Abstract
BackgroundCats infected with exogenous feline leukemia virus (exFeLV) have a higher chance of lymphoma development than uninfected cats. Furthermore, an increased exFeLV transcription has been detected in lymphomas compared to non-malignant tissues. The possible mechanisms of lymphoma development by exFeLV are insertional mutagenesis or persistent stimulation of host immune cells by viral antigens, bringing them at risk for malignant transformation. Vaccination of cats against exFeLV has in recent years decreased the overall infection rate in most countries. Nevertheless, an increasing number of lymphomas have been diagnosed among exFeLV-negative cats. Endogenous feline leukemia virus (enFeLV) is another retrovirus for which transcription has been observed in cat lymphomas. EnFeLV provirus elements are present in the germline of various cat species and share a high sequence similarity with exFeLV but, due to mutations, are incapable of producing infectious viral particles. However, recombination between exFeLV and enFeLV could produce infectious particles.ResultsWe examined the FeLV expression in cats that have developed malignant lymphomas and discussed the possible mechanisms that could have induced malignant transformation. For expression analysis we used next-generation RNA-sequencing (RNA-Seq) and for validation reverse transcription quantitative PCR (RT-qPCR). First, we showed that there was no expression of exFeLV in all samples, which eliminates the possibility of recombination between exFeLV and enFeLV. Next, we analyzed the difference in expression of three enFeLV genes between control and lymphoma samples. Our analysis showed an average of 3.40-fold decreased viral expression for the three genes in lymphoma compared to control samples. The results were confirmed by RT-qPCR.ConclusionsThere is a decreased expression of enFeLV genes in lymphomas versus control samples, which contradicts previous observations for the exFeLV. Our results suggest that a persistent stimulation of host immune cells is not an appropriate mechanism responsible for malignant transformation caused by feline endogenous retroviruses.Electronic supplementary materialThe online version of this article (doi:10.1186/s12917-015-0378-9) contains supplementary material, which is available to authorized users.
Highlights
Cats infected with exogenous feline leukemia virus have a higher chance of lymphoma development than uninfected cats
As a pairwise sequence alignment reported that the analyzed strains of Endogenous feline leukemia virus (enFeLV) and exogenous feline leukemia virus (exFeLV) are 74.10% identical, we counted only the reads mapped to virus specific parts of U3 regions in the Long terminal repeats (LTR) (Figure 1) to estimate the enFeLV or exFeLV specific expression strength
On average 46.33 reads mapped to the enFeLV specific region (35 bp) and in tumor samples, on average 14.80 reads mapped to the same region
Summary
Cats infected with exogenous feline leukemia virus (exFeLV) have a higher chance of lymphoma development than uninfected cats. EnFeLV provirus elements are present in the germline of various cat species and share a high sequence similarity with exFeLV but, due to mutations, are incapable of producing infectious viral particles. Endogenous feline leukemia virus (enFeLV) sequences are found in the genomes of domestic cats (Felis catus) and related wild cat species [1,2]. Transcription and translation of enFeLV proviruses were detected in various tissues and cell lines, no infectious viruses are produced, due to mutations within essential parts of the viral genome [9,10,11]. Recombination between enFeLV sequences with exFeLVs can generate infectious virus particles [11,12,13,14,15]
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