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1                                              GALV-like viruses have also been discovered in several S
2                                              GALV-S and SSAV have the same host range with the except
3 at threonine at 550 inactivates ChoPit1 as a GALV receptor.
4 is sufficient to render PiT2 functional as a GALV receptor.
5 to the woolly monkey virus (WMV), which is a GALV strain that likely originated in a gibbon host.
6                       The second record of a GALV in M. burtoni provides further evidence that M. bur
7                           The discovery of a GALV in the most western part of the Australo-Papuan dis
8 f Wallace's Line, the woolly monkey virus (a GALV) and the closely related koala retrovirus (KoRV) ha
9          We hypothesized that vectors with a GALV pseudotype might perform better based on our previo
10 ion were constructed and tested, showing (a) GALV and/or Fcy::Fur expression did not affect virus gro
11 ition in region A can vary without affecting GALV entry.
12 imilar pattern of cell tropism as KoRV-A and GALV.
13  with vectors targeting both amphotropic and GALV receptors may prove to be of additional benefit in
14 xplain previous observations that FeLV-B and GALV, which primarily uses Pit1, display nonreciprocal i
15  cells with equivalent numbers of FeLV-C and GALV or RD114 and GALV-pseudotyped retroviruses for inje
16 le adaptive differences between the KoRV and GALV envelope genes account for differences in their rec
17 Southeast Asian rodent species for KoRV- and GALV-like sequences, using hybridization capture and hig
18 date hosts from Southeast Asia for KoRV- and GALV-like sequences.
19                                      MLV and GALV RBDs are not able to render FeLV-T infectious.
20 ignificant differences between the RD114 and GALV-pseudotype vectors.
21 lent numbers of FeLV-C and GALV or RD114 and GALV-pseudotyped retroviruses for injection into fetal s
22 lts suggest that fusion-defective FeLV-T and GALV are restricted to homologous RBD rescue of infectiv
23 rus envelope proteins (from Friend virus and GALV or xenotropic viruses) assemble into heteromers whe
24 teins, suggesting that the block to XMRV and GALV infection is mediated at the level of envelope-rece
25 n immunoblot analysis demonstrated that anti-GALV antisera reacted with three proteins in PK-15 cells
26 xtracellular regions of HaPiT2 functioned as GALV receptors.
27  expression did not affect virus growth; (b) GALV expression causes cell fusion and increases the tum
28 o studies involving vectors chimeric between GALV and KoRV-B established that variable regions A and
29 ver, CHOK1 conditioned medium does not block GALV entry into E36, indicating the secreted inhibitors
30 rs, E36 cells are highly susceptible to both GALV and A-MLV in the absence of tunicamycin.
31 ells conferred strong susceptibility to both GALV and A-MLV, and similar overexpression of CHO Pit1 c
32                      MMMol cells infected by GALV are resistant to subsequent infection not only by G
33  abolish Pit1-mediated cellular infection by GALV and FeLV-B.
34  these cells are susceptible to infection by GALV.
35 esistant to subsequent infection not only by GALV but also by amphotropic murine leukemia virus.
36 n be trans-activated for infectivity only by GALV RBDs.
37             Surprisingly, transactivation by GALV RBD enabled wild-type or H10A mutant PERVs of all t
38 hips with the other previously characterized GALVs.
39 itive repopulation assay to directly compare GALV-pseudotype retrovirus vectors produced by either Ph
40  have constructed several vectors containing GALV-S/SSAV chimeric envelope proteins to map the region
41                             Unlike with E36, GALV and A-MuLV exhibited reciprocal interference when i
42 enerated complete genomic sequences for each GALV strain using hybridization capture and high-through
43 , or +1), and yet Pit1 remained an efficient GALV receptor.
44 viously published ones from highly efficient GALV receptors revealed that every position in region A
45 sera specific for the Gag proteins of either GALV or simian sarcoma-associated virus reacted with the
46 sceptibility of several cell lines to either GALV-S or SSAV infection.
47  extracellular domain of Pit1 is crucial for GALV entry and that an acidic residue at position 550 is
48 , shown by several studies to be crucial for GALV infection.
49 ssed the significance of this difference for GALV infection by replacing the aspartate 550 in Pit1 wi
50 sequence of the critical receptor domain for GALV infection in the Indonesian M. burtoni subsp. was c
51         Whether native ChoPit1 functions for GALV was determined by interference assays using Lec8, a
52 ide domain IV are specifically important for GALV infection.
53 substitution rendered Pit1 nonfunctional for GALV and suggests that threonine at 550 inactivates ChoP
54               Even Pit2 is nonfunctional for GALV only because it has lysine at the first position in
55 s from Wallacea (Indonesia) was positive for GALV.
56 t time that Pit1 is the binding receptor for GALV and not a coreceptor or another type of GALV entry
57 region of Pit2, a nonfunctional receptor for GALV.
58 s, and CHO Pit1 is a functional receptor for GALV.
59 nd ChoPit1 therefore differ as receptors for GALV; ChoPit1 is either inactivated by secreted factors
60 he region of the HaPiT2 protein required for GALV receptor function.
