Pathogenesis and treatment of HTLV-I associated myelopathy.

Abstract

That HTLV-I is not a latent infection is indicated by the detection of mRNA in the peripheral blood and CNS of patients with HTLV-I infection and by the persisting humoral and cellular immune responses. Indeed the frequency of anti-HTLV CTL is extremely high. The reduction in anti-TAX CTL frequency following reduction in proviral load suggests that removal of viral antigen may result in a reduced inflammatory response at least in peripheral blood and although the clinical data should be interpreted with caution, perhaps in the CNS. Patients with more advanced disease, and possibly fixed deficits may not benefit from either anti-inflammatory or antiretroviral treatment. The patients with most to gain are those with least deficit in whom early diagnosis and treatment will depend on raising awareness of HTLV-I beyond the neurological community. Many patients with HAM first present to a urologist or gynaecologist with bladder dysfunction or may have been seen in the genitourinary clinical with impotence or positive treponemal serology, which in the older patient is often the result of childhood infection with Treponema pallidum pertenue. Investigation of these patients should include HTLV-I serology and further investigation of HTLV-I positive patients should include proviral load measurements as well as markers of inflammation. Treatments whether antiviral or anti-inflammatory should be assessed for their effect on both as well as a clinical response.