Epigenetic landscape of the host during arbovirus infection

Abstract

Arboviral diseases are transmitted to humans through arthropod vectors, such as dengue and chikungunya. Increasing evidence indicates that viral infections can induce epigenetic modifications in the host, thereby facilitating viral replication and propagation. Identifying these interactions provides mechanistic insights into infection processes and supports the development of advanced research strategies capable of addressing the current lack of effective therapeutic and intervention tools. This study aimed to assess, in vitro, the modulation of distinct epigenetic mechanisms following DENV and CHIKV infection. Primary lymphocyte cultures were infected with CHIKV and DENV, and the expression of writers, erasers, and modulators involved in epigenetic regulation was analyzed using SYBR Green qPCR. Gene expression was quantified at 0, 24, 48, 72, 96, and 120 hours post-infection and compared with non-infected controls. Among the four epigenetic mechanisms evaluated, significant changes were observed in genes associated with DNA methylation. At 72 hours post-infection, most of the differentially expressed genes were upregulated, including DNMT3B, which participates in de novo methylation, and the MBD gene family, which plays a transcriptional repression role and contributes to gene silencing. No significant alterations were detected in most genes linked to the other mechanisms analyzed. These findings suggest that arboviral infection preferentially activates the methylation pathway and specific genes across other regulatory processes. However, further investigation is required to identify the genomic regions affected and clarify whether these epigenetic changes contribute to enhanced viral transcription or replication.