Hypothesis: AA amyloidosis is a factor causing systemic complications after coronavirus disease

Area of Science:

• Immunology
• Pathology
• Infectious Diseases

Background:

• Severe COVID-19 is associated with systemic chronic inflammation and thrombosis.
• High cytokine levels during severe COVID-19 correlate with Serum amyloid A (SAA) protein overproduction.
• Existing research primarily identifies elevated SAA as a biomarker for COVID-19.

Purpose of the Study:

• To propose a novel hypothesis linking AA amyloidosis to the systemic complications observed in severe COVID-19.
• To explore the potential role of SAA overproduction and subsequent amyloidosis in COVID-19 pathogenesis.

Main Methods:

• This study presents a hypothesis based on existing literature and clinical observations.
• It involves a comparative analysis of the clinical manifestations of severe COVID-19 and AA amyloidosis.

Main Results:

• The clinical picture of severe COVID-19 complications shares striking similarities with AA amyloidosis.
• SAA overproduction, a known consequence of severe COVID-19, can lead to systemic AA amyloidosis.
• SAA amyloid deposits are cytotoxic, inducing inflammation and thrombosis in various organs.

Conclusions:

• AA amyloidosis is hypothesized to be a contributing factor to the systemic complications following severe COVID-19 infection.
• Further research is warranted to investigate the direct causal link between SAA-induced amyloidosis and COVID-19 pathogenesis.