COVID-19 is estimated to be three times more contagious than influenza, SARS and MERS. Variants in symptoms range from mild illness to significant hypoxia. The gastrointestinal (GI) tract is a notable site of infection, producing symptoms such as diarrhea, nausea, and vomiting; however, the virus can be present in the GI tract and persist asymptomatically. SARS-CoV-2 uses a spike (S) protein to inhibit angiotensin-converting enzyme 2 (ACE2), which is present on epithelial cells lining the lungs and GI tract. This enzyme is an important regulator in the GI tract for innate immunity, microbiome ecology, and susceptibility to inflammatory conditions; therefore, the inhibition of ACE2 can result in intestinal inflammation. Kim, H. S. (2021) suggests that gut health at the time of infection is a critical indicator of symptom development. In patients with disrupted gut barriers such as “leaky gut” syndrome, SARS-CoV-2 binds to ACE2 in the GI tract and can enter the blood stream, producing systemic symptoms. Patients with healthy gut barrier and flora did not exhibit GI symptoms and excreted the virus in their feces. Healthy GI tracts have higher numbers of Treg cells, which are activated by butyrate. Proposed treatments include increasing beneficial gut bacteria with next-generation probiotics and butyrate-producing microbes. Additionally, increasing dietary fibre, which can be utilized by beneficial gut bacteria to produce butyrate, can significantly improve gut health.