# Sindbis Virus–Host Interactions in Human Neuroblastoma Cells: Implications for Viral Pathogenesis and Replication

## TL;DR

This study explores how Sindbis virus interacts with human neuroblastoma cells, revealing insights into viral replication, cell death, and immune responses.

## Contribution

The study provides new insights into Sindbis virus replication dynamics and immune gene modulation in a neuronal cell model.

## Key findings

- SINV replication in SH-SY5Y cells was detectable as early as 3 hours post-infection.
- UV-C light effectively inactivated SINV after three 30-second exposures.
- SINV triggered apoptosis and upregulated innate immune genes peaking between 12–16 hours post-infection.

## Abstract

Sindbis virus (SINV) is a mosquito-borne alphavirus capable of causing neurological and immunological symptoms in humans, yet its effects on neural/immune systems remain insufficiently characterized. This study aimed to examine SINV replication, UV-C light inactivation, apoptosis induction, and immune gene modulation in human SH-SY5Y neuroblastoma cells. Following viral adaptation and infectious dose determination, SINV replication and inactivation were assessed using RT-qPCR and dsRNA immunofluorescence. Apoptotic markers (caspase-3, Bax, Bcl-2) were analyzed by immunofluorescence and immune genes expression kinetics (TLR3/7, RIGI, MDA5, IL-1β, IL-6, TNFα, IL-10, IFNβ and β-catenin) were measured at defined time points post-infection by RT-qPCR. SH-SY5Y cells supported productive SINV infection, with viral RNA detectable as early as 3 hpi and marked cytopathic effects by 24 hpi. A custom-built UV-C chamber achieved complete viral inactivation following 3 × 30 s exposures. We observed SINV time-course replication and UV-C inactivation with conspicuous morphological alterations in SH-SY5Y cells. Furthermore, SINV triggered caspase-dependent apoptosis and robust transcriptional upregulation of innate immune genes, peaking between 12–16 hpi and declining by 30 hpi. These findings elucidate the temporal dynamics of SINV replication, cell death mechanisms, and immune activation in a neuronal context, contributing to a better understanding of SINV neuropathogenesis.