ライフサイエンスコーパス: FIV

1 FIV also encodes a multifunctional OrfA accessory protei

2 FIV employs a distinct strategy to target helper T cells

3 FIV Env might exclude tetherin locally or direct assembl

4 FIV Gag is a nuclear shuttling protein that utilizes the

5 FIV infection causes AIDS-like disease and mortality in

6 FIV integrated across the entire length of the transcrip

7 FIV integration preferences are more similar to those of

8 FIV intra-individual evolution rates were noted to be eq

9 FIV subtype D was not detected in any submitted specimen

10 FIV Vif colocalized with feline APOBEC3 (fA3) proteins,

11 FIV virions bearing 39 out of 63 mutant glycoproteins tr

12 FIV was determined on short-term follow-up imaging in tw

13 FIV-34TF10 in which the OrfA reading frame is open (OrfA

14 FIV-based lentiviral vectors can transfect CE with shRNA

15 FIV-positive cats had significantly less lymph-node enla

16 Of 101 FIV antibody-positive feline blood specimens submitted f

17 In addition, 143 of 226 FIV-infected animals (63%) also expressed antibodies to

18 60, 100% (FI), 71.8% (FII/FIII), and 20.5% (FIV to FVI) of samples from individuals initiating treat

19 For example, clade A FIV-PPR is predominantly neurotropic and causes a mild d

20 In addition, FIV(HuMOR) prevented the attendant sensitization of trig

21 Alix-binding motif in FIV Gag did not affect FIV release.

22 ed and unvaccinated cats were infected after FIV-PPR challenge and exhibited similar plasma virus loa

23 st, nine cats became antibody positive after FIV vaccination but remained negative in the FIV PCR.

24 s in HIV diagnosis, serum antibodies against FIV classically serve as an indicator of infection statu

25 y was blocked, implying that most if not all FIV Gag normally undergoes nuclear cycling.

26 Virtually all FIV Gag rapidly became intranuclear when the CRM1 export

27 nd previous studies showing efficacy with an FIV-pPPRDelta vif DNA vaccine.

28 an selection, presumably due to an ancestral FIV infection.

29 e been selected for escape from an ancestral FIV.

30 The others restrict HIV-1 and FIV but not HIV-2.

31 We conclude that HIV-1 and FIV Gag differ strikingly in a key intracellular traffic

32 In addition, HIV-1 and FIV genomes accumulated with Gag in late endosomal foci,

33 se CRM1 (mCRM1) minimally affected HIV-1 and FIV production and did not antagonize hCRM1.

34 an immunodeficiency virus type 1 (HIV-1) and FIV Gag may differ.

35 0 mul for 6 weeks) reduced CXCL10, IL-6, and FIV RNA detection in brain, although PPAR-gamma in glia

36 ix (Alix-V) did not disrupt FIV budding, and FIV Gag peptides showed no affinity for Alix-V.

37 gene transcription driven by the FIV-C36 and FIV-PPR LTRs were identical.

38 ic viruses were prepared between FIV-C36 and FIV-PPR, with reciprocal exchanges involving (i) the 3'

39 Moreover, macrophage CD134 expression and FIV infection were enhanced by activation in response to

40 ee l-glutamic acid at 6 times, while FII and FIV were due to succinic acid at more than 30 times thei

41 ration or IFN-gamma responses to the HIV and FIV peptide pools.

42 f SIV > HIV-1 > BIV and EIAV > MLV, RSV, and FIV.

43 sly discriminates between FIV-vaccinated and FIV-infected cats.

44 Unlike other tetherin antagonists, FIV Env cannot act in trans to rescue vpu-deficient HIV-

45 is both restriction factor and cofactor, as FIV requires tetherin for optimal particle release.

46 rains (tissue culture adapted [TCA]) such as FIV-34TF10 can bind to HSPG, whereas SU from field strai

47 , whereas SU from field strains (FS) such as FIV-PPR cannot.

