Inflammatory brain injury after severe viral infection is not unique to COVID-19

Abstract

This scientific commentary refers to ‘Brain injury in COVID-19 is associated with dysregulated innate and adaptive immune responses’ by Needham et al. (https://doi.org/10.1093/brain/awac321).

Figure 1

Severe SARS-CoV-2 and influenza infection both lead to peripheral inflammation and brain damage. Elevated levels of brain injury biomarkers—namely the axonal protein neurofilament light (NfL), the microtubule-associated protein tau and the astroglial marker glial fibrillary acidic protein (GFAP)—are found in peripheral blood at the acute time point after SARS-CoV-2 infection (0–14 days from hospital admission), with the observed increases being severity-dependent. Injury biomarkers are most likely released by the destruction of neurons (N) and astrocytes (A), which probably occurs due to the excessive proinflammatory cytokine release in peripheral blood by leucocytes (L) and as a consequence, inside the CNS via microglial cells (M). A sustained cytokine response is also found in convalescent patients (>80 days from admission), with an IgM response to various antigens dominating an IgG response, by plasma blasts (P). An increased release of tau protein up to 4 months post-admission suggests a second process. In influenza patients at the subacute time point, an immune response was detected that was similar to that seen with SARS-CoV-2 infection, accompanied by a similar release of brain injury biomarkers in the peripheral blood. Altogether these findings suggest that components of the innate and adaptive immune response may interact with cells of the CNS and may be central actors in COVID-19 disease and its post-acute sequelae. Created with BioRender.com.