Role of Neuroimmune Interactions in COVID-19-related Cardiovascular Damage

Abstract

Coronavirus disease 2019 (COVID-19) has caused a global pandemic impacting over 200 countries/regions and more than 200 million patients worldwide. Among the infected patients, there is a high prevalence of COVID-19-related cardiovascular injuries. However, the specific mechanisms linking cardiovascular damage and COVID-19 remain unclear. The COVID-19 pandemic also has exacerbated the mental health burden of humans. Considering the close association between neuroimmune interactions and cardiovascular disease, this review assessed the complex pathophysiological mechanisms connecting neuroimmune interactions and cardiovascular disease. It was revealed that the mental health burden might be a pivotal accomplice causing COVID-19-associated cardiovascular damage. Specifically, the proinflammatory status of patients with a terrible mood state is closely related to overdrive of the hypothalamus-pituitary-adrenal (HPA) axis, sympathovagal imbalance, and endothelial dysfunction, which lead to an increased risk of developing cardiovascular injury during COVID-19. Therefore, during the prevention and treatment of cardiovascular complications in COVID-19 patients, particular attention should be given to relieve the mental health burden of these patients.

Immune Mechanisms Underpinning Long COVID: Collegium Internationale Allergologicum Update 2024

“…There is widespread cellular distribution of ACE2 within the nervous system [93] and direct neural invasion has been demonstrated [94]. Mechanistically, SARS-CoV-2 can be actively transported throughout neurons via the dynein-kinesin mechanism and transported in a retrograde manner via transsynaptic transfer [95][96][97].…”