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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 icient ASLV receptors to demonstrate that an ASLV CPE can be uncoupled from the death-promoting funct
15  were fully susceptible to infection with an ASLV-A vector.
16 ffector cells expressing Env from ASLV-A and ASLV-B and target cells expressing cognate receptors.
17  pseudotyped on HIV-1 virions, the A-MLV and ASLV-A Envs also exhibit a T = 1 entry stoichiometry.
18 sed on a total of 110 gag gene sequences and ASLV-host phylogenies based on mitochondrial 12S ribosom
19                                   Thus, anti-ASLV-SU-A mc8C5-4 proves to be a unique new immunoreagen
20 ectly, we have now followed subgroup A ASLV (ASLV-A) virions entering cells via either the transmembr
21 independent virus, and with subgroups A or B ASLV Env proteins.
22 ied the association between ASLV subgroup B (ASLV-B) and liposomes and fusion between effector cells
23 ytosol, we demonstrated that virions bearing ASLV Env, but not HIV-1 Env, enter the cytosol in a low-
24 f low pH, we studied the association between ASLV subgroup B (ASLV-B) and liposomes and fusion betwee
25               We assessed congruence between ASLV phylogenies based on a total of 110 gag gene sequen
26 fically blocking infection of avian cells by ASLV(A) with a 90% inhibitory concentration of approxima
27 amily (grouse and ptarmigan) is supported by ASLV monophyletic groups reflecting geographic distribut
28 inding a soluble form of the receptor caused ASLV-B to hydrophobically associate with liposome membra
29  enhancers derived from vertebrates (chicken ASLV, mouse IgM, and human cTNT) promote splicing of two
30 in glial cells and the replication-competent ASLV long terminal repeat with a splice acceptor/tv-a gl
31         In this study, replication-competent ASLV mutant subgroup A [ASLV(A)] variants with these cys
32                                    Congruent ASLV and host phylogenies for two species of Perdix, two
33 quenced were not previously known to contain ASLVs.
34  report of a complete, replication-defective ASLV provirus sequence from any bird other than the dome
35 loyed cells that express signaling-deficient ASLV receptors to demonstrate that an ASLV CPE can be un
36  multiple rounds of infection with different ASLV vectors.
37 stance to infection by subgroups B, D, and E ASLV is explained by the presence of a single base pair
38 equired to convert hLDL-A5 into an efficient ASLV-A receptor.
39 5, were identified as critical for efficient ASLV(C) infection.
40 in repeat 22 (LDL-A22), to mediate efficient ASLV-A entry.
41 egion are critical determinants of efficient ASLV infection.
42 delay the acid-induced fusion of endocytosed ASLV.
43 g chimeras in which two authentic enhancers (ASLV and FP) were substituted for the native NRS purine
44                                          For ASLV subgroup A (ASLV-A), association with its receptor
45 odule of Tva is an important determinant for ASLV-A entry.
46                       Trp48 is important for ASLV-A infectivity.
47                         Soluble receptor for ASLV-A induces a lipophilic character in the envelope wh
48 odel, indicating that low pH is required for ASLV Env-dependent viral penetration into the cytosol an
49 ently debated whether low pH is required for ASLV infection.
50 nctional determinants of Tvc responsible for ASLV(C) receptor activity.
51 Tva) ligand-binding module is sufficient for ASLV-A infectivity.
52 equences to infer coevolutionary history for ASLVs and their hosts.
53 n between effector cells expressing Env from ASLV-A and ASLV-B and target cells expressing cognate re
54  the Avian Sarcoma and Leukosis Virus genus (ASLV-A), was studied by examining mutants derived by vir
55                                     However, ASLV fusion seems to proceed to a lipid mixing stage at
56 eraction with the viral glycoprotein EnvA in ASLV-A entry.
57 he amino terminus of the Tva LDL-A module in ASLV-A infection.
58 ines flanking the internal fusion peptide in ASLV TM are critical for efficient function of the ASLV
59 garding the structure and function of Tva in ASLV-A entry.
60 rtments, was found to only partially inhibit ASLV fusion with early endosomes.
61 re, we evaluated the requirements for intact ASLV-A particles to bind to target bilayers and fuse wit
62  human HeLa cells and show that HTLV-1, like ASLV, does not specifically target transcription units a
63  30 is preferred to rescue the C9,45S mutant ASLV(A).
64 en TVA residues to bind wild-type and mutant ASLV(A) glycoproteins with a high affinity and recover t
65 Our previous work characterized three mutant ASLV(A) isolates that could efficiently bind and infect
66 reliminary phylogenetic taxonomy for the new ASLVs, in which named taxa denote monophyletic groups.
