-A Envs also exhibit a T = 1 entry stoichiometry.

19 sed on a total of 110 gag gene sequences and ASLV-host phylogenies based on mitochondrial 12S ribosom

20 Thus, anti-ASLV-SU-A mc8C5-4 proves to be a unique new immunoreagen

21 ectly, we have now followed subgroup A ASLV (ASLV-A) virions entering cells via either the transmembr

22 independent virus, and with subgroups A or B ASLV Env proteins.

23 ied the association between ASLV subgroup B (ASLV-B) and liposomes and fusion between effector cells

24 ytosol, we demonstrated that virions bearing ASLV Env, but not HIV-1 Env, enter the cytosol in a low-

25 f low pH, we studied the association between ASLV subgroup B (ASLV-B) and liposomes and fusion betwee

26 We assessed congruence between ASLV phylogenies based on a total of 110 gag gene sequen

27 fically blocking infection of avian cells by ASLV(A) with a 90% inhibitory concentration of approxima

28 amily (grouse and ptarmigan) is supported by ASLV monophyletic groups reflecting geographic distribut

29 inding a soluble form of the receptor caused ASLV-B to hydrophobically associate with liposome membra

30 enhancers derived from vertebrates (chicken ASLV, mouse IgM, and human cTNT) promote splicing of two

31 in glial cells and the replication-competent ASLV long terminal repeat with a splice acceptor/tv-a gl

32 In this study, replication-competent ASLV mutant subgroup A [ASLV(A)] variants with these cys

33 Congruent ASLV and host phylogenies for two species of Perdix, two

34 quenced were not previously known to contain ASLVs.

35 report of a complete, replication-defective ASLV provirus sequence from any bird other than the dome

36 loyed cells that express signaling-deficient ASLV receptors to demonstrate that an ASLV CPE can be un

37 multiple rounds of infection with different ASLV vectors.

38 stance to infection by subgroups B, D, and E ASLV is explained by the presence of a single base pair

39 equired to convert hLDL-A5 into an efficient ASLV-A receptor.

40 5, were identified as critical for efficient ASLV(C) infection.

41 in repeat 22 (LDL-A22), to mediate efficient ASLV-A entry.

42 egion are critical determinants of efficient ASLV infection.

43 delay the acid-induced fusion of endocytosed ASLV.

44 g chimeras in which two authentic enhancers (ASLV and FP) were substituted for the native NRS purine

45 For ASLV subgroup A (ASLV-A), association with its receptor

46 odule of Tva is an important determinant for ASLV-A entry.

47 Trp48 is important for ASLV-A infectivity.

48 Soluble receptor for ASLV-A induces a lipophilic character in the envelope wh

49 odel, indicating that low pH is required for ASLV Env-dependent viral penetration into the cytosol an

50 ently debated whether low pH is required for ASLV infection.

51 nctional determinants of Tvc responsible for ASLV(C) receptor activity.

52 Tva) ligand-binding module is sufficient for ASLV-A infectivity.

53 equences to infer coevolutionary history for ASLVs and their hosts.

54 n between effector cells expressing Env from ASLV-A and ASLV-B and target cells expressing cognate re

55 the Avian Sarcoma and Leukosis Virus genus (ASLV-A), was studied by examining mutants derived by vir

56 However, ASLV fusion seems to proceed to a lipid mixing stage at

57 eraction with the viral glycoprotein EnvA in ASLV-A entry.

58 he amino terminus of the Tva LDL-A module in ASLV-A infection.

59 ines flanking the internal fusion peptide in ASLV TM are critical for efficient function of the ASLV

60 garding the structure and function of Tva in ASLV-A entry.

61 rtments, was found to only partially inhibit ASLV fusion with early endosomes.

62 re, we evaluated the requirements for intact ASLV-A particles to bind to target bilayers and fuse wit

63 human HeLa cells and show that HTLV-1, like ASLV, does not specifically target transcription units a

64 30 is preferred to rescue the C9,45S mutant ASLV(A).

65 en TVA residues to bind wild-type and mutant ASLV(A) glycoproteins with a high affinity and recover t

66 Our previous work characterized three mutant ASLV(A) isolates that could efficiently bind and infect

67 reliminary phylogenetic taxonomy for the new ASLVs, in which named taxa denote monophyletic groups.

68 Comparing the distribution of de novo ASLV integration sites to ERVs indicated that purifying

69 In contrast, de novo ASLV integration sites within TUs showed no orientation

70 pe protein, we have evaluated the ability of ASLV-A to infect receptor-deficient cell lines in the pr

71 eterminant of an interferon-induced block of ASLV release.

72 ide insertion stabilizes the conformation of ASLV Env into a form that can be acted upon by low pH.

