Speaker
Description
Zika virus (ZIKV), a re-emerging arbovirus of the Flavivirus genus, is linked to severe neurological outcomes such as Guillain-Barré syndrome and congenital microcephaly. Understanding host transcriptional responses to ZIKV is essential to uncover mechanisms of viral pathogenesis. The virus is transmitted by Aedes mosquito, and symptoms start to manifest 3-7 days after infection.
In this study we investigated the effect of Zika virus infection on the transcriptome and general stress response.
We utilized two groups of lung adenocarcinoma cells lines (A549), one group infected with Zika virus(ZIKA) and the other as control(MOCK). Single cell sequencing was performed for both groups. Analysis were performed utilizing STAR alignment, DESeq2, rMATs, maser, to assess the changes is gene expression, alternative splicing activity and gene ontology was performed with metascape.
Principal components analysis showed clear clustering between our two groups indicating differences in gene expression. There were substantial upregulation of genes in the Zika infected cells. ISG15, IF16, and ATF3. ATF3 upregulation indicated activation of the integrated stress response. Gene ontology showed that most of these genes were associated with immunity against viral infection and were mostly interferon stimulated. Substantial difference in alternative splicing activity was also observed, with most genes associated with cilium assembly.
The study shows that Zika virus infection induces upregulation of genes and activation of integrated stress response, and changes in splicing events. This study offers insight into the molecular changes that occurs during infection and contribute to understanding the pathogenessis of the infection.