Abstract
Parvovirus B19 infection is mostly asymptomatic in immunocompetent individuals but may cause severe manifestations when humoral immunity is impaired. Anti-CD20 therapies such as rituximab induce prolonged B-cell depletion and hypogammaglobulinemia, affecting the immune coordination and lowering the threshold for viral neuroinvasion and persistence within the central nervous system (CNS). We present a case of a 61-year-old patient who developed new-onset seizures 9 months after completing rituximab as fourth-line therapy for immune-mediated thrombocytopenia. Brain MRI showed a focal hyperintense lesion in the left peri-insular region with edema. Parvovirus B19 DNA was detected in the cerebrospinal fluid via polymerase chain reaction, while extensive testing for other infectious and autoimmune causes of encephalitis was negative. Immunological work-up demonstrated persistent depletion of CD19(+) B lymphocytes and severe hypogammaglobulinemia. This case highlights the role of impaired humoral immunity in facilitating viral persistence within the CNS and emphasizes the need to consider parvovirus B19 and other uncommon pathogens as a potential cause of encephalitis in patients with prior anti-CD20 therapy, even months after treatment completion.