Open Access Research

Increased seroreactivity to HERV-K10 peptides in patients with HTLV myelopathy

Raisa Perzova1, Elliot Graziano1, Swathi Sanghi1, Caitlin Welch1, Patricia Benz1, Lynn Abbott1, Danielle Lalone1, Jordan Glaser2, Thomas Loughran3, William Sheremata4 and Bernard J Poiesz1*

Author Affiliations

1 Department of Medicine, Division of Hematology/Oncology, State University of New York, Upstate Medical University, Syracuse, NY 13210, USA

2 Division of Infectious Diseases, Department of Medicine, Staten Island Hospital, New York, NY, USA

3 Penn State Cancer Institute, Penn State Milton S. Hershey Medical Center, Hershey, PA, USA

4 Department of Neurology, University of Miami, Miami, FL, USA

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Virology Journal 2013, 10:360  doi:10.1186/1743-422X-10-360

Published: 23 December 2013



Previously, we had shown that persons infected with human T-cell lymphoma leukemia virus 1 or 2 (HTLV-1 or 2) had an increased prevalence of antibodies to a peptide in the Pol protein of the retrovirus HERV-K10, homologous to a peptide in HTLV gp21 envelope protein. The prevalence rate was higher in those with myelopathy vs. non-myelopathy. We have now extended our observations to a cohort restricted to North America in whom the diagnosis of HTLV myelopathy was rigorously confirmed to also test for reactivity to another HERV-K10 peptide homologous to the HTLV p24 Gag protein.


Sera from 100 volunteer blood donors (VBD), 53 patients with large granular lymphocytic leukemia (LGLL), 74 subjects with HTLV-1 or 2 infection (58 non-myelopathy and 16 myelopathy) and 83 patients with multiple sclerosis (MS) were evaluated in ELISA assays using the above peptides.


The HTLV myelopathy patients had a statistically significant increased prevalence of antibodies to both HERV-K10 peptides (87.5%) vs. the VBD (0%), LGLL patients (0%), MS patients (4.8%), and the HTLV positive non-myelopathy subjects (5.2%).


The data suggest that immuno-cross-reactivity to HERV-K10 peptides and/or transactivation of HERV-K10 expression by the HTLV Tax protein may be involved in the pathogenesis of HTLV-associated myelopathy/tropical spastic paraparesis and spastic ataxia.