Infection is a major cause of morbidity and mortality individuals with mitochondrial disease, frequently triggering metabolic decompensation, multiorgan dysfunction, and neurologic deterioration. In the context of the recent COVID19 pandemic, people with mitochondrial disease are at increased risk for severe disease and poor outcomes if infected. However, the mechanisms for this link between infection and clinical decline are incompletely understood. Given that people with mitochondrial disease are particularly susceptible to infection and may experience delayed recovery, we hypothesize that this is in part due to immune factors that influence host-pathogen interactions. The purpose of this protocol is to collect biological specimens to identify immune signatures that contribute to the phenotype of infection and outcomes in patients with mitochondrial disease who become ill during the COVID19 pandemic. In order to compare these cases with others of similar genetic backgrounds and environmental exposures, we will also collect specimens from family members. We will then examine how these signatures correlate with comprehensive quantifiable clinical measures throughout the course of disease, from presenting symptoms, through acute decompensation, stabilization and convalescence. While this protocol is developed during the COVID-19 pandemic with a focus on a specific infectious pathogen, we hope that this study will extend beyond the pandemic in an effort to more broadly understand acute infectious illness in patients with mitochondrial disease. Additionally, it will serve as a remote adjunct to the NIH MINI Study, a natural history study focused on the immunophenotype of mitochondrial disease that is conducted at the NIH Clinical Center.