In a well-characterized model of HIV-1 infection in human MDM, we have shown that IFN-α treatment or HIV-1 infection of MDM activates STAT1 phosphorylation to bind to and upregulate the GLS1 promoter activity, and subsequently increased glutaminase and glutamate production (Fig. 4, 5). This evidence concerns the gene IFNA1 and HIV-1 infection.