61 his sequence is a definitive requirement for GALV infection has also remained unclear; certain recept
62 ing regions of KoRV that distinguish it from GALV were introduced into the GALV genome, and their fun
63 ent of this transactivation was a functional GALV receptor on the cells.
64                      Using dually functional GALV/A-MLV receptors, we examined the role of receptor w
65 d in MDTF, a cell line that lacks functional GALV receptors and is resistant to GALV.
66 apua New Guinea and no bat species harboring GALV-like retroviruses.
67 en determined for all of the five identified GALV strains, nor has a comprehensive evolutionary analy
68 the genome sequence of this newly identified GALV, the critical domain for infection of its potential
69                              Fusion-impaired GALV envelope mutants can be trans-activated for infecti
70                  Disruption of this motif in GALV results in vectors with reduced syncytia forming ca
71        Mitochondrial dysfunction occurred in GALV-FMG-induced syncytia prior to loss of viability wit
72                 Four of the GALVs, including GALV strain SEATO (GALV-S), were originally isolated fro
73  KoRV's attenuation from a highly infectious GALV-like progenitor virus has allowed the identificatio
74 ugh unable to infect E36 cells, SSAV infects GALV-resistant murine cells expressing the E36-derived v
75 th an insertion C-terminal to the PHQ motif (GALV I(10)) bind Pit1 but fail to infect cells.
76              BHK cells bind neither XMRV nor GALV envelope proteins.
77 yped vector correlated with higher levels of GALV receptor RNA compared with the amphotropic receptor
78 he SSAV SU protein and C-terminal portion of GALV-S fail to infect E36 cells.
79 ubstituted for the corresponding residues of GALV, resulted in vectors exhibiting substantially reduc
80 ly Murinae, may play a role in the spread of GALV-like viruses.
81 provirus very closely related to a strain of GALV.
82                          The four strains of GALV isolated from gibbons formed a monophyletic clade t
83 er ERVs, is substantially lower than that of GALV.
84 GALV and not a coreceptor or another type of GALV entry factor.
85  Asia and broadens the known distribution of GALVs in wild rodents.
86            Despite the biomedical utility of GALVs as viral vectors and in cancer gene therapy, full
87 llular domain of MolPit1 and MolPit2 have on GALV receptor function, chimeric receptors were made by
88 g equivalent titers of either amphotropic or GALV pseudotyped vectors containing the neo gene.
89 mposition (e.g., they contain either SSAV or GALV-S envelope protein) to show that the envelope of SS
90 ssing the appropriate receptors bind XMRV or GALV envelope proteins.
91  respectively, can mediate efficient XMRV or GALV infection.
92 ced by fusing BHKXpr1 or BHKPiT1 to XMRV- or GALV-resistant cells, respectively, can mediate efficien
93 raction was cocultivated on irradiated PG13 (GALV-pseudotype) packaging cells for 48 hours.
94 and we evaluated vectors produced by Phoenix-GALV for their ability to transduce hematopoietic progen
95 e engraftment of cells transduced by Phoenix-GALV-pseudotype vectors.
96  In 3 additional baboons we compared Phoenix-GALV-derived vectors to more recently developed lentivir
97 etrovirus vectors produced by either Phoenix-GALV or by the NIH 3T3-derived packaging cell line, PG13
98 ibbon ape leukemia virus pseudotype (Phoenix-GALV), and we evaluated vectors produced by Phoenix-GALV
99 aboon CD34(+) cells, suggesting that Phoenix-GALV-derived oncoretroviral vectors may be even more eff
100 s was significantly higher using the Phoenix-GALV-derived vector as compared with the PG13-derived ve
101 encing, in the attempt to identify potential GALV and KoRV hosts.
102  is exogenous, suggesting that KoRV predates GALV and that gibbons and koalas acquired the virus at d
103 kemia virus hyperfusogenic envelope protein (GALV-FMG) resulted in the formation of multinucleated sy
104 mes identified two highly conserved regions, GALV (residues 309-312) and ESRP (residues 329-332).
105     Incubation with soluble GALV RBD renders GALV I(10) particles infectious, whereas incubation with
106 r of the GALVs, including GALV strain SEATO (GALV-S), were originally isolated from gibbon apes, wher
107 gesting that host immune pressure is shaping GALV evolution.
108                      Incubation with soluble GALV RBD renders GALV I(10) particles infectious, wherea
109                                       Tagged GALV envelope proteins bind specifically to cells expres
110  present at significantly higher levels than GALV-pseudotyped vectors.
