Unique Long Terminal Repeat and Surface Glycoprotein Gene Sequences of Feline Leukemia Virus as Determinants of Disease Outcome

Chandhasin, Chandtip; Coan, Patricia N.; Pandrea, Ivona; Grant, Chris K.; Lobelle‐Rich, Patricia; Puetter, Adriane; Lévy, Laurence

doi:10.1128/jvi.79.9.5278-5287.2005

Cited by 20 publications

(33 citation statements)

References 36 publications

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“…In FeLV-945 LTR, three 21-bp repeats form 2 junctions: 1 junction is formed by the fi rst repeat and the adjacent second repeat; the other is formed by the second and third repeats. Each junction includes a c-Myb binding site that increases the rate of viral replication through the recruitment of transcriptional coactivator binding protein (cAMP response element) (11). FeLV-Pco LTR sequences had 1 copy of the repeat junction ( 945 causes multicentric lymphoma, myeloproliferative disorder, and anemia and has never been associated with thymic lymphoma (26).…”

Section: Discussionmentioning

confidence: 99%

“…Because FeLV-945 is well characterized and highly virulent in the domestic cat (11,25), sequence elements associated with disease determination (env) and transcription enhancement (LTR) in FeLV-945 were examined in FeLV-Pco. In the envelope protein, 10 signature amino acid residues (found within the surface glycoprotein) that were shared between FeLV-Pco and FeLV-945 were distinctive from other strains of FeLV ( Figure 5).…”

Section: Phylogenetic Analysismentioning

confidence: 99%

“…Although the mechanism of immunopathogenesis is unclear, viral envelope proteins may be involved (9). FeLV envelope (env) and the long terminal repeat (LTR) sequences have been suggested as being involved in determination of disease sequelae, virus transactivation, and virus replication (10)(11)(12). There are 4 naturally occurring viral subgroups of exogenous FeLV (A, B, C, and T) that are distinguished genetically by sequence differences in the env gene and functionally by receptor interactions required for cell entry (13).…”

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confidence: 99%

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Genetic Characterization of Feline Leukemia Virus from Florida Panthers

Brown

Cunningham

Roca

et al. 2008

Emerg. Infect. Dis.

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Section: Discussionmentioning

confidence: 99%

Section: Phylogenetic Analysismentioning

confidence: 99%

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confidence: 99%

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Genetic Characterization of Feline Leukemia Virus from Florida Panthers

Brown

Cunningham

Roca

et al. 2008

Emerg. Infect. Dis.

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“…However, other roles, such as inducing hyperproliferation in a preleukemic stage by interaction with other host cell factors, may also be important (15). Interestingly, we found that recombinants with endogenous retroviral sequences were a rare event in 10A1 infections and were only Variations in the env gene have also been implicated in the altered leukemia specificity in feline leukemia viruses, although this may involve a receptor-independent mechanism (12,14,28). Fli1: the common denominator in erythro(blastic) leukemia?…”

Section: Discussionmentioning

confidence: 73%

Importance of Receptor Usage, Fli1 Activation, and Mouse Strain for the Stem Cell Specificity of 10A1 Murine Leukemia Virus Leukemogenicity

Rodenburg

Fischer

Engelmann

et al. 2007

J Virol

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Murine leukemia viruses (MuLV) induce leukemia through a multistage process, a critical step being the activation of oncogenes through provirus integration. Transcription elements within the long terminal repeats (LTR) are prime determinants of cell lineage specificity; however, the influence of other factors, including the Env protein that modulates cell tropism through receptor recognition, has not been rigorously addressed. The ability of 10A1-MuLV to use both PiT1 and PiT2 receptors has been implicated in its induction of blast cell leukemia. Here we show that restricting receptor usage of 10A1-MuLV to PiT2 results in loss of blast cell transformation capacity. However, the pathogenicity was unaltered when the env gene is exchanged with Moloney MuLV, which uses the Cat1 receptor. Significantly, the leukemic blasts express erythroid markers and consistently contain proviral integrations in the Fli1 locus, a target of Friend MuLV (F-MuLV) during erythroleukemia induction. Furthermore, an NB-tropic variant of 10A1 was unable to induce blast cell leukemia in C57BL/6 mice, which are also resistant to F-MuLV transformation. We propose that 10A1-and F-MuLV actually induce identical (erythro)blastic leukemia by a mechanism involving Fli1 activation and cooperation with inherent genetic mutations in susceptible mouse strains. Furthermore, we demonstrate that deletion of the Icsbp tumor suppressor gene in C57BL/6 mice is sufficient to confer susceptibility to 10A1-MuLV leukemia induction but with altered specificity. In summary, we validate the significance of the env gene in leukemia specificity and underline the importance of a complex interplay of cooperating oncogenes and/or tumor suppressors in determining the pathogenicity of MuLV variants.

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“…FeLV-A is weakly pathogenic in nature but is associated in unvaccinated animals with the induction of leukemia and lymphoma. Experimental infection with FeLV-A typically results in thymic lymphoma of Tcell origin after prolonged latency of one to three years (6)(7)(8).…”

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confidence: 99%