73 itical for the binding affinity and entry of ASLV(A) using the mutant glycoproteins and viruses to pr

74 ble for interacting with the glycoprotein of ASLV(C).

75 complexes that simulate the interactions of ASLV virions with cells.

76 nd a small pore are the key intermediates of ASLV fusion.

77 tent with the proposed two-step mechanism of ASLV entry that involves receptor-priming followed by lo

78 Lipid mixing of ASLV-A was inhibited by a peptide designed to prevent si

79 Previously, some interesting mutants of ASLV-A have been selected by others which can use chicke

80 hich requires low pH for fusion), but not of ASLV-A, with host cells.

81 odel in which the internal fusion peptide of ASLV-A EnvA exists as a loop that is stabilized by a dis

82 at is unique to the chain reversal region of ASLV EnvA controls the pH at which ASLV entry occurs.

83 ssion of chicken BST-2 blocks the release of ASLV in chicken cells and of human immunodeficiency viru

84 t of the presence of the cytoplasmic tail of ASLV Env.

85 he integration sites of HTLV-1 with those of ASLV, HIV, simian immunodeficiency virus, MLV, and foamy

86 Widespread distribution of ASLVs among diverse, endemic galliform host species sugg

87 An inference of horizontal transmission of ASLVs among some members of the Tetraoninae subfamily (g

88 The effects on ASLV(C) glycoprotein binding and infection efficiency we

89 The effect of the hr2 mutations on ASLV envelope-mediated infection did not parallel the ef

90 y transcriptional profiling of uninfected or ASLV-infected CEF cells.

91 tified as critical determinants in the other ASLV(A-E) receptors for a proper interaction with ASLV g

92 Similar to other viral FPDs, the putative ASLV FPD has been modeled as an amphipathic helix where

93 We also provided evidence that ASLV-C fuses with cells at neutral pH.

94 hetically labeled with pyrene, we found that ASLV-A mixes its lipid envelope with cells within 5 to 1

95 We found that ASLV-A particles bind stably to liposomes in a receptor-

96 ysis of the integration products showed that ASLV integrase can use a wide variety of substrate seque

97 pH is sufficient to activate EnvA, such that ASLV-A particles bind hydrophobically to and merge their

98 The ASLV TM glycoprotein has been proposed to adopt a struct

99 The ASLV(A) envelope glycoproteins are organized into functi

100 trate that receptor binding can activate the ASLV-A envelope protein and convert it to a fusogenic co

101 rocess were elucidated by characterizing the ASLV(A) glycoprotein interactions with the TVA receptor

102 s demonstrate that the basic residues in the ASLV envelope have roles in both receptor recognition an

103 ings suggest that the central proline in the ASLV fusion peptide is important for the formation of th

104 hese cysteines, we mutated C9 and C45 in the ASLV subtype A Env (EnvA), individually and together, to

105 Analysis of the ASLV envelope sequences revealed a cluster of basic resi

106 Robson-Garnier structure predictions of the ASLV fusion peptide and immediate surrounding sequences

107 but not by the transmembrane isoform of the ASLV receptor.

108 M are critical for efficient function of the ASLV viral glycoproteins in mediating entry.

109 most of the initial characterization of the ASLV(A) TVA, and the chicken TVA receptor, which is 65%

110 ctivate fully the fusogenic potential of the ASLV-A envelope protein, we have evaluated the ability o

111 action of virions with a soluble form of the ASLV-A receptor at 37 degrees C, the metastable form of

112 This suggests that the ASLV glycoproteins may share a common mechanism of recep

113 LV LTR promoter, but it does not bind to the ASLV promoter.

114 lian retroviral vectors pseudotyped with the ASLV-A envelope glycoprotein (EnvA).

115 ction with a MLV vector pseudotyped with the ASLV-A envelope protein but were fully susceptible to in

116 ical transmission and cospeciation for these ASLVs and hosts.

117 ptide was sufficient not only for binding to ASLV-B but also for activating viral entry into mammalia

118 ostly outside TUs, including ERVs related to ASLV.

119 , developed to assess the binding of sTva to ASLV envelope glycoprotein, demonstrates that sTva has a

120 locus, TVA, that controls susceptibility to ASLV-A.

121 The TVA800/ASLV-A system should prove useful for the molecular anal

122 Using ASLV-A particles biosynthetically labeled with pyrene, w

123 a virus (MLV), avian sarcoma leucosis virus (ASLV) and prototype foamy virus (PFV).

