However, they displayed gene signatures previously reported during and after SARS-CoV-2 infection including, downregulation of MHC genes (HLA-C, HLA-B, and HLA-DPB1) and CCL5 (a cytokine associated with immune recruitment during respiratory infection) [6], upregulation of immunomodulatory genes regulating inflammation and cell stress (SFTPA1, EGR1), and elevated expression of genes associated with mitochondrial dysfunctions and increased oxidative stress responses (i.e., LARS2). This evidence concerns the gene LARS2 and respiratory tract infectious disorder.