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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Gene Review

env  -  Env polyprotein

Feline leukemia virus

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Disease relevance of env

  • Thus, the pathogenic and the host range determinants of the feline aplastic anemia retrovirus colocalize to a 3' pol-5' env region of the FSC genome and likely reside within a region encoding 241 amino acid residues of the N terminus of the extracellular glycoprotein [1].
  • The presence of env recombinant FeLV (FeLV-B) showed a negative correlation with proviral insertion at fit-1, possibly due to the rapid onset of these tumors [2].
  • The order of genes with respect to viral RNA is 5'-gag-fms-env-3', in which the entire feline leukemia virus env gene and an almost complete gag sequence are represented [3].
  • In contrast, only 1 of 22 naturally arising FeLV-negative feline LSAs contained recombinant proviruses, and no recombinant env gene was detected in seven samples from normal tissues or tissues from FeLV-positive animals that died from other diseases [4].
  • Cloning of enFeLV cDNA from two FeLV-free lymphoma cell lines (3201 and MCC) revealed a long open reading frame (ORF) encoding a truncated env gene product corresponding to the N-terminal portion of gp70env [5].

High impact information on env

  • In preparation for in vivo experiments to study the cell-to-cell pathway for the spread of the virus from the site of inoculation, the green fluorescent protein (GFP) transgene fused to an internal ribosome entry site (IRES) was inserted after the last nucleotide of the env gene in the ecotropic FeLV-A Rickard (FRA) provirus [6].
  • We PCR amplified the exogenous feline leukemia virus (FeLV)-related env gene species from lymphosarcomas induced by intradermally administered plasmid DNA of either the prototype FeLV, subgroup A molecular clone, F6A, or a new molecular clone, FeLV-A, Rickard strain (FRA) [7].
  • At least two RNA species were detected, a 4.5-kb RNA containing gag, env, and long terminal repeat sequences and a 2-kb RNA containing env and long terminal repeat sequences [5].
  • These were examined for virus-induced rearrangements of the c-myc, flvi-2 (bmi-1), fit-1, and pim-1 loci, for T-cell receptor (TCR) gene rearrangements, and for the presence of env recombinant FeLV (FeLV-B) [2].
  • Recombination between feline leukemia virus subgroup B or C and endogenous env elements alters the in vitro biological activities of the viruses [8].

Biological context of env

  • Immunoprecipitation analysis of the extracellular glycoproteins of 61E and EECC, a replication-competent viral construct composed of the 61C env and 3' long terminal repeat fused to the 61E gag-pol genes, demonstrated that the gp70 of EECC could be distinguished from that of 61E by both feline immune serum and a murine monoclonal antibody [9].
  • Nucleotide sequence analysis of the 3' end of the proviral genome and comparison with the published sequence of FeLV-B/Gardner-Arnstein showed that the most extensive differences are located within the 5' domain of the env gene [10].
  • This region, required for the pathogenic phenotype, cannot be larger than 1.5 kilobase pairs, a size only slightly more than that sufficient to encode the nonglycosylated precursor of the gp52 env gene product [11].
  • Restriction endonuclease mapping of four different clones indicates that there are a number of similarities among them, notably the presence of a 6.0- to 6.4-kilobase pair (kbp) EcoRI hybridizing fragment containing portions of sequences homologous to the gag, pol, env, and long terminal repeat-like elements of the infectious FeLV [12].
  • These findings indicate that T-cell killing is a consequence of superinfection and that the mutations in env critical to pathogenicity of the immunosuppressive variant result in a failure to establish superinfection interference in infected cells [13].

Anatomical context of env

  • T-cell killing depended on changes within a 7-amino-acid region near the C terminus of the gp70 env gene or was achieved independently by changes within a 109-amino-acid region encompassing the N terminus of gp70 [13].

Associations of env with chemical compounds

  • For each of the four tumor DNAs, nucleotide sequence analysis was performed on multiple clones of rFeLV-specific PCR products derived from the surface glycoprotein (SU) portion of the recombinant proviral env gene [14].

