Dataset Information

Two endogenous retroviral loci appear to contribute to Multiple Sclerosis.

ABSTRACT:

Background

Two endogenous retroviral loci seem to be involved in the human disease Multiple sclerosis (MS).

Results

The two retroviral loci synergize in and contribute to MS (shown by ANOVA). Synergy probably means recombination or complementation of the activated viruses. Similar observations may be true for Type 1 Diabetes and Rheumatoid arthritis. In MS the genes also synergize with the immune system; this could well be a common phenomenon.

Conclusion

We formulate various theories about the role of the viruses. Also, the concept is developing that some forms of autoimmunity should be treatable with antiretrovirals. In the case of MS, this idea is gradually gaining weight.

SUBMITTER: Nexo BA

PROVIDER: S-EPMC4851805 | biostudies-literature | 2016 Apr

REPOSITORIES: biostudies-literature

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Publications

Two endogenous retroviral loci appear to contribute to Multiple Sclerosis.

Nexø Bjørn A BA Jensen Sara B SB Nissen Kari K KK Hansen Bettina B Laska Magdalena J MJ

BMC neurology 20160430

<h4>Background</h4>Two endogenous retroviral loci seem to be involved in the human disease Multiple sclerosis (MS).<h4>Results</h4>The two retroviral loci synergize in and contribute to MS (shown by ANOVA). Synergy probably means recombination or complementation of the activated viruses. Similar observations may be true for Type 1 Diabetes and Rheumatoid arthritis. In MS the genes also synergize with the immune system; this could well be a common phenomenon.<h4>Conclusion</h4>We formulate variou ...[more]

PMID: 27130045

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Project description:Feline leukemia virus (FeLV) is an exogenous retrovirus that causes malignant hematopoietic disorders in domestic cats, and its virulence may be closely associated with viral sequences. FeLV is classified into several subgroups, including A, B, C, D, E, and T, based on viral receptor interference properties or receptor usage. However, the transmission manner and disease specificity of the recombinant viruses FeLV-D and FeLV-B remain unclear. The aim of this study was to understand recombination events between exogenous and endogenous retroviruses within a host and elucidate the emergence and transmission of recombinant viruses. We observed multiple recombination events involving endogenous retroviruses (ERVs) in FeLV from a family of domestic cats kept in one house; two of these cats (ON-T and ON-C) presented with lymphoma and leukemia, respectively. Clonal integration of FeLV-D was observed in the ON-T case, suggesting an association with FeLV-D pathogenesis. Notably, the receptor usage of FeLV-B observed in ON-T was mediated by feline Pit1 and feline Pit2, whereas only feline Pit1 was used in ON-C. Furthermore, XR-FeLV, a recombinant FeLV containing an unrelated sequence referred to the X-region, which is homologous to a portion of the 5'-leader sequence of Felis catus endogenous gammaretrovirus 4 (FcERV-gamma4), was isolated. Genetic analysis suggested that most recombinant viruses occurred de novo; however, the possibility of FeLV-B transmission was also recognized in the family. This study demonstrated the occurrence of multiple recombination events between exogenous and endogenous retroviruses in domestic cats, highlighting the contribution of ERVs to pathogenic recombinant viruses.IMPORTANCEFeline leukemia virus subgroup A (FeLV-A) is primarily transmitted among cats. During viral transmission, genetic changes in the viral genome lead to the emergence of novel FeLV subgroups or variants with altered virulence. We isolated three FeLV subgroups (A, B, and D) and XR-FeLV from two cats and identified multiple recombination events in feline endogenous retroviruses (ERVs), such as enFeLV, ERV-DC, and FcERV-gamma4, which are present in the cat genome. This study highlights the pathogenic contribution of ERVs in the emergence of FeLV-B, FeLV-D, and XR-FeLV in a feline population.

Dataset Information

Two endogenous retroviral loci appear to contribute to Multiple Sclerosis.

Background

Results

Conclusion

Publications

Two endogenous retroviral loci appear to contribute to Multiple Sclerosis.

Similar Datasets

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