# Comprehensive Transcriptomic Profiling Reveals Rotavirus-Induced Alterations in Both Coding and Long Non-Coding RNA Expression in MA104 Cells

## TL;DR

This study maps how rotavirus infection changes both coding and non-coding RNA in cells, highlighting new long non-coding RNAs involved in immune responses.

## Contribution

The study identifies novel lncRNA targets and provides a genome-wide transcriptomic resource for host–rotavirus interactions.

## Key findings

- RV infection caused significant upregulation of 3651 mRNAs and 4655 lncRNAs in MA104 cells.
- Key immune pathways like RIG-I-like receptor and Toll-like receptor were activated, while metabolic pathways were suppressed.
- Two novel lncRNAs and immune-related mRNAs (OASL and C3) were validated at both RNA and protein levels.

## Abstract

Rotavirus (RV) is the primary cause of severe gastroenteritis in young children, yet the long noncoding RNA (lncRNA) regulatory landscape governing the host response remains largely unmapped. To address this gap, the present study performed an integrated transcriptomic analysis of mRNA and lncRNA expression profiles in RV-infected MA104 cells at 24 h post-infection. Deep sequencing identified 11,919 high-confidence lncRNAs, revealing a massive transcriptional shift: 3651 mRNAs and 4655 lncRNAs were differentially expressed, with both populations predominantly upregulated. Functional enrichment analysis confirmed the strong activation of key innate immunity pathways, including the RIG-I-like receptor, Toll-like receptor, and TNF signaling pathways. Conversely, fundamental metabolic pathways were found to be suppressed. Crucially, the analysis of lncRNA targets highlighted their involvement in coordinating the host antiviral defense, particularly through transregulation. Experimental validation confirmed the significant upregulation of key immune-related mRNAs (OASL and C3) as well as two novel lncRNAs (lncRNA-6479 and lncRNA-4290) by qRT-PCR. The significant upregulation of OASL and C3 was validated at the protein level, confirming the biological relevance of the transcriptomic data. This study provides a foundational, genome-wide resource, identifying novel lncRNA targets for future mechanistic investigation into host–RV interactions.