Influenza A virus (IAV) creates a significant burden of disease in the human population every year, including millions of cases of severe illness, and hundreds of thousands of deaths. Like all viruses, IAV is an obligate parasite: it requires the host cell to carry out its replication cycle and produce its progeny. In order to hijack the host cell machinery, IAV induces significant changes to the subcellular architecture, including the remodeling of several membrane-bound organelles. Some of these organelle changes have been well-characterized, including the production of genome replication compartments in the nucleus; fission and fusion of the mitochondria for metabolic regulation; the folding of the plasma membrane for virus entry and egress; and fusion between the virus and endosomal membranes. One subcellular organelle that is not well-characterized during IAV infection is the peroxisome which supports lipid metabolism and immune signaling in uninfected contexts. In this work, I studied the peroxisome during infection, observing a steady decrease in abundance, rapid increases in surface area and volume, a steady increase in surface area to volume ratio, and an increase in tethering to the microtubules and endoplasmic reticulum. Next, I characterized the protein-protein interactions driving these changes to peroxisomal morphology and motility. I hypothesize that IAV-induced peroxisomal regulation enables the virus to rewire cellular lipid metabolism for the production of the envelopes of its progeny. Conversely, the inhibition of the lipid metabolism pathways on which IAV is dependent, and the upregulation of peroxisomal immune signaling represent potential mechanisms for therapeutic intervention.