To describe the risk factors, symptoms, treatment, and outcomes of anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis occurring in people living with HIV (PLWH).

Herpes simplex virus encephalitis is a known trigger of anti-NMDAR encephalitis. In recent years, multiple case reports also document anti-NMDAR encephalitis in PLWH, especially those who develop cerebrospinal fluid (CSF) escape, defined by an elevated CSF viral load in the setting of plasma viral suppression. Although the relationship between HIV and other viruses with anti-NMDAR encephalitis has not been fully elucidated, possible mechanisms include molecular mimicry or viral-induced release of NMDAR and other proteins as a result of neurotoxicity. HIV-induced functional dysregulation of CD4+ cell subtypes is another plausible contributor.

We conducted a literature search for published cases of autoimmune encephalitis in PLWH. We added an unpublished case from our center and described the clinical features of this unique cohort.

Eight published cases of anti-NMDAR encephalitis among PLWH were identified, as well as one unpublished case from our center. Common trends in these 9 cases include elevated CSF HIV viral load, T2 hyperintense lesions on MRI, and clinical improvement with immunomodulation. Our patient was a 51-year-old woman who presented off of antiretroviral therapy (recent CD4 range 199-252 cells/mm³) with status epilepticus and was found to have an elevated CSF HIV viral load and multiple non-enhancing T2-hyperintense lesions on brain MRI. Anti-NMDAR antibodies were positive in the serum and CSF. She did not respond to steroids or intravenous immunoglobulins, but began to improve after plasma exchange and was subsequently treated with rituximab.

Anti-NMDAR encephalitis is an important, treatable consideration in PLWH who present with altered mental status or new seizures. Patients with an elevated CSF viral load may be at higher risk for this syndrome, and immunomodulation may be indicated even in patients who are immunosuppressed.