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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
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
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
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
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
20 ectly, we have now followed subgroup A ASLV (ASLV-A) virions entering cells via either the transmembr
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
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
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
37 stance to infection by subgroups B, D, and E ASLV is explained by the presence of a single base pair
43 g chimeras in which two authentic enhancers (ASLV and FP) were substituted for the native NRS purine
48 odel, indicating that low pH is required for ASLV Env-dependent viral penetration into the cytosol an
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
58 ines flanking the internal fusion peptide in ASLV TM are critical for efficient function of the ASLV
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
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.
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
75 tent with the proposed two-step mechanism of ASLV entry that involves receptor-priming followed by lo
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.
82 he integration sites of HTLV-1 with those of ASLV, HIV, simian immunodeficiency virus, MLV, and foamy
84 An inference of horizontal transmission of ASLVs among some members of the Tetraoninae subfamily (g
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
91 hetically labeled with pyrene, we found that ASLV-A mixes its lipid envelope with cells within 5 to 1
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
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
103 Robson-Garnier structure predictions of the ASLV fusion peptide and immediate surrounding sequences
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
112 ction with a MLV vector pseudotyped with the ASLV-A envelope protein but were fully susceptible to in
114 ptide was sufficient not only for binding to ASLV-B but also for activating viral entry into mammalia
116 , developed to assess the binding of sTva to ASLV envelope glycoprotein, demonstrates that sTva has a
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
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
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,
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
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
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
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
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
158 bgroup C avian sarcoma and leukosis viruses [ASLV(C)], i.e., Tvc, a protein most closely related to m
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
164 determinants important for interacting with ASLV(C) glycoproteins, at least two aromatic amino acid
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