Host transcriptome in human 239T cells infected with HPIV3 expressing wild-type virus versus its matrix-deleted counterpart

Paramyxoviruses (PMVs) exploit the host's translation machinery to enhance their replication. We found that the PMV matrix protein is crucial in this process, inhibiting host protein synthesis while boosting viral protein production. This occurs through interactions with the core exon-junction complex (cEJC), a key player in mRNA biogenesis. Disruption of this interaction using siRNA led to increased viral replication but did not affect other viruses like SARS-CoV-2. Our study unveils a novel mechanism by which PMVs hijack host cell resources, offering new targets for antiviral therapy. Overall design: HEK 293T cells were mock-infected or infected with either HPIV3-WT or HPIV3 delta M at an MOI of 3 for 48 hours. Total RNA was extracted from the cells and subjected to polysome profiling followed by RNA sequencing analysis using poly(A) enrichment.