67        Comparing the distribution of de novo ASLV integration sites to ERVs indicated that purifying
68                         In contrast, de novo ASLV integration sites within TUs showed no orientation
69 pe protein, we have evaluated the ability of ASLV-A to infect receptor-deficient cell lines in the pr
70 ide insertion stabilizes the conformation of ASLV Env into a form that can be acted upon by low pH.
71 itical for the binding affinity and entry of ASLV(A) using the mutant glycoproteins and viruses to pr
72 ble for interacting with the glycoprotein of ASLV(C).
73  complexes that simulate the interactions of ASLV virions with cells.
74 nd a small pore are the key intermediates of ASLV fusion.
75 tent with the proposed two-step mechanism of ASLV entry that involves receptor-priming followed by lo
76                              Lipid mixing of ASLV-A was inhibited by a peptide designed to prevent si
77      Previously, some interesting mutants of ASLV-A have been selected by others which can use chicke
78 hich requires low pH for fusion), but not of ASLV-A, with host cells.
79 odel in which the internal fusion peptide of ASLV-A EnvA exists as a loop that is stabilized by a dis
80 at is unique to the chain reversal region of ASLV EnvA controls the pH at which ASLV entry occurs.
81 t of the presence of the cytoplasmic tail of ASLV Env.
82 he integration sites of HTLV-1 with those of ASLV, HIV, simian immunodeficiency virus, MLV, and foamy
83                   Widespread distribution of ASLVs among diverse, endemic galliform host species sugg
84   An inference of horizontal transmission of ASLVs among some members of the Tetraoninae subfamily (g
85                               The effects on ASLV(C) glycoprotein binding and infection efficiency we
86           The effect of the hr2 mutations on ASLV envelope-mediated infection did not parallel the ef
87 y transcriptional profiling of uninfected or ASLV-infected CEF cells.
88 tified as critical determinants in the other ASLV(A-E) receptors for a proper interaction with ASLV g
89    Similar to other viral FPDs, the putative ASLV FPD has been modeled as an amphipathic helix where
90               We also provided evidence that ASLV-C fuses with cells at neutral pH.
91 hetically labeled with pyrene, we found that ASLV-A mixes its lipid envelope with cells within 5 to 1
92                                We found that ASLV-A particles bind stably to liposomes in a receptor-
93 ysis of the integration products showed that ASLV integrase can use a wide variety of substrate seque
94 pH is sufficient to activate EnvA, such that ASLV-A particles bind hydrophobically to and merge their
95                                          The ASLV TM glycoprotein has been proposed to adopt a struct
96                                          The ASLV(A) envelope glycoproteins are organized into functi
97 trate that receptor binding can activate the ASLV-A envelope protein and convert it to a fusogenic co
98 rocess were elucidated by characterizing the ASLV(A) glycoprotein interactions with the TVA receptor
99 s demonstrate that the basic residues in the ASLV envelope have roles in both receptor recognition an
100 ings suggest that the central proline in the ASLV fusion peptide is important for the formation of th
101 hese cysteines, we mutated C9 and C45 in the ASLV subtype A Env (EnvA), individually and together, to
102                              Analysis of the ASLV envelope sequences revealed a cluster of basic resi
103  Robson-Garnier structure predictions of the ASLV fusion peptide and immediate surrounding sequences
104  but not by the transmembrane isoform of the ASLV receptor.
105 M are critical for efficient function of the ASLV viral glycoproteins in mediating entry.
106  most of the initial characterization of the ASLV(A) TVA, and the chicken TVA receptor, which is 65%
107 ctivate fully the fusogenic potential of the ASLV-A envelope protein, we have evaluated the ability o
108 action of virions with a soluble form of the ASLV-A receptor at 37 degrees C, the metastable form of
109                       This suggests that the ASLV glycoproteins may share a common mechanism of recep
110 LV LTR promoter, but it does not bind to the ASLV promoter.
111 lian retroviral vectors pseudotyped with the ASLV-A envelope glycoprotein (EnvA).
112 ction with a MLV vector pseudotyped with the ASLV-A envelope protein but were fully susceptible to in
113 ical transmission and cospeciation for these ASLVs and hosts.
114 ptide was sufficient not only for binding to ASLV-B but also for activating viral entry into mammalia
115 ostly outside TUs, including ERVs related to ASLV.
116 , developed to assess the binding of sTva to ASLV envelope glycoprotein, demonstrates that sTva has a
117  locus, TVA, that controls susceptibility to ASLV-A.
118                                   The TVA800/ASLV-A system should prove useful for the molecular anal
119                                        Using ASLV-A particles biosynthetically labeled with pyrene, w
120 a virus (MLV), avian sarcoma leucosis virus (ASLV) and prototype foamy virus (PFV).
