Previous studies of SARS-coronaviruses have described the proliferation of pro-inflammatory cytokines that are active in promoting blood–barrier breakdown, namely interleukin-8 (IL8) and monocyte chemoattractant protein-1 (MCP1) [10, 11]. A description of coronavirus infections in a Japanese encephalitis mouse model demonstrated CNS viral infection induced astrocyte and microglia proliferation, leading to increased release of IL-8 in the CSF [10]. MCP1 is another pro-inflammatory mediator that is expressed in CNS cells including astrocytes, neurons, and microglia. MCP1 may be up-regulated in conditions which target and degrade the blood–brain barrier and can recruit additional inflammatory cells as the monocytes migrate across the blood–brain barrier [11]. We hypothesize that as a result of the accumulation of inflammatory markers, there may be local cortical irritation that precipitates seizures related to COVID-19 infection. Although cerebrospinal fluid may contain markers of inflammation, the treatment of this infection is largely supportive, and with the additional risk of coagulopathy precipitated by SARS-CoV-2, a lumbar puncture may not be justifiable unless there is an alternative diagnosis to be sought. A limitation of our case series is that cerebrospinal fluid was unable to be obtained due to patient factors that made a lumbar puncture relatively contraindicated and that a CSF-PCR test for SARS-CoV-2 was not yet commercially available. As this disease continues to spread, we will continue to learn about its direct and/or indirect epileptogenesis.