M. tuberculosis and HIV-1 syndemic interactions are a major global health concern. Despite the clinical significance of co-infection, our understanding of the cellular pathophysiology and the therapeutic pharmacodynamic impact of co-infection is limited. Here, we use single-round infectious HIV-1 pseudo-typed viral-particles expressing GFP alongside M. tuberculosis expressing mCherry to study pathogenesis and treatment. We report that HIV-1 infection inhibited intracellular replication of M. tuberculosis and demonstrate the therapeutic activity of antiviral treatment (efavirenz) and antimicrobial treatment (rifampicin). The described method could be applied for detailed mechanistic studies to inform the development of novel treatment strategies
