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The continuous and rapid emergence of new viral strains calls for a better understanding of the fundamental changes occurring within the host cell upon viral infection. In this study, we analyzed RNA-seq transcriptome data from Calu-3 human lung epithelial cells infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) compared to five other viruses namely, severe acute respiratory syndrome coronavirus (SARS-CoV), Middle East Respiratory Syndrome (SARS-MERS), influenzavirus A (FLUA), influenzavirus B (FLUB), and rhinovirus (RHINO) compared to mock-infected cells and characterized their coding and noncoding RNA transcriptional portraits. The induction of interferon, inflammatory, and immune response was a hallmark of SARS-CoV-2 infection. Comprehensive bioinformatics revealed the activation of immune response and defense response to the virus as a common feature of viral infection. Interestingly however, the degree of functional categories and signaling pathways activation varied among different viruses. Ingenuity pathways analysis highlighted altered conical and casual pathways related to TNF, IL1A, and TLR7, which are seen more predominantly during SARS-CoV-2 infection. Nonetheless, the activation of chemotaxis and lipid synthesis was prominent in SARS-CoV-2-infected cells. Despite the commonality among all viruses, our data revealed the hyperactivation of chemotaxis and immune cell trafficking as well as the enhanced fatty acid synthesis as plausible mechanisms that could explain the inflammatory cytokine storms associated with severe cases of COVID-19 and the rapid spread of the virus, respectively.