# Coincidental Coexistence of Human T-lymphotropic Virus Type 1 (HTLV-1)-Associated Myelopathy/Tropical Spastic Paraparesis and Myasthenia Gravis in a Patient With Chronic HTLV-1 Infection: A Case Report

## TL;DR

A patient with a long-term HTLV-1 infection developed both HAM/TSP and myasthenia gravis, suggesting a possible link between the virus and autoimmune diseases.

## Contribution

This case report adds to the limited evidence suggesting HTLV-1 may contribute to the development of autoimmune conditions like myasthenia gravis.

## Key findings

- A patient with chronic HTLV-1 infection developed myasthenia gravis confirmed by anti-acetylcholine receptor autoantibodies.
- The patient responded well to acetylcholinesterase inhibitors, indicating a typical autoimmune response.
- The absence of thymoma suggests HTLV-1 may trigger autoimmunity without structural thymic abnormalities.

## 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.