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Updated: May 7, 2026

RNA-seq Analysis of Transcriptomes in Thrombin-treated and Control Human Pulmonary Microvascular Endothelial Cells

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Published on: February 13, 2013

Blood transcriptomic profiling reveals gene expression alterations in patients with SFTS-associated encephalitis.

DaiQing Wu¹, AoFan Wang¹, Junjie Shi²

¹Department of Clinical Laboratory, Nanjing Drum Tower Hospital, Clinical College of Jiangsu University, Nanjing, Jiangsu, China.

Microbiology Spectrum

|September 23, 2025

Summary

Severe fever with thrombocytopenia syndrome (SFTS) can cause fatal encephalitis. This study identified six key immune genes linked to brain damage in SFTS patients, offering potential diagnostic and therapeutic targets.

Keywords:

encephalitis peripheral blood mononuclear cells (PBMC)severe fever with thrombocytopenia syndrome transcriptomic analysis

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Isolating Human Peripheral Blood Mononuclear Cells and CD4+ T cells from Sézary Syndrome Patients for Transcriptomic Profiling

Isolating Human Peripheral Blood Mononuclear Cells and CD4+ T cells from Sézary Syndrome Patients for Transcriptomic Profiling

Published on: October 14, 2021

Area of Science:

Infectious Diseases
Neuroscience
Immunology

Background:

Severe fever with thrombocytopenia syndrome (SFTS) is a dangerous tick-borne illness caused by SFTSV.
SFTSV infection can lead to fatal encephalitis, characterized by neurological symptoms like seizures and consciousness disorders.
The precise mechanisms of SFTSV neuroinvasion and associated brain injury are not well understood.

Purpose of the Study:

To investigate the molecular mechanisms underlying SFTS-induced brain damage.
To identify host immune responses contributing to encephalitis in SFTS patients.

Main Methods:

Analysis of clinical laboratory parameters from SFTS patients.
Transcriptomic analysis of peripheral blood mononuclear cells (PBMCs) from SFTS patients with and without encephalitis.
Comparison of gene expression profiles between encephalitis and non-encephalitis groups.

Main Results:

Central nervous system manifestations in SFTSV infection correlate with altered immune gene expression.
Six differentially expressed immune genes (MET, KIT, IL1R2, MAFF, CD69, CEBPD) were identified between SFTS encephalitis and non-encephalitis groups.
These genes may play a role in the pathogenesis of SFTS-associated encephalitis.

Conclusions:

Host immune gene expression changes are associated with SFTS-related encephalitis.
The identified genes provide potential targets for understanding SFTSV pathogenesis.
Further research into the host immune response could lead to improved treatments for SFTS-associated neurological complications.