48 e if cats are co-infected with an attenuated FIV strain (PLV).

49 Budding of bald FIV and HIV particles was blocked by carnivore tetherins

50 ypes and unambiguously discriminates between FIV-vaccinated and FIV-infected cats.

51 ino acid sequences are not identical between FIV and HIV, the ability of FIV to bind and utilize both

52 The interaction between FIV and CD134 was probed using MAb 7D6 and soluble CD134

53 ants, chimeric viruses were prepared between FIV-C36 and FIV-PPR, with reciprocal exchanges involving

54 ine groups after challenge with a biological FIV isolate (FIV-PPR) at 13 weeks postimmunization.

55 ed anti-CD134 and anti-SU antibodies blocked FIV infection ex vivo.

56 RDelta vif proviral plasmid DNA or with both FIV-pPPRDelta vif DNA and a feline IFN-gamma expression

57 ants important for HSPG and CXCR4 binding by FIV SU and thus further define the importance of the V3

58 th the selective targeting of these cells by FIV.

59 es and meniscal tissue were also infected by FIV(HuMOR), which presumably exerted an antiinflammatory

60 elid species, disease etiology introduced by FIV infection are less clear, but recent studies indicat

61 ncing can be achieved in cells transduced by FIV vectors coexpressing reporter genes and 3' untransla

62 ld disease in the periphery, whereas clade C FIV-C36 causes fulminant disease with CD4(+) T-cell depl

63 lear export pathway with leptomycin B causes FIV Gag but not HIV-1 Gag to accumulate in the nucleus.

64 study we sought to identify and characterize FIV late domain(s) and elucidate cellular machinery invo

65 Five well-characterized FIV subtypes, A, B, C, D, and E, are recognized worldwid

66 00 nM DRV or TL-3, whereas parental chimeric FIV could not.

67 ially the same in the wild-type and chimeric FIVs.

68 specificity of Gag cleavage so that chimeric FIVs were not infectious.

69 None of the chimeric FIVs recapitulated the replication rate of FIV-C36, alth

70 Furthermore, imaging of intron-containing FIV RNA showed that hCRM1 increased RNA export to the cy

71 ndence on this protein: particles containing FIV Env need tetherin for optimal release from the cell,

72 ave received the FIV vaccine, which contains FIV subtype A and D inactivated virions.

73 correlated to responses to their counterpart FIV pools.

74 feline A3Z3 variants suppress vif-defective FIV infectivity.

75 ding domain of Alix (Alix-V) did not disrupt FIV budding, and FIV Gag peptides showed no affinity for

76 oviral genome of two geographically distinct FIV subtypes isolated from free-ranging lions.

77 chronic activation of CD8(+) T cells during FIV infection results in chromatin remodeling at the IL-

78 HIV-1 molecular clones that encode FIV Vif or SIVmac Vif (HIV-1(VF) and HIV-1(VS)) were the

79 Furthermore, FIV-enveloped FIV particles actually required tetherin for optimal rel

80 All blood samples from experimentally FIV-infected cats (n=5) were antibody positive and highl

81 ll known FIV strains and differentiates five FIV subtypes.

82 ompares intra-individual evolution rates for FIV, SIV, and HIV following systematic review of the lit

83 The primary receptor for FIV is CD134, a member of the tumor necrosis factor rece

84 ositive feline blood specimens submitted for FIV PCR diagnosis, 61 were positive (60%).

85 l machinery, may affect gene expression from FIV vectors.

86 in Alix stimulates the release of virus from FIV-expressing human cells.

87 he observed specificity distinctions with FS FIV.

88 Furthermore, FIV-enveloped FIV particles actually required tetherin f

89 but similar to the Ebola virus glycoprotein, FIV Env did not reduce intracellular or cell surface tet

90 cy virus (FIV)-based lentivirus vector (GP64-FIV) to murine nasal epithelia.

