CD8+ T-cell encephalitis (CD8E) is a rare subacute disease caused by autoreactive CD8+ T lymphocytes that attack CD4+ T cells infected by HIV, leading to viral replication and increased CD8+ cell counts in cerebrospinal fluid (CSF). Diagnosis involves a combination of clinical assessment, neuroimaging, and CSF analysis. Brain magnetic resonance imaging (MRI) is essential to identify typical changes, such as white matter lesions. We report the case of a PLWHA with poor adherence to antiretroviral therapy (ART) who developed CD8E. The patient, a 22-year-old male university student, presented with poor ART adherence, HIV viral load of 123 copies, and CD4 count of 449 cells. He was initially hospitalized for bradypsychia, ataxia, tremors, and cognitive decline. Contrast-enhanced brain CT showed diffuse hypodensity of white matter and cerebellum, with accentuated sulci and fissures. Brain MRI revealed diffuse, bilateral, and symmetrical FLAIR hypointensity in white matter. CSF analysis showed 30 cells (87% lymphocytes, some atypical), protein 157 mg/dL, glucose 43 mg/dL, lactate 14 mg/dL, detectable EBV PCR, HIV viral load 457 copies/mL, CD8 count 7 cells/mm³, and CD4 count 2 cells/mm³. Based on these findings, CD8E was suspected. Pulse therapy with methylprednisolone was initiated. The patient was discharged with clinical and CSF improvement, still under corticosteroid treatment. One year later, he was readmitted for diplopia. MRI showed improvement in previous lesions and a new thalamic lesion suggestive of Wernicke’s syndrome. CSF was unremarkable, and HIV plasma viral load was undetectable. He improved with thiamine. Seven months later, after another period of poor ART adherence, the patient presented again with recurrence of neurological symptoms similar to those during the first hospitalization. MRI revealed new bilateral lesions, worse in the right temporal region. CSF showed 10 cells, protein 138 mg/dL, and elevated plasma HIV viral load; viral panel was negative. Recurrence/progression of CD8E due to probable viral escape was considered. New pulse corticosteroid therapy and ART reinitiation were administered. On the second day of hospitalization, the patient developed decreased consciousness and respiratory failure, requiring intubation and ICU transfer, where additional corticosteroid pulses led to progressive improvement. After extubation, he continued tapering corticosteroids, though neurological sequelae persisted. After discharge, he remained on ART with multidisciplinary follow-up. CD8E is directly related to ART adherence and undetectable HIV viral load, with frequent relapses among patients with poor adherence. It is a rare and severe condition, and neurological sequelae may be permanent.
Montebeller et al. (Sun,) studied this question.