Biology subjects

Puig-Torrents, M.

Publications and source records attributed to Puig-Torrents, M..

3 recordsLinked to original sources

bioRxiv2026

Arbovirus persistence in mosquitoes is characterized by translation repression of viral RNAs

Arboviruses induce acute lytic infection in human cells but establish persistent infection in their mosquito vectors, a viral strategy that is essential for sustained viral transmission. How mosquito cells maintain continuous production of viral progeny without compromising host cell viability remains a fundamental unresolved question. Because arbovirus replication in human cells relies on viral takeover of the host translational machinery, we investigated how translation is regulated during persistent infection in mosquito cells using chikungunya virus (CHIKV) as a model. A temporal analysis of viral RNA translation in RNAi-competent and RNAi-deficient Aedes albopictus cells revealed that persistence was associated with reduced viral protein production resulting from translation repression of viral RNAs. Subcellular localization analyses of the viral protein nsP2 and LC-MS/MS analyses of host tRNAs showed that, in contrast to human cells, CHIKV infection in mosquito cells neither induced nuclear relocalization of viral nsP2 to induce global host mRNA depletion, nor reshaped the tRNA modification landscape to compensate for the suboptimal codon usage of viral RNAs. Together, our results indicate that persistent infection in mosquito cells is characterized by a balanced host-virus translational state, in which limited viral translation is maintained while viral takeover of the host translational machinery is avoided. Notably, translation repression of viral RNAs was also observed during Zika virus (ZIKV) infection, suggesting that this mechanism may represent a general RNAi-independent feature of arbovirus persistence in mosquito cells.

microbiology↗

bioRxiv2025

Translational repression of viral RNA mediates arbovirus persistence in mosquitoes

Persistent infection of mosquito cells is essential for the transmission of arboviruses, yet how these viruses produce sufficient progeny without compromising host cell fitness remains unclear. Arbovirus genomes exhibit suboptimal codon usage for both human and mosquito hosts, raising questions about how they achieve efficient translation in such distinct cellular environments. Using chikungunya virus (CHIKV) as a model, we conducted a temporal, genome-wide analysis of transcription, translation, and tRNA modifications in Aedes albopictus C6/36 cells. Unlike in human cells, CHIKV infection does not alter the tRNA modification landscape in mosquitoes to overcome codon bias, nor does it induce widespread degradation of host transcripts. Instead, viral persistence is marked by a progressive, virus-specific repression of CHIKV RNA translation, occurring alongside a recovery of host mRNA translation. This translational balance, maintained independently of the RNAi system, enables sustained viral production without major disruption to host gene expression. Our findings identify translational control as a central mechanism underlying persistent arbovirus infection in mosquito cells.

microbiology↗

bioRxiv2023

N6-methyladenosine modification is not a general trait of viral RNA genomes

Despite the nuclear localization of the m6A machinery, the genomes of multiple exclusively-cytoplasmic RNA viruses, such as chikungunya (CHIKV) and dengue (DENV), are reported to be extensively m6A-modified. However, these findings are mostly based on m6A-seq, an antibody-dependent technique with a high rate of false positives. Here, we addressed the presence of m6A in CHIKV and DENV RNAs. For this, we combined m6A-seq and the antibody-independent SELECT and nanopore direct RNA sequencing techniques with functional, molecular, and mutagenesis studies. Following this comprehensive analysis, we found no evidence of m6A modification in CHIKV or DENV transcripts. Furthermore, depletion of key components of the host m6A machinery did not affect CHIKV or DENV infection. Moreover, CHIKV or DENV infection had no effect on the m6A machinerys localization. Our results challenge the prevailing notion that m6A modification is a general feature of cytoplasmic RNA viruses and underscore the importance of validating RNA modifications with orthogonal approaches.

microbiology↗