91 t integrase-transportin 3 binding hierarchy: FIV, HIV-1, and BIV > SIV and MLV > EIAV.

92 However, FIV is also macrophage tropic, and in chronic infection

93 rates between LV-FIV and LV-FIV encoding HV-FIV Vif.

94 (referred to here as high-virulence FIV [HV-FIV]), and a less-pathogenic strain, FIV-PPR (referred t

95 rates equivalent to those of the virulent HV-FIV parental virus.

96 ch vif, orfA, or both genes from virulent HV-FIV replaced equivalent genes in LV-FIV.

97 herefore, this PCR quantitatively identifies FIV subtypes and unambiguously discriminates between FIV

98 actions involved in virus budding.IMPORTANCE FIV is a nonprimate lentivirus that infects domestic cat

99 In FIV-infected feline cells, some intranuclear Gag was det

100 TNF- alpha improved listericidal activity in FIV-negative control cats but not in FIV-positive cats,

101 ther, our results demonstrated a decrease in FIV diversity in bone marrow in the presence of PLV.

102 onserved sites and transition frequencies in FIV genes differ among tissues of dual and single infect

103 , whereas IL-10 modestly reduced function in FIV-negative control cats.

104 IL-15 improved innate function in FIV-positive cats and increased the percentage of natura

105 ncluding both memory and motor functions, in FIV(+) animals.

106 the role of vif and orfA accessory genes in FIV replication and pathogenicity, we generated chimeras

107 and elucidate cellular machinery involved in FIV release.

108 HIV-1-equivalent substitutions were made in FIV PR, and cleavage of each Gag-Pol polyprotein was the

109 genesis of a potential Alix-binding motif in FIV Gag did not affect FIV release.

110 termined that mutagenesis of a PSAP motif in FIV Gag, small interfering RNA-mediated knockdown of Tsg

111 vity in FIV-negative control cats but not in FIV-positive cats, whereas IL-10 modestly reduced functi

112 uted in structurally equivalent positions in FIV PR were prepared in order to study the molecular bas

113 of the canonical Alix-binding L-domain(s) in FIV Gag.

114 loads and a better overall health status in FIV(+) cats, whereas anti-SU antibodies were present ind

115 of these chimeras is more straightforward in FIV than in primate lentiviruses, since FIV accessory ge

116 After the introduction of an inactivated FIV vaccine, this approach has become problematic, since

117 is of minor allele frequencies at individual FIV genome sites revealed 242 sites significantly affect

118 However, infectious FIV particles were resistant, and spreading FIV replicat

119 ly explain the failure to produce infectious FIVs bearing these mutations.

120 feline APOBEC3, APOBEC3Z3 (A3Z3), to inhibit FIV replication.

121 g fragment of Tsg101 (TSG-5') each inhibited FIV release.

122 wever, PCR detection of host-cell-integrated FIV DNA will differentiate infection-derived antibody fr

123 , Q99V, and P100N mutations were cloned into FIV Gag-Pol, and those constructs that best approximated

124 It must be incorporated specifically into FIV virions to be active.

125 ter challenge with a biological FIV isolate (FIV-PPR) at 13 weeks postimmunization.

126 amplifies single-target copies of all known FIV strains and differentiates five FIV subtypes.

127 omparative analyses of available full-length FIV consisting of subtypes A, B and C from FIVFca, Palla

128 pe surface unit (SU) with CXCR4, full-length FIV SU-Fc as well as constructs with deletions of extend

129 ted and placed in the context of full-length FIV-34TF10.

130 n of replication rates between LV-FIV and LV-FIV encoding HV-FIV Vif.

131 equalization of replication rates between LV-FIV and LV-FIV encoding HV-FIV Vif.

132 R (referred to here as low-virulence FIV [LV-FIV]).

133 ulent HV-FIV replaced equivalent genes in LV-FIV.

134 o compared to the replication kinetics of LV-FIV.

