Post-transcriptional RNA modifications, known as the epitranscriptome, impact infection outcomes and host immune responses, including cytokine production, signaling pathways, and immune cell activation. Investigating these dynamic and reversible chemical modification changes within host cells after infection provides crucial insights into cellular immune functions. Advances in sequencing technologies now enable the unbiased detection of chemical modifications across the entire mRNA transcript. In this study, we utilized Oxford Nanopore Technology's direct RNA-sequencing (dRNA-seq) to examine the epitranscriptomic alterations in cellular mRNA during viral infections. Normal Human Bronchial Epithelial (NHBE) cells were differentiated at an air-liquid interface to form a pseudostratified epithelium of basal, ciliated, club and goblet cells, and then infected with the 2009 pandemic strain of influenza virus A(H1N1)pdm09. A time-course experiment was conducted, and the cellular mRNA was analyzed using dRNA-seq. The raw electric signal data from dRNA-seq allowed us to computationally measure RNA methylation and polyA tail length. This analysis identified transcript-specific changes, including m6A, m5C modifications, isoform usage, and polyA tail length, highlighting significant differences between infected and control samples over time. Pathway analysis further revealed that genes with differential methylation in infected samples are associated with innate immune pathways and mRNA stability. Our results underscore the potential of direct RNA sequencing to study host responses at the subcellular RNA level, enhancing our understanding of viral infections and paving the way for new research into post-transcriptional RNA regulation in the context of pathogen-host interactions.