Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) currently spread worldwide, causing the COVID-19 pandemic. The rate of its positive cases increases daily due to the unavailability of approved antivirals and a lack of knowledge of its pathophysiology in host-based antiviral discovery. Previous clinical data proved that SAS-CoV-2 infects human alveolar macrophages and naïve CD4+T cells in lymphocytes in severe COVID-19 patients through cytokine storms. Like other viruses, SARS-CoV-2 infection reprograms cellular metabolism and deactivates innate immune systems and rely on metabolic changes in immune-specific cells for its optimal replication and pathogenesis. The interplay between cellular metabolism and innate immunity is thus of great interest in the development of host-based antivirals. Genome-scale metabolic networks of SARS-CoV-2-alveolar macrophage (iAB-AMØ-1410) and SARS-CoV-2-naïve CD4+T cells (CD4T1670) have previously been reconstructed from the RECON1 model. These metabolic network models will be helpful for studying the interplay of cellular metabolism with immune responses in virus-infected and uninfected immune-specific cells. Such metabolic models could be used for a better understanding of its pathophysiology and host-based antiviral development.

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