135 reas Ca(2+) -sensitive K(+) channels mediate FIV via an NO-independent pathway.

136 Moreover, FIV has evolved dependence on this protein: particles co

137 alyze the specificity changes in each mutant FIV PR expressed in the context of the natural Gag-Pol p

138 t with ex vivo results obtained using mutant FIVs.

139 The SHVH-P-FV (</=1kDa) and SHVH-N-FIV (3-1kDa) fractions showed the best ACE-inhibitory ac

140 ics, and myristoylation properties of native FIV MA with a mutant protein containing a consensus feli

141 t with the above observations, OrfA-negative FIV-34TF10 productively infects CrFK (CD134-negative) an

142 V3 MAbs weakly neutralized FIV infection using target cells expressing both CD134 a

143 Approximately 21% of FIV integrations within transcriptional units occurred i

144 dentical between FIV and HIV, the ability of FIV to bind and utilize both feline and human CXCR4 make

145 However, many molecular aspects of FIV replication remain poorly understood.

146 We also observed direct binding of FIV Gag peptides to Tsg101.

147 Alix is sufficient to rescue the budding of FIV mutants devoid of canonical L-domains.

148 A component of FIV that is Kir independent is abrogated by blocking Ca(

149 ficiency achieved following a single dose of FIV expressing mouse erythropoietin was insufficient to

150 additively following each of seven doses of FIV delivered over consecutive weeks (1 dose/week), with

151 ng IFN-gamma did not enhance the efficacy of FIV-pPPRDelta vif DNA immunization.

152 ent inherent differences in the evolution of FIV relative to that of primate lentiviruses, which may

153 Lentiviruses, with the exception of FIV, display a requirement for transportin 3 in comparis

154 8+ T cells, concordant with the expansion of FIV into CD8+ T cells with progression of the infection.

155 A higher frequency of FIV-specific T-cell proliferation responses was observed

156 The chimera carrying the 3' half of FIV-C36 demonstrated an intermediate disease course with

157 pe FIVs and chimeras carrying the 3' half of FIV-C36 or the 3' LTR and Rev2 regions of FIV-C36 on the

158 A single injection of FIV(HuMOR) into the temporomandibular joints of Col1-IL-

159 ect evidence for a sequential interaction of FIV Env with CD134 and CXCR4 and reveal the presence of

160 capitulate the species-specific monophyly of FIV marked by high levels of genetic diversity both with

161 rapid-growth phenotype and pathogenicity of FIV-C36 are the result of evolutionary fine tuning throu

162 Prediction of FIV with ATI was slightly better compared to ATS.

163 c FIVs recapitulated the replication rate of FIV-C36, although most replicated to levels similar to t

164 Our data suggest a greater reduction of FIV with IAT compared with either IVT or NRT.

165 DNA in regions of FIV insertion sites exhibited a "bendable" structure and

166 of FIV-C36 or the 3' LTR and Rev2 regions of FIV-C36 on the PPR background.

167 discrete substitutions in the active site of FIV PR with structurally equivalent residues of HIV-1 PR

168 e receptor utilization of diverse strains of FIV and found that all strains tested utilized CD134 as

169 However, strains of FIV differ in utilization of CD134; the prototypic strai

170 ost replicated to levels similar to those of FIV-PPR.

171 approximately 20-fold greater than those of FIV-PPR.

172 d that multiple factors, including timing of FIV-pPPRDelta vif inoculations and challenge, as well as

173 of primary sensory neurons via transport of FIV vectors from peripheral nerve endings to sensory gan

174 ith disease progression, the cell tropism of FIV broadens such that B cells and monocytes/macrophages

175 The optimized FIV-based RNAi expression vectors will find broad use gi

176 mmunized with either FIVDelta vifATGgamma or FIV-pPPRDelta vif plus pCDNA-IFNgamma, while virus-speci

177 ccinated with either FIVDelta vifATGgamma or FIV-pPPRDelta vif proviral plasmid DNA or with both FIV-

178 e similar to Pallas cat FIVOma than to other FIV.

