Myasthenie.com

Cureus. 2025 Jul 17;17(7):e88163. doi: 10.7759/cureus.88163. eCollection 2025 Jul.

ABSTRACT

Human T-lymphotropic virus type 1 (HTLV-1) infection profoundly alters central immune regulation via molecular mechanisms involving the viral proteins transactivator X and HTLV-1 basic leucine zipper factor, which promote the proliferation of autoreactive T lymphocytes and the dysfunction of regulatory T cells, resulting in persistent inflammation of the central nervous system. These alterations not only explain the occurrence of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) but have also been associated with the development of autoimmune diseases such as myasthenia gravis (MG). While the connection between chronic HTLV-1 infection and MG is still anecdotal, a small number of case studies and limited molecular research suggest a potential link. Recent investigations have identified HTLV-1 tax and pol gene sequences in thymic tissue from MG patients, supporting the idea that the virus can persistently infect the thymus and interfere with the negative selection of T lymphocytes. Here, we present the case of a patient with HAM/TSP for over 12 years who subsequently experienced a myasthenic crisis, confirmed by the detection of anti-acetylcholine receptor autoantibodies. The patient responded favorably to treatment with acetylcholinesterase inhibitors. The absence of thymoma, together with a history of chronic retroviral infection, reinforced the potential role of HTLV-1 as a trigger for autoimmunity in the absence of structural abnormalities. This case illustrates the clinical and molecular convergence between retroviral infection and immune dysfunction, providing further support for a model of virally induced autoimmunity.

PMID:40821191 | PMC:PMC12357591 | DOI:10.7759/cureus.88163


Source: https://pubmed.ncbi.nlm.nih.gov/4082119 ... t9+e462414