Amyloidosis is characterized by depositing insoluble fibrillar proteins that misfold into beta-pleated sheets. This phenomenon occurs on a systemic or local level and may interfere with the function of various organs, including the heart, kidneys, and liver. Among those presenting with amyloidosis, hepatic, gastrointestinal, renal, cardiac, vitreous, and immunological involvement may occur. These manifestations are linked to several clinical presentations, varying from abdominal pain and hepatomegaly to restrictive cardiomyopathy and chronic renal failure. The two most common types of amyloid proteins are amyloid light chain (AL) and serum amyloid A (AA) proteins. AL produced by immunoglobulin light chains kappa and lambda (κ, λ) circulate systemically and accumulate in organs. At the same time, serum AA proteins are acute-phase reactants seen in infectious, chronic inflammatory states. In an immune-mediated infection such as COVID-19, serum AA levels may be a predictive factor of disease severity and a valuable biomarker to monitor the clinical course of COVID-19 patients. This report highlights a case in which infection with COVID-19 provoked an effective immune response that may have contributed to the accelerated progression of systemic amyloidosis with hepatic involvement. The study further investigates the involvement of AL and AA proteins in COVID-19 infections, including their role in synergistically exacerbating an already grueling clinical course.