179 ding to their high ACE-inhibitory potential, FIV and FV were fractionated by RP-HPLC and then analyze

180 ferent molecular and biochemical properties, FIV represents an attractive model for the development o

181 e given the extensive tropism of pseudotyped FIV vectors for many cell types in vitro and in vivo.

182 r at presentation, IAT significantly reduced FIV (46 cm3 with IAT vs 149 cm3 with IVT or NRT; P < .00

183 (full-range of threshold settings regarding FIV prediction) maps were coregistered in 3D with FIV us

184 e envelope glycoprotein (Env), which rescued FIV from carnivore tetherin restriction when expressed i

185 emonstrate that the Alix Bro1 domain rescues FIV mutants lacking a functional TSG101-interacting moti

186 he Okavango Delta in Botswana, both resemble FIV genome sequence from puma, Pallas cat and domestic c

187 onfers on pgtTRIMCyp the ability to restrict FIV in the presence of cyclosporin A, a drug that normal

188 We found that co-infection with PLV shifts FIV diversity from bone marrow to lymph node and spleen.

189 cal IL-1 receptor type I (IL-1RI) signaling, FIV(IL-1Ra) vector was injected into the cisterna magna

190 d in FIV than in primate lentiviruses, since FIV accessory gene open reading frames have very little

191 FIV particles were resistant, and spreading FIV replication was uninhibited.

192 dividuals who initiated ART at later stages (FIV to FVI) and averaged 1.9 +/- 0.7 log(10) copies/mill

193 FIV [HV-FIV]), and a less-pathogenic strain, FIV-PPR (referred to here as low-virulence FIV [LV-FIV])

194 t and a greater L. monocytogenes burden than FIV-negative control cats.

195 Our data demonstrate that FIV relies predominantly on a Tsg101-binding PSAP motif

196 Our review consistently documents that FIV evolution rates within individuals are significantly

197 less clear, but recent studies indicate that FIV causes moderate to severe CD4 depletion.

198 Microarray data indicated that FIV integration favored actively transcribed genes.

199 We observed that FIV evolves more slowly than HIV and SIV at the intra-in

200 Gag behaviors and raise the possibility that FIV genome encapsidation may initiate in the nucleus.

201 The results show that FIV Envs mediate a distinctive tetherin evasion.

202 The results show that FIV-C36 replicates ex vivo and in vivo to levels approxi

203 These results suggest that FIV peptides could be used in an HIV-1 vaccine.

204 The FIV accessory protein Vif abrogates the inhibition of in

205 The FIV gp95 glycoprotein (SU) from laboratory-adapted strai

206 transferase gene transcription driven by the FIV-C36 and FIV-PPR LTRs were identical.

207 antibody positive and highly positive in the FIV PCR.

208 FIV vaccination but remained negative in the FIV PCR.

209 striatum, and hippocampus were higher in the FIV(+)/insulin-treated group compared with the FIV(+)/PB

210 When expressed individually, the FIV matrix (MA), capsid (CA), and nucleocapsid-p2 (NC-p2

211 In order to map the interaction of the FIV envelope surface unit (SU) with CXCR4, full-length F

212 Our data consisted of the 3' half of the FIV genome from three tissues of animals infected with F

213 Our findings indicate that residues of the FIV myristoylation sequence play roles in replication be

214 s used to map the secondary structure of the FIV packaging signal RNA.

215 rkedly reduce cell surface expression of the FIV primary binding receptor.

216 Based on the FIV results, we hypothesize that the Gag-genome associat

217 n, all of the mutant PRs still processed the FIV polyprotein but the apparent order of processing was

218 ns were from cats known to have received the FIV vaccine, which contains FIV subtype A and D inactiva

219 It turns out that the FIV tetherin antagonist is also its Env protein, but the

220 onses to the HIV-1 peptide pools than to the FIV peptide pools, except for peptide-pool F3.

