Novel Perspectives Focused on the Relationship Between Herpesvirus Encephalitis and Anti-GFAP-Antibody-Positive Astrocytopathy.

Abstract

Virus encephalitis (VE), recognized as one of the common kinds of central nervous system (CNS) diseases after virus infection, has a surprising correlation with autoimmune encephalitis (AE) when autoimmune antibodies emerge in cerebrospinal fluid (CSF) or serum. Herpes simplex virus and Epstein-Barr virus are the most critical agents worldwide. By molecular mimicry, herpes viruses can invade the brain directly or indirectly. As a type-III intermediate filament, glial fibrillary acidic protein (GFAP) can be seen in both the central and peripheral nervous system and is regarded as a marker of astrocyte activation. Autoimmune glial fibrillary acidic protein astrocytopathy (GFAP-A), an autoimmune inflammatory CNS disorder with unearthed pathogenic mechanism yet, is correlated with CD8 + T cells and AQP4 astrocytopathy in TNF signaling. It brings a new concept of VE and GFAP coexisting, which has been documented in several case reports. Considering the infectious role of herpes viruses in CNS, EBV contributes to GFAP-IgG significantly and may result in GFAP-A. Coincidently, the existence of GFAP-IgG in patients with infection of herpes viruses has been documented as well. There exist multiple diagnoses of VE, ranging from traditional diagnostic criteria, such as CSF examination and electronic techniques, to a novel approach, according to case reports, the detection of GFAP-lgG. In terms of treatment, except for (IVIG), the explorations for new curative targets and optimal diagnostic time are of great necessity. In conclusion, emphasis given to the CNS autoimmune effect brought by the virus infection is highly worthy.