2022年11月又有一篇新的研究顯示Spike protein的類澱粉生成(Amyloidogenicity)特性：
The Increased Amyloidogenicity of Spike RBD and pH-Dependent Binding to ACE2 May Contribute to the Transmissibility and Pathogenic Properties of SARS-CoV-2 Omicron as Suggested by In Silico Study---International Journal of Molecular Sciences
https://www.mdpi.com/1422-0067/23/21/13502/htm

Amyloid是Prion-like protein聚集後沉積在組織或器官中的物質。Spike protein在血中與Fibrinogen碰撞後，可促使Fibrinogen直接發生聚集(Spike protein啟動Fibrinogen聚集，但不參與Fibrinogen聚集)。正常情況下，Fibrinogen在血中要經過Thrombin切割成Fibrin，由Fibrin聚集成血液凝固的主要成份。Fibrin aggregate可被血中的Plasmin切割而溶解，但Fibrinogen aggregate不行。下圖是Fibrin aggregate與Fibrinogen aggregate的差別：

 
https://portlandpress.com/bioscirep/article/41/8/BSR20210611/229418/SARS-CoV-2-spike-protein-S1-induces-fibrin-ogen
(A)純化的螢光-Fibrinogen經Thrombin切割後形成有規則的Fibrin aggregate (Alexa Fluor 88螢光)。
(B)正常血液除掉血小板(此時Fibrinogen不會被Thrombin切割)，加入Spike protein後，Fibrinogen直接聚集成不規則如棉絮狀的Fibrinogen aggregate (Thioflavin T對Amyloid的螢光染色)。

如果你打了新冠疫苗，疫苗中有Bioactive Spike protein，進入血液中就促使Fibrinogen形成(B)圖的聚集。Long COVID syndrome的病因是感染新冠病毒發生肺炎，病毒從肺泡微血管溜進血液中，Spike protein就有機會促使Fibrinogen形成(B)圖的聚集。Fibrinogen是一種Prion-like protein，一旦發生異常聚集，便會把血中的Fibrinogen拉過來進行鏈鎖聚集，越聚越多，越聚越大(不會停止，但快慢因人而異)，形成Amyloid血栓，血栓造成的猝死可能發生在注射疫苗數月、數年或數十年後。

下圖是正常人與Long COVID syndrome病人的去血小板血漿，用Thioflavin T染Amyloid。
 
A: 正常人的去血小板血漿，用Thioflavin T只染到微量的Amyloid (不是Fibrinogen aggregate)。
B、C、D: Long COVID sydrome病人的去血小板血漿，用Thioflavin T染到奇形怪狀的大形Amyloid。
https://portlandpress.com/biochemj/article/479/4/537/230829/A-central-role-for-amyloid-fibrin-microclots-in

Spike protein與Amyloid形成的論文集如下：
A comprehensive mini-review on amyloidogenesis of different SARS-CoV-2 proteins and its effect on amyloid formation in various host proteins---3 biotech, October 2022
https://link.springer.com/article/10.1007/s13205-022-03390-1

SARS-CoV-2, long COVID, prion disease and neurodegeneration---Frontiers in Neuorscience, September 2022
https://www.frontiersin.org/articles/10.3389/fnins.2022.1002770/full

SARS-CoV-2 Spike protein S2 subunit modulates γ-secretase and enhances amyloid-β production in COVID-19 neuropathy---Cell Discovery, September 2022
https://www.nature.com/articles/s41421-022-00458-3

SARS-CoV-2 spike protein aggregation is triggered by bacterial lipopolysaccharide, FEBS Letters, September 2022
https://febs.onlinelibrary.wiley.com/doi/full/10.1002/1873-3468.14490

Amyloidogenesis of SARS-CoV-2 Spike Protein---Journal of the American Chemical Society, May 2022
https://pubs.acs.org/doi/10.1021/jacs.2c03925

Adverse effects of COVID-19 mRNA vaccines: the spike hypothesis---Trends in Molecular Science, April 2022
https://www.cell.com/trends/molecular-medicine/fulltext/S1471-4914(22)00103-4

The Possible Role of Prion-Like Viral Protein Domains on the Emergence of Novel Viruses as SARS-CoV-2---Journal of Molecular Evolution, April 2022
https://link.springer.com/article/10.1007/s00239-022-10054-4

Prion-like Domains in Spike Protein of SARS-CoV-2 Differ across Its Variants and Enable Changes in Affinity to ACE2---Microorganisms, January 2022
https://www.mdpi.com/2076-2607/10/2/280

Highly efficient intercellular spreading of protein misfolding mediated by viral ligand-receptor interactions---Nature Communications, October 2021
https://www.nature.com/articles/s41467-021-25855-2

SARS-CoV-2 spike protein S1 induces fibrin(ogen) resistant to fibrinolysis: implications for microclot formation in COVID-19---Bioscience Reports, August 2021
https://portlandpress.com/bioscirep/article/41/8/BSR20210611/229418/SARS-CoV-2-spike-protein-S1-induces-fibrin-ogen

SARS-CoV-2 spike protein interactions with amyloidogenic proteins: Potential clues to neurodegeneration---Biochemical and Biophysical Research Communication, May 2021
https://www.sciencedirect.com/science/article/pii/S0006291X2100499X