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Soluble IL‐2 receptor and beta‐2 microglobulin as possible serologic markers of neurologic disease in HTLV‐1 infection
Author(s) -
ToledoCornell Cristina,
Santos Silvane,
Orge Gloria,
Glesby Marshall J.,
Carvalho Edgar M.
Publication year - 2014
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.23711
Subject(s) - beta 2 microglobulin , medicine , tropical spastic paraparesis , serology , overactive bladder , myelopathy , disease , immunology , receptor , human t lymphotropic virus , gastroenterology , antibody , pathology , spinal cord , alternative medicine , psychiatry
The human T‐cell leukemia virus (HTLV‐1) is the causative agent of a variety of neurologic diseases, including HTLV‐1 Associated Myelopathy (HAM/TSP) and overactive bladder. Investigation of immune markers such as soluble interleukin‐2 receptor (sIL‐2R) and beta‐2 microglobulin (B2M) has shown some promising results in distinguishing patients with neurologic disease from those with carrier status. The objective of the present study was to determine if plasma levels of sIL‐2R and B2M are markers of neurologic disease in individuals infected with HTLV‐1. The present study was divided into two parts. A cross‐sectional study and a nested case control study. In the cross‐sectional study, HAM/TSP patients had higher plasma levels of B2M and sIL‐2R than patients with overactive bladder and HTLV‐1 carriers ( P < 0.01 for all comparisons). For the nested case control study, the sIL‐2 receptor test was able to distinguish patients with HAM/TSP from patients in the combined group of carriers and patients with overactive bladder with a sensitivity of 75.8% and false positive rate of 25.4%. Plasma levels of these markers did not change with the development of HAM/TSP and overactive bladder in HTLV‐1 carrier patients. The present study has shown the importance of sIL‐2 receptor in helping identifying HAM/TSP. However, the levels of these makers did not change significantly with the development of neurologic disease. J. Med. Virol. 86:315–321, 2014 . © 2013 Wiley Periodicals, Inc.