124 GACAACA-3' for avian sarcoma-leukosis virus (ASLV) and 5'-AACA(A/C)AGCA-3' for human immunodeficiency

125 integration of avian sarcoma-leukosis virus (ASLV) and human immunodeficiency virus (HIV) DNA in the

126 process of avian sarcoma and leukosis virus (ASLV) and human immunodeficiency virus type 1 (HIV-1) as

127 ian retrovirus avian sarcoma/leukosis virus (ASLV) and the filovirus ebolavirus Zaire.

128 the oncovirus avian sarcoma/leukosis virus (ASLV) contains an internal fusion peptide flanked by two

129 retrovirus avian sarcoma and leukosis virus (ASLV) enters cells via pH-independent membrane fusion.

130 ns bearing avian sarcoma and leukosis virus (ASLV) envelope glycoprotein (Env) and the cell membrane.

131 peptide of the avian sarcoma/leukosis virus (ASLV) envelope protein (Env) is internal, near the N ter

132 ess of the avian sarcoma and leukosis virus (ASLV) family of retroviruses requires first a specific i

133 , we found avian sarcoma and leukosis virus (ASLV) gag genes in 19 species of birds in the order Gall

134 , we found avian sarcoma and leukosis virus (ASLV) gag genes in 26 species of galliform birds from No

135 The avian sarcoma/leukosis virus (ASLV) is activated for fusion by a two-step mechanism.

136 bgroups of avian sarcoma and leukosis virus (ASLV) is associated with viral Env activation of the dea

137 n cells by avian sarcoma and leukosis virus (ASLV) or EnvA-pseudotyped murine leukemia virus, respect

138 retrovirus avian sarcoma and leukosis virus (ASLV) predicts that upon binding cell surface receptors,

139 ed with an avian sarcoma and leukosis virus (ASLV) receptor resistance allele, tvb(r).

140 integration of avian sarcoma-leukosis virus (ASLV) shows little preference either for genes, transcri

141 Binding of avian sarcoma and leukosis virus (ASLV) to its cognate receptor on the cell surface causes

142 on from an avian sarcoma and leukosis virus (ASLV) vector.

143 ruses, such as avian sarcoma/leukosis virus (ASLV), employ a two-step mechanism in which receptor bin

144 ed for the avian sarcoma and leukosis virus (ASLV), whereby interaction with specific cell surface re

145 ion of the avian sarcoma and leukosis virus (ASLV), with endosomes.

146 t range of the avian sarcoma/leukosis virus (ASLV)-based RCASBP vectors produced two viral vectors, R

147 ty against avian sarcoma and leukosis virus (ASLV).

148 etrovirus, avian sarcoma and leukosis virus (ASLV).

149 ediated by the avian sarcoma-leukosis virus (ASLV-A) envelope glycoproteins can be neutralized by an

150 subgroup A avian sarcoma and leukosis virus (ASLV-A), in viral entry.

151 subgroup A avian sarcoma and leukosis virus (ASLV-A), induces conformational changes in the viral env

152 subgroup A avian sarcoma and leukosis virus (ASLV-A), the five cell lines were resistant to infection

153 subgroup A avian sarcoma and leukosis virus (ASLV-A).

154 subtype A avian sarcoma and leukosis virus (ASLV-A).

155 In avian sarcoma and leukemia viruses (ASLV), PR forms the C-terminal domain of Gag.

156 Avian sarcoma and leukosis viruses (ASLV) are unusual among retroviruses in that the region

157 icity in avian sarcoma and leukosis viruses (ASLV) maps to the central region of the envelope surface

158 bgroup A avian sarcoma and leukosis viruses (ASLV-A) was recently identified by a gene transfer strat

159 D, and E avian sarcoma and leukosis viruses (ASLVs) is a tumor necrosis factor receptor-related prote

160 bgroup A avian sarcoma and leucosis viruses [ASLV(A)] with the TVA receptor required to infect cells

161 bgroup A avian sarcoma and leukosis viruses [ASLV(A)] is the cellular glycoprotein Tva.

162 bgroup C avian sarcoma and leukosis viruses [ASLV(C)], i.e., Tvc, a protein most closely related to m

163 region of ASLV EnvA controls the pH at which ASLV entry occurs.

164 Nineteen of the 26 host species from whom ASLVs were sequenced were not previously known to contai

165 al determinants of the binding affinity with ASLV(A) envelope glycoproteins and to mediate efficient

166 fected chicken embryo fibroblasts (CEF) with ASLV or HIV and sequenced 863 junctions between host and

167 A determinants critical for interacting with ASLV(A) glycoproteins is proposed.

168 determinants important for interacting with ASLV(C) glycoproteins, at least two aromatic amino acid

169 A-E) receptors for a proper interaction with ASLV glycoproteins.

170 In addition, we show with ASLV EnvA that the bulky hydrophobic residue following t