目的 探讨儿童人类疱疹病毒7型（HHV-7）脑炎引起的病毒性脑炎（VE）后自身免疫性脑炎（PVEAE）的临床特点及免疫机制。方法 回顾性分析4例患儿VE期和PVEAE期两个病程阶段临床表现、头颅MRI、脑电图等临床资料，检测PVEAE期脑脊液（CSF）中细胞因子、自身免疫性脑炎相关抗体等临床指标，分析HHV-7脑炎并发PVEAE的临床特点及免疫机制，总结诊治经验。结果 4例患儿中位发病年龄7岁，HHV-7脑炎首发距PVEAE症状出现的平均时间间隔为17d。4例患儿PVEAE期均出现发热、抽搐、精神行为异常、认知障碍、言语障碍等症状。PVEAE期抗NMDAR抗体阳性3例，抗neurexin-3a抗体阳性1例，CSF中IL-6、IL-8水平均显著升高。PVEAE期头颅MRI出现新发病灶3例，主要累及额顶叶及胼胝体压部、右侧丘脑、左侧海马。4例患儿接受一线免疫抑制治疗，随访6~12个月均预后良好，但遗留注意力缺陷及记忆力下降等轻微神经行为后遗症，1例遗留轻症遗尿症及难治性癫痫。结论 HHV-7脑炎患儿病情缓解期出现病情反常恶化，需考虑合并PVEAE，PVEAE期CSF细胞因子IL-6、IL-8水平显著升高，免疫炎症反应是PVEAE的主要发病机制。

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.