ArticleVirologica Sinica2017
Expression of human cytomegalovirus components in the brain tissues of patients with Rasmussen's encephalitis.
Article in Virologica Sinica, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Rasmussen's encephalitis is characterized by relatively lower production of IFN-β and activated cytotoxic T cell upon herpes viruses infection.Journal of neuroinflammation · 2022Article
- HCMV infection and IFITM3 rs12252 are associated with Rasmussen's encephalitis disease progression.Annals of clinical and translational neurology · 2021Article
- Genetic Factors in Rasmussen's Encephalitis Characterized by Whole-Exome Sequencing.Frontiers in neuroscience · 2021Article
- Rasmussen's encephalitis: mechanisms update and potential therapy target.Therapeutic advances in chronic disease · 2020Review
- Detection of EBV and HHV6 in the Brain Tissue of Patients with Rasmussen's Encephalitis.Virologica Sinica · 2018Article
- Elevated expression of EBV and TLRs in the brain is associated with Rasmussen's encephalitis.Virologica Sinica · 2017Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rasmussen's encephalitis (RE) is a rare and severe progressive epileptic syndrome with unknown etiology. Infection by viruses, including human cytomegalovirus (HCMV), has been speculated to be a potential trigger for RE. However, no viral antigens have been detected in the brains of patients with RE; thus, a possible clinical linkage between viral infections and RE has not been firmly established. In this study, we evaluated the expression of HCMV pp65 antigen in brain sections from 26 patients with RE and 20 non-RE patients by immunohistochemistry and in situ hybridization, and assessed the associations between HCMV infection and clinical parameters. Elevated expression of HCMV pp65 protein and DNA was observed in 88.5% (23/26) and 69.2% (18/26) of RE cases, respectively. In the non-RE group, HCMV pp65 antigen was detected only in two cases (10%), both of which were negative for DNA staining. Additionally, the intensity of HCMV pp65 staining was correlated with a shorter duration of the prodromal stage, younger age of seizure onset, and more severe unilateral cortical atrophy. Elevated expression of HCMV pp65 was observed in RE brain tissue and was correlated with the clinical features of RE disease. In summary, our results suggested that HCMV infection may be involved in the occurrence and progression of RE disease. Thus, further studies are needed to determine whether early treatment with anti-HCMV antibodies could modulate the course of RE.
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