Objective To investigate the clinical features and immune mechanisms of post-viral encephalitis autoimmune encephalitis (PVEAE) caused by human herpesvirus 7 (HHV-7) encephalitis in children. Methods A retrospective analysis of clinical manifestations, cranial MRI, electroencephalogram (EEG), and other clinical data from four pediatric patients during the viral encephalitis (VE) phase and post-viral encephalitis with autoimmune encephalitis (PVEAE) phase. Clinical indicators including cytokines and antibodies associated with autoimmune encephalitis in cerebrospinal fluid (CSF) during the PVEAE phase were measured. The clinical characteristics and immune mechanisms of HHV-7 encephalitis complicated by PVEAE were analyzed, and diagnostic and therapeutic experiences were summarized. Results The median age of onset in the 4 pediatric patients was 7 years. The average interval between the onset of HHV-7 encephalitis and the emergence of PVEAE symptoms was 17 days. All 4 patients exhibited symptoms during the PVEAE phase, including fever, seizures, psychiatric and behavioral abnormalities, cognitive impairment, and speech disorders. During the PVEAE phase, 3 patients tested positive for anti-NMDAR antibodies and 1 for anti-neurexin-3a antibodies. CSF levels of IL-6 and IL-8 were significantly elevated in all cases. New lesions were identified on cranial MRI in 3 patients during the PVEAE phase, primarily involving the frontal-parietal lobes, commissural region of the corpus callosum, right thalamus, and left hippocampus. Four patients received first-line immunosuppressive therapy. All demonstrated favorable outcomes at 6-to 12-month follow-up, though mild neurobehavioral sequelae persisted, including attention deficits and memory impairment. One patient developed mild enuresis and refractory epilepsy. Conclusion In children with HHV-7 encephalitis, paradoxical deterioration during the remission phase warrants consideration of concurrent PVEAE. During the PVEAE phase, CSF cytokine levels of IL-6 and IL-8 significantly increase, indicating that immune-inflammatory responses constitute the primary pathogenesis of PVEAE.