221 Using the FIV model for lentiviral persistence, these studies prov

222 oliferation responses were observed with the FIV peptide pools than with the HIV peptide pools.

223 V(+)/insulin-treated group compared with the FIV(+)/PBS-treated group.

224 Finally, Kir channels also contribute to FIV in human subcutaneous microvessels.

225 Endothelial Kir channels contribute to FIV of mouse mesenteric arteries via an NO-dependent mec

226 olution rates were noted to be equivalent to FIV interindividual rates.

227 at position 65 determines the resistance to FIV Vif-mediated degradation.

228 orthy that feline A3Z3 hap V is resistant to FIV Vif-mediated degradation and still inhibits vif-prof

229 ant, restrictive, and naturally resistant to FIV Vif-mediated degradation.

230 In transit, FIV Gag and genomic RNA accumulated independently of eac

231 l cortex and white matter of insulin-treated FIV(+) animals, with associated preservation of cortical

232 glia was increased compared with PBS-treated FIV(+) control animals.

233 ion and phorbol myristate acetate treatment, FIV could be reactivated in tissues from 4 cats.

234 ogenicity, we generated chimeras between two FIV molecular clones with divergent disease potentials:

235 oral cleavage pattern generated by wild-type FIV PR, while maintaining HIV-like inhibitor specificity

236 red relative to that observed with wild-type FIV PR.

237 ests were performed in vivo on the wild-type FIVs and chimeras carrying the 3' half of FIV-C36 or the

238 MA(NOS) chimera, suggesting that the unusual FIV sequence is conserved to promote exposure and effici

239 elium-dependent flow-induced vasodilatation (FIV) assayed in pressurized mesenteric arteries pre-cons

240 FIV-C36 (referred to here as high-virulence FIV [HV-FIV]), and a less-pathogenic strain, FIV-PPR (re

241 , FIV-PPR (referred to here as low-virulence FIV [LV-FIV]).

242 tions, to test whether diversity of virulent FIV in lymphoid tissues is altered in the presence of PL

243 cted with the feline immunodeficiency virus (FIV) (Cre) vector in the right and left temporomandibula

244 Feline immunodeficiency virus (FIV) and human immunodeficiency virus type 1 (HIV-1) pro

245 2 (HIV-2) and feline immunodeficiency virus (FIV) but not HIV-1.

246 nfection with feline immunodeficiency virus (FIV) causes an immunosuppressive disease whose consequen

247 Feline immunodeficiency virus (FIV) causes progressive immunodeficiency in domestic cat

248 tors based on feline immunodeficiency virus (FIV) could be used for coexpression of reporter construc

249 ) facilitated feline immunodeficiency virus (FIV) entry into CXCR4-positive, cell surface CD134-negat

250 usly observed feline immunodeficiency virus (FIV) Gag accumulating at the nuclear envelope during liv

251 region of the feline immunodeficiency virus (FIV) Gag protein.

252 In feline immunodeficiency virus (FIV) infected cats, daily intranasal insulin treatment (

253 Feline immunodeficiency virus (FIV) infection in cats provides an excellent model to ex

254 the course of feline immunodeficiency virus (FIV) infection suppress CD8(+) CTL function in a TGF-bet

255 that in vitro feline immunodeficiency virus (FIV) infection, but not UV-inactivated virus, activates

256 Feline immunodeficiency virus (FIV) infects many species of cat, and is related to HIV,

257 Feline immunodeficiency virus (FIV) is a lentivirus that causes AIDS in domestic cats,

258 Feline immunodeficiency virus (FIV) is among the most common infectious agents of cats.

259 tic cats with feline immunodeficiency virus (FIV) is an important model system for studying human imm

260 Feline immunodeficiency virus (FIV) naturally infects multiple species of cat and is re

261 Feline immunodeficiency virus (FIV) OrfA is an accessory protein that is critical for p

262 poration onto feline immunodeficiency virus (FIV) particles, transduction efficiency, receptor bindin

