Viral evolution is driven in part by the need to evade immune responses of the host. Through a process of random mutations and selection pressure by the immune system of the host, viruses can develop novel variants that can escape immune responses of both antibodies and T-cells. We are developing computational immunoinformatic tools to predict which mutations are likely driven by immune pressure, including both T-cell and antibody responses. We have been applying these tools to study the evolution of influenza and SARS-CoV-2. Identification of such mutations may help improve vaccine design to combat rapidly evolving pathogens such as SARS-CoV-2.