Analytical, diagnostic and therapeutic context of env


  1. Pathogenic and host range determinants of the feline aplastic anemia retrovirus. Riedel, N., Hoover, E.A., Dornsife, R.E., Mullins, J.I. Proc. Natl. Acad. Sci. U.S.A. (1988) [Pubmed]
  2. Genetic determinants of feline leukemia virus-induced lymphoid tumors: patterns of proviral insertion and gene rearrangement. Tsatsanis, C., Fulton, R., Nishigaki, K., Tsujimoto, H., Levy, L., Terry, A., Spandidos, D., Onions, D., Neil, J.C. J. Virol. (1994) [Pubmed]
  3. McDonough feline sarcoma virus: characterization of the molecularly cloned provirus and its feline oncogene (v-fms). Donner, L., Fedele, L.A., Garon, C.F., Anderson, S.J., Sherr, C.J. J. Virol. (1982) [Pubmed]
  4. Recombinant feline leukemia virus genes detected in naturally occurring feline lymphosarcomas. Sheets, R.L., Pandey, R., Jen, W.C., Roy-Burman, P. J. Virol. (1993) [Pubmed]
  5. Defective endogenous proviruses are expressed in feline lymphoid cells: evidence for a role in natural resistance to subgroup B feline leukemia viruses. McDougall, A.S., Terry, A., Tzavaras, T., Cheney, C., Rojko, J., Neil, J.C. J. Virol. (1994) [Pubmed]
  6. A replication-competent feline leukemia virus, subgroup A (FeLV-A), tagged with green fluorescent protein reporter exhibits in vitro biological properties similar to those of the parental FeLV-A. Chang, Z., Pan, J., Logg, C., Kasahara, N., Roy-Burman, P. J. Virol. (2001) [Pubmed]
  7. A novel truncated env gene isolated from a feline leukemia virus-induced thymic lymphosarcoma. Shi, Y., Roy-Burman, P. J. Virol. (2000) [Pubmed]
  8. Recombination between feline leukemia virus subgroup B or C and endogenous env elements alters the in vitro biological activities of the viruses. Pandey, R., Ghosh, A.K., Kumar, D.V., Bachman, B.A., Shibata, D., Roy-Burman, P. J. Virol. (1992) [Pubmed]
  9. Posttranslational modifications distinguish the envelope glycoprotein of the immunodeficiency disease-inducing feline leukemia virus retrovirus. Poss, M.L., Mullins, J.I., Hoover, E.A. J. Virol. (1989) [Pubmed]
  10. Nucleotide sequences of a feline leukemia virus subgroup A envelope gene and long terminal repeat and evidence for the recombinational origin of subgroup B viruses. Stewart, M.A., Warnock, M., Wheeler, A., Wilkie, N., Mullins, J.I., Onions, D.E., Neil, J.C. J. Virol. (1986) [Pubmed]
  11. Envelope gene sequences which encode the gp52 protein of spleen focus-forming virus are required for the induction of erythroid cell proliferation. Linemeyer, D.L., Menke, J.G., Ruscetti, S.K., Evans, L.H., Scolnick, E.M. J. Virol. (1982) [Pubmed]
  12. Molecular cloning and characterization of endogenous feline leukemia virus sequences from a cat genomic library. Soe, L.H., Devi, B.G., Mullins, J.I., Roy-Burman, P. J. Virol. (1983) [Pubmed]
  13. Viral genetic determinants of T-cell killing and immunodeficiency disease induction by the feline leukemia virus FeLV-FAIDS. Donahue, P.R., Quackenbush, S.L., Gallo, M.V., deNoronha, C.M., Overbaugh, J., Hoover, E.A., Mullins, J.I. J. Virol. (1991) [Pubmed]
  14. In vivo evolution and selection of recombinant feline leukemia virus species. Bechtel, M.K., Mathes, L.E., Hayes, K.A., Phipps, A.J., Roy-Burman, P. Virus Res. (1998) [Pubmed]
  15. Strong sequence conservation among horizontally transmissible, minimally pathogenic feline leukemia viruses. Donahue, P.R., Hoover, E.A., Beltz, G.A., Riedel, N., Hirsch, V.M., Overbaugh, J., Mullins, J.I. J. Virol. (1988) [Pubmed]
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