ABSTRACT
Objective:To investigate the clinical features of adenoviral encephalitis (AE), and to provide reference for clinical diagnosis and treatment of adenoviral encephalitis.Methods:From January 2012 to December 2020, 1 185 cerebrospinal fluid (CSF) samples of hospitalized children with suspected central nervous system infection in the Second Affiliated Hospital of Shantou University Medical College were collected for the detection of 22 common respiratory pathogens and common pathogens for encephalitis by polymerase chain reaction. Records of patients with adenovirus positive in CSF were reviewed and relevant clinical manifestations, laboratory tests and imaging examination results were collected for analysis.Results:Among 1 185 CSF samples, 242 samples were positive for viral nucleic acid, with detection rate of 20.4%, including 1.9%(23/1 185) of adenovirus. As for 23 children diagnosed with AE, 18 were male, five were female, with the age of (44.8±35.9) months, ranging from two months and 19 days to 10 years. Of 23 children, 21(91.3%) presented with fever, followed by convulsions (16 cases, 69.6%), headache (four cases, 17.4%), vomiting (11 cases, 47.8%), consciousness change (11 cases, 47.8%) and emotion disturbance (three cases, 13.0%). Among 23 children, eight cases had white blood cell counts (WBC) of (6 to <10)×10 9/L, 10 cases had WBC of (10 to 20)×10 9/L and the white blood cell classification was mainly neutrophils (21 cases, 91.3%), and C reactive protein of 20 cases (87.0%) was in the normal range. Cerebrospinal fluid examination showed that WBC were less than 15×10 6/L in 20 cases (87.0%), and WBC ≥15×10 6/L in three cases, which were up to 500×10 6/L; the protein of 19 cases was in the normal range, the glucose of 15 cases was in the normal range, and the chloride of 19 cases was in the normal range. Among 16 cases with brain magnetic resonance imaging examination, eight cases did not show abnormality, six cases with local meningeal linear enhancement, one case with small intracranial malacia, and one case with extensive intracranial lesions. For 13 cases who received electroencephalogram (EEG) test, seven cases showed normal EEG or marginal state, four cases showed extensive medium and high amplitude slow wave, one case showed spike wave or spike slow wave and one case had both of the above two changes. Among 23 children, 22 cases recovered including one case had secondary epilepsy, and the remaining one case had severe brain dysfunction and was unable to suck when discharged, with an indwelling gastric tube and accompanied by secondary epilepsy. Conclusions:The clinical manifestations and auxiliary examinations of children with AE have no obvious specificity. Most children with AE have a good prognosis, but a small number of them may have serious sequelae.
ABSTRACT
Objective: To investigate the innate immune response of influenza virus-infected glial cells,the transcription levels in chemokines in mouse microglia and astrocytes were detected which pre-infected by human H1N1 or avian H5N1 influenza viruses.Methods: The glial cells isolated from neonatal mice cerebral cortex were cultured and further microglia and astrocytes were purified.The primary mouse microglia and astrocytes were infected in vitro by H1N1 or H5N1 influenza viruses in a multiplicity of infection (MOI) 2.Eight hours post infection,the influenza virus nucleoprotein (NP) was detected by immunofluorescence to identify the proportion of infected cells.The cellular RNA were extracted at 6 h and 24 h to detect the transcriptional level of chemokines by semi-quantitative RT-PCR.Results: More than 95% of the microgha and astrocytes which isolated from mice were infected.The transcription levels of CCL-3,CCL-5,CXCL-2,CXCL-9 and CXCL-10 from infected microglia and astrocytes were upregulated.Futhermore,the mRNA level of CXCL-10 increased much more.In addition,avian H5N1 influenza virus could induce more stronger upregulation of those chemokines than human H1N1 did.Conclusion: The mouse microglia and astro cytes which are infected by H1N1 influenza virus or H5N1 influenza virus could induce upregulation of transcription level of chemokines.