COVID-19 Exposure Unmasking Systemic Amyloidosis With Hepatic Predominance

Russe-Russe, Jose R.; Abramowitz, Chiya; Pellegrini, James R.; Betancourt, Alejandro Alvarez; Cohen, Ricky; Baldino, Michael; Crandall, Ronald; Kagolanu, Deepthi; Mejía, José Fernando; Rizvon, Kaleem

doi:10.7759/cureus.31092

Cited by 2 publications

(2 citation statements)

References 11 publications

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“…The SAA1 i.e. the AA precursor protein is synthesized in the liver and could be triggered by COVID-19 infection and associated with AL-amyloid seeds [ 138 ]. This case would strengthen the hypothesis of AA amyloidosis is a factor causing systemic complications after COVID-19 disease [ 139 ].…”

Section: Covid-19 Sequelae With Similarities and Possible Connections...mentioning

confidence: 99%

Viruses and amyloids - a vicious liaison

Hammarström

Nyström

2023

Prion

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The crosstalk between viral infections, amyloid formation and neurodegeneration has been discussed with varying intensity since the last century. Several viral proteins are known to be amyloidogenic. Post-acute sequalae (PAS) of viral infections is known for several viruses. SARS-CoV-2 and COVID-19 implicate connections between amyloid formation and severe outcomes in the acute infection, PAS and neurodegenerative diseases. Is the amyloid connection causation or just correlation? In this review we highlight several aspects where amyloids and viruses meet. The evolutionary driving forces that dictate protein amyloid formation propensity are different for viruses compared to prokaryotes and eukaryotes, while posttranslational endoproteolysis appears to be a common mechanism leading up to amyloid formation for both viral and human proteins. Not only do human and viral proteins form amyloid irrespective of each other but there are also several examples of co-operativity between amyloids, viruses and the inter-, and intra-host spread of the respective entity. Abnormal blood clotting in severe and long COVID and as a side effect in some vaccine recipients has been connected to amyloid formation of both the human fibrin and the viral Spike-protein. We conclude that there are many intersects between viruses and amyloids and, consequently, amyloid and virus research need to join forces here. We emphasize the need to accelerate development and implementation in clinical practice of antiviral drugs to preclude PAS and downstream neurological damage. There is also an ample need for retake on suitable antigen targets for the further development of next generation of vaccines against the current and coming pandemics.

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Section: Covid-19 Sequelae With Similarities and Possible Connections...mentioning

confidence: 99%

Viruses and amyloids - a vicious liaison

Hammarström

Nyström

2023

Prion

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“…It is well known that SAA lies at the center of AA amyloidosis pathogenesis, so it could be expected that any elevation of serum SAA can accelerate the progression of amyloidosis in patients with this disease. Such an assumption was valid during the COVID-19 infection, where the rise in SAA levels worsened the existing AA amyloidosis (55). In patients without amyloidosis, there are some indications that SARS-CoV-2 envelope protein can speed up the formation of SAA amyloid.…”

Section: Serum Amyloid a And Amyloidosis In Covid-19mentioning

confidence: 99%

Significance of serum amyloid A for the course and outcome of SARS-CoV-2 infection

Jegorović,

Šipetić-Grujičić,

Ignjatović

2023

Medicinski podmladak

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The occurrence of a new coronavirus, Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), quickly became a global threat after it had spread across the continents in just a few months. Over the next three years, it caused infections in over 646.6 million people and resulted in over 6.6 million deaths. As a novel disease, Coronavirus Disease 19 (COVID-19) became the subject of intensive research. Due to various clinical manifestations of the infection with possible fatal outcomes, it became evident that a finer understanding of COVID-19 pathogenesis, clinical manifestations, and complications is necessary. Investigation of acute-phase reaction as a component of the immune system response to infection can be very helpful. Serum amyloid A (SAA) was investigated for this purpose as one of the acute-phase reactants primarily synthesized by the hepatocytes in response to pro-inflammatory cytokines. It has been found that elevated SAA levels were independent factors for gastrointestinal manifestations and liver injury during COVID-19 but also one of the factors in COVID19-associated coagulopathy. Studies showed that SAA levels positively correlate with disease severity and prognosis. Patients with severe infection demonstrated significantly higher levels of SAA. Higher SAA levels were observed in COVID-19 patients with chronic diseases such as diabetes mellitus, hypertension, cerebrovascular diseases, and obesity, all recognized as independent risk factors for critical disease and poor prognosis. Patients with COVID-19 who died had higher levels of SAA than survivors. This short review will summarize current studies and knowledge about SSA in COVID-19, its role in the pathogenesis of SARS-CoV-2 infection, and its clinical usefulness in COVID-19 patients.

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COVID-19 Exposure Unmasking Systemic Amyloidosis With Hepatic Predominance

Cited by 2 publications

References 11 publications

Viruses and amyloids - a vicious liaison

Viruses and amyloids - a vicious liaison

Significance of serum amyloid A for the course and outcome of SARS-CoV-2 infection

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