121 GACAACA-3' for avian sarcoma-leukosis virus (ASLV) and 5'-AACA(A/C)AGCA-3' for human immunodeficiency
122 integration of avian sarcoma-leukosis virus (ASLV) and human immunodeficiency virus (HIV) DNA in the
123 process of avian sarcoma and leukosis virus (ASLV) and human immunodeficiency virus type 1 (HIV-1) as
124 ian retrovirus avian sarcoma/leukosis virus (ASLV) and the filovirus ebolavirus Zaire.
125  the oncovirus avian sarcoma/leukosis virus (ASLV) contains an internal fusion peptide flanked by two
126 retrovirus avian sarcoma and leukosis virus (ASLV) enters cells via pH-independent membrane fusion.
127 ns bearing avian sarcoma and leukosis virus (ASLV) envelope glycoprotein (Env) and the cell membrane.
128 peptide of the avian sarcoma/leukosis virus (ASLV) envelope protein (Env) is internal, near the N ter
129 ess of the avian sarcoma and leukosis virus (ASLV) family of retroviruses requires first a specific i
130 , we found avian sarcoma and leukosis virus (ASLV) gag genes in 19 species of birds in the order Gall
131 , we found avian sarcoma and leukosis virus (ASLV) gag genes in 26 species of galliform birds from No
132            The avian sarcoma/leukosis virus (ASLV) is activated for fusion by a two-step mechanism.
133 bgroups of avian sarcoma and leukosis virus (ASLV) is associated with viral Env activation of the dea
134 n cells by avian sarcoma and leukosis virus (ASLV) or EnvA-pseudotyped murine leukemia virus, respect
135 retrovirus avian sarcoma and leukosis virus (ASLV) predicts that upon binding cell surface receptors,
136 ed with an avian sarcoma and leukosis virus (ASLV) receptor resistance allele, tvb(r).
137 integration of avian sarcoma-leukosis virus (ASLV) shows little preference either for genes, transcri
138 Binding of avian sarcoma and leukosis virus (ASLV) to its cognate receptor on the cell surface causes
139 on from an avian sarcoma and leukosis virus (ASLV) vector.
140 ruses, such as avian sarcoma/leukosis virus (ASLV), employ a two-step mechanism in which receptor bin
141 ed for the avian sarcoma and leukosis virus (ASLV), whereby interaction with specific cell surface re
142 ion of the avian sarcoma and leukosis virus (ASLV), with endosomes.
143 t range of the avian sarcoma/leukosis virus (ASLV)-based RCASBP vectors produced two viral vectors, R
144 ediated by the avian sarcoma-leukosis virus (ASLV-A) envelope glycoproteins can be neutralized by an
145 subgroup A avian sarcoma and leukosis virus (ASLV-A), in viral entry.
146 subgroup A avian sarcoma and leukosis virus (ASLV-A), induces conformational changes in the viral env
147 subgroup A avian sarcoma and leukosis virus (ASLV-A), the five cell lines were resistant to infection
148 subgroup A avian sarcoma and leukosis virus (ASLV-A).
149 subgroup A avian sarcoma and leukosis virus (ASLV-A).
150  subtype A avian sarcoma and leukosis virus (ASLV-A).
151       In avian sarcoma and leukemia viruses (ASLV), PR forms the C-terminal domain of Gag.
152          Avian sarcoma and leukosis viruses (ASLV) are unusual among retroviruses in that the region
153 icity in avian sarcoma and leukosis viruses (ASLV) maps to the central region of the envelope surface
154 bgroup A avian sarcoma and leukosis viruses (ASLV-A) was recently identified by a gene transfer strat
155 D, and E avian sarcoma and leukosis viruses (ASLVs) is a tumor necrosis factor receptor-related prote
156 bgroup A avian sarcoma and leucosis viruses [ASLV(A)] with the TVA receptor required to infect cells
157 bgroup A avian sarcoma and leukosis viruses [ASLV(A)] is the cellular glycoprotein Tva.
158 bgroup C avian sarcoma and leukosis viruses [ASLV(C)], i.e., Tvc, a protein most closely related to m
159 region of ASLV EnvA controls the pH at which ASLV entry occurs.
160    Nineteen of the 26 host species from whom ASLVs were sequenced were not previously known to contai
161 al determinants of the binding affinity with ASLV(A) envelope glycoproteins and to mediate efficient
162 fected chicken embryo fibroblasts (CEF) with ASLV or HIV and sequenced 863 junctions between host and
163 A determinants critical for interacting with ASLV(A) glycoproteins is proposed.
164  determinants important for interacting with ASLV(C) glycoproteins, at least two aromatic amino acid
165 A-E) receptors for a proper interaction with ASLV glycoproteins.
166                    In addition, we show with ASLV EnvA that the bulky hydrophobic residue following t

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