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Updated: Jul 4, 2026

Viral Tracing of Genetically Defined Neural Circuitry

Viral Tracing of Genetically Defined Neural Circuitry

Published on: October 17, 2012

Cross-System Transcriptomics Suggests Enterovirus A71 Exploits Wound Healing Programs to Target Neural Progenitors in

Nibras Mohammed Ali Hashim¹, Noor N Al-Hayani², Bushra Jabbar Hamad¹

¹Department of Biology, College of Science, University of Thi-Qar, Nasiriyah, Iraq.

Infectious Disorders Drug Targets

|July 3, 2026

Summary

Enterovirus 71 (EV-A71) infection targets neural stem cells by hijacking their regenerative programs. This study identifies a macrophage gene signature to distinguish active EV-A71 infection from vaccine responses.

Keywords:

ALOX5 Enterovirus A71 PMEPA1 immune evasion macrophages neural progenitors spinal cord organoids transcriptomics

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Published on: June 30, 2021

Area of Science:

Virology
Neuroscience
Computational Biology

Background:

Enterovirus A71 (EV-A71) immune evasion and neuroinvasion mechanisms remain unclear.
Inactivated vaccines offer protection without the detrimental effects of active infection, such as inflammation and viral persistence.

Purpose of the Study:

To investigate the dichotomy between active EV-A71 infection and vaccine-induced immunity using computational transcriptomics.
To identify specific neural cell populations susceptible to enteroviral infection.

Main Methods:

Compared bulk RNA-seq data from THP-1 macrophages infected with active versus inactivated EV-A71.
Developed a 10-gene consensus signature and projected it onto a human spinal cord organoid single-cell RNA-seq atlas.
Utilized an iterative Area Under the Curve (AUC)-based optimization strategy to refine candidate genes.

Main Results:

Active EV-A71 infection activates a wound-healing program (PMEPA1, ALOX5, CCL1, SPRED3), while inactivated virus elicits an anti-inflammatory response.
EV-A71 infection leads to an immunosuppressive M2 phenotype with decreased inflammatory factors (ADORA2A, CCR1, CXCL1).
The 10-gene signature identified cycling neural progenitors as the likely reservoir for EV-A71 replication.

Conclusions:

A macrophage gene signature computationally identifies EV-A71 infection versus vaccine protection.
EV-A71 targets proliferative and regenerative programs in neural stem cells within human spinal cord organoids.