111                 We have also determined that GALV particles bearing SU proteins with an insertion C-t
112                      These results show that GALV-pseudotyped vectors are capable of transducing babo
113                We have previously shown that GALV can infect E36 cells by using both its own receptor
114                           This suggests that GALV can enter MMMol via not only the GALV receptor (Mol
115                                          The GALV-WMV clade in turn formed a sister group to the koal
116 ith concentration in the env gene across the GALV strains that were particularly oncogenic and KoRV s
117 rt here the full genome sequences of all the GALV strains and demonstrate that diversifying selection
118                                 Although the GALV Env protein is commonly used to make high-titer pse
119  The region has also been proposed to be the GALV binding site, but this lacks empirical support.
120                  It is intended to enter the GALV/Fcy::Fur expressing virus into clinical development
121 esis and ITC established that changes in the GALV and ESRP regions affected Phe binding and feedback
122 nguish it from GALV were introduced into the GALV genome, and their functional consequences were asse
123   We propose that region A itself is not the GALV binding motif and that other sequences are required
124 erefore, that the combined expression of the GALV protein and Fcy::Fur provides a highly potent oncol
125 es comprised of the N-terminal region of the GALV-S SU protein and the C-terminal region of SSAV infe
126 s that GALV can enter MMMol via not only the GALV receptor (MolPit1) but also the amphotropic murine
127 sion in Southeast Asia and China suggest the GALV-KoRV clade originates in the former region and furt
128 rs and 7.1%, 11.3%, <15%, and 26.4% with the GALV pseudotyped vector.
129 The higher gene transfer efficiency with the GALV-pseudotyped vector correlated with higher levels of
130                                  Four of the GALVs, including GALV strain SEATO (GALV-S), were origin
131                                   Therefore, GALV and KoRV may have arisen via a cross-species transf
132 sistance of receptor-expressing BHK cells to GALV or XMRV, as shown by tunicamycin treatment and muta
133 overed to date are only distantly related to GALV.
134 unctional GALV receptors and is resistant to GALV.
135                    A virus highly similar to GALV has been identified in an Australian native rodent
136 nt with the susceptibility of the species to GALV infection.
137 while Pit2 does not confer susceptibility to GALV.
138 sion of CHO Pit1 conferred susceptibility to GALV.
139 ressing these chimeras became susceptible to GALV, whereas cells expressing wild-type Pit2 remained r
140 ter lung E36 cells, which are susceptible to GALV-S but not SSAV.
141          The detected vertically transmitted GALV-like viruses in Australo-Papuan fauna compared to s
142                          In this study using GALV-pseudotype vectors, we examined additional variable
143  to infections by gibbon ape leukemia virus (GALV) and amphotropic murine leukemia virus (A-MLV) unle
144 gammaretroviruses gibbon ape leukemia virus (GALV) and feline leukemia virus subgroup B (FeLV-B) can
145                   Gibbon ape leukemia virus (GALV) and koala retrovirus (KoRV) most likely originated
146 receptors for the gibbon ape leukemia virus (GALV) and the amphotropic murine leukemia virus (A-MuLV)
147                   Gibbon ape leukemia virus (GALV) and the koala retrovirus (KoRV) are very closely r
148 LTR and using the gibbon ape leukemia virus (GALV) Env for internalization were efficient at transduc
149 ogically reactive gibbon ape leukemia virus (GALV) envelope proteins, tagged with a feline leukemia v
150 ve members of the gibbon ape leukemia virus (GALV) family of type C retroviruses.
151 nce implicated in gibbon ape leukemia virus (GALV) infection, and an acidic residue at the first posi
152 d virus (XMRV) or gibbon ape leukemia virus (GALV) infection, even when their respective receptors, X
153  receptor and the gibbon ape leukemia virus (GALV) receptor Pit-1 were used concurrently.
154 e leukemia virus, gibbon ape leukemia virus (GALV), and simian sarcoma-associated virus was demonstra
155 highly infectious gibbon ape leukemia virus (GALV), the infectivity of KoRV, like that of other ERVs,
156 glycoprotein from gibbon ape leukemia virus (GALV), which it was hoped would aid the spread of the ac
157 e of KoRV and the gibbon ape leukemia virus (GALV), with virion morphology and Mn(2+)-dependent virio
158 e cocultivated on gibbon ape leukemia virus (GALV)-based retrovirus vector-producing cells.
159 nd LNX) or by the gibbon ape leukemia virus (GALV)-pseudotype packaging cells PG13 (LNY).
160 ing cells using a gibbon ape leukemia virus (GALV)-pseudotype retroviral vector.
161 tein derived from gibbon ape leukemia virus (GALV).
162 uLVs but also for gibbon ape leukemia virus (GALV).
163 ally resistant to gibbon ape leukemia virus (GALV).
164 ence with that of gibbon ape leukemia virus (GALV).
165  gammaretrovirus, gibbon ape leukemia virus (GALV).
166 able exception is gibbon ape leukemia virus (GALV).
167 D) derived from a gibbon ape leukemia virus (GALV).
168 irus (A-MuLV) and gibbon ape leukemia virus (GALV); E36 cells are highly susceptible to both viruses,
169             The gibbon ape leukemia viruses (GALVs) are among the most medically relevant retroviruse
170                 Gibbon ape leukemia viruses (GALVs) are part of a larger group of pathogenic gammaret
171 e Wallace Line, gibbon ape leukemia viruses (GALVs) have been isolated from captive gibbons.
172 led a simple retrovirus with a chimeric VL30/GALV-like structure.
173          KoRV is endogenous in koalas, while GALV is exogenous, suggesting that KoRV predates GALV an
174                             To determine why GALV cannot infect CHOK1, we cloned and sequenced ChoPit
175 nkey and shares 78% amino acid identity with GALV-S.

 
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