What HIV in the brain can teach us about SARS-CoV-2 neurologic complications?

Al-Harthi, Lena; Campbell, Edward M; Schneider, Julie A; Bennett, David A

Severe acute respiratory syndrome coronavirus 2 (SARS- CoV-2) is the etiologic agent of COVID-19, a disease that as of July 10, 2020, has infected over 12 million people and killed over 500,000. COVID-19 infection leads to Acute Respiratory Distress Syndrome (ARDS) in a subset of patients and is a primary driver of acute morbidity in infected persons. However, it is becoming increasingly clear that SARS-CoV-2 infection drives dysfunction and pathology outside the lungs, including reports of renal, cardiac and neurological complications. Here, we summarize the known incidence and evidence of neurological complications associated with SARS-CoV-2 infection and other pathogenic coronaviruses. These studies describe a poorly understood spectrum of COVID-19 CNS symptoms, ranging from common and subclinical issues such as anosmia and headache to more concerning reports of stroke and encephalopathy. We discuss potential mechanisms of pathogenesis, including a discussion of how the understanding of neurological complications known to occur in HIV-1 patients may provide insight into SARS-CoV-2 associated neurologic manifestations. Specifically, three hypotheses are discussed which are informed by decades of knowledge about HIV pathogenesis in the brain, which include a potential direct viral effect, an indirect viral effect, and/or a neuroimmune axis effect. Individually or in combination these potential effects may contribute to COVID-19 neurologic complications.