263 We have used feline immunodeficiency virus (FIV) protease (PR) as a mutational system to study the m

264 A feline immunodeficiency virus (FIV) provirus with a vif gene deletion (FIVDelta vifATGg

265 n and blocked feline immunodeficiency virus (FIV) replication in lymphoid and nonlymphoid feline cell

266 1 (HIV-1) and feline immunodeficiency virus (FIV) reverse transcriptases (RT), were identified using

267 Feline immunodeficiency virus (FIV) shares with T-cell tropic strains of human immunode

268 The feline immunodeficiency virus (FIV) targets activated CD4-positive helper T cells prefe

269 1 (HIV-1) and feline immunodeficiency virus (FIV) the least.

270 ce, using the feline immunodeficiency virus (FIV) vector, which is capable of stably transducing divi

271 us (BIV), and feline immunodeficiency virus (FIV) Vif appear specific to the A3Z3-type protein of the

272 expression of feline immunodeficiency virus (FIV) Vif-green fluorescent protein (GFP) in HIV-1 entry

273 ular clone of feline immunodeficiency virus (FIV), a range of viral variants emerged with distinct mo

274 ), HIV-1, and feline immunodeficiency virus (FIV), and have been postulated to encode proteins import

275 virus (EIAV), feline immunodeficiency virus (FIV), and Rous sarcoma virus (RSV) to critically address

276 strict HIV-1, feline immunodeficiency virus (FIV), equine infectious anemia virus (EIAV), or N-tropic

277 lentiviruses-feline immunodeficiency virus (FIV), simian immunodeficiency virus (SIV), and human imm

278 receptor for feline immunodeficiency virus (FIV), targeting the virus preferentially to activated CD

279 receptor for feline immunodeficiency virus (FIV), targeting the virus preferentially to activated CD

280 reasons, the feline immunodeficiency virus (FIV), which infects both domestic and wild cats, encodes

281 lication of a feline immunodeficiency virus (FIV)-based lentivirus vector (GP64-FIV) to murine nasal

282 ansfer with a feline immunodeficiency virus (FIV)-based lentivirus vector.

283 in sera from feline immunodeficiency virus (FIV)-infected and uninfected cats.

284 h 10(2)-10(6) feline immunodeficiency virus (FIV)-infected T cells.

285 ous HIV-1 and feline immunodeficiency virus (FIV).

286 ns of HIV and feline immunodeficiency virus (FIV).

287 vif-defective feline immunodeficiency virus (FIV).

288 ious chimeric feline immunodeficiency virus (FIV)/HIV strain carrying six HIV-like protease (PR) muta

289 As (HIV-1 and feline immunodeficiency virus [FIV]) vis-a-vis their Gag proteins in live cells.

290 olving virus (feline immunodeficiency virus, FIV) can reveal details of the contemporary population s

291 e feline and human immunodeficiency viruses (FIV and HIV) target helper T cells selectively, and in d

292 ed with significant immunopathology in vivo, FIV-C36 (referred to here as high-virulence FIV [HV-FIV]

293 al therapy in reducing final infarct volume (FIV) in intracranial large-vessel occlusions (ILVOs) are

294 ding the prediction of final infarct volume (FIV).

295 dies have demonstrated that the way in which FIV interacts with its primary receptor, CD134, alters a

296 rediction) maps were coregistered in 3D with FIV using voxel-wise overlap measurement.

297 ngly, the lack of protection associated with FIV-pPPRDelta vif DNA immunization contrasted with findi

298 e of A3Z3 polymorphism in domestic cats with FIV Vif has not yet been addressed.

299 from three tissues of animals infected with FIV alone, or with FIV and PLV, sequenced by 454 technol

300 of animals infected with FIV alone, or with FIV and PLV, sequenced by 454 technology.