The Spike Protein’s Presence, Long COVID, COVID Infection and Parkinson’s Neutrophil Elastase cleaves the Spike Protein into amyloidogenic fragments which may stabilize αS-dimer allowing neurotoxic aggregate seeding. WALTER M CHESNUT SEP 22
The Spike Protein’s Presence, Long COVID, COVID Infection and Parkinson’s Neutrophil Elastase cleaves the Spike Protein into amyloidogenic fragments which may stabilize αS-dimer allowing neurotoxic aggregate seeding. WALTER M CHESNUT SEP 22
READ IN APP
It has been over three years since I wrote about how I believed Neutrophil Elastase in the presence of the Spike Protein could lead to a new kind of prionopathy – multiple amyloidoses.
A paper published in late August of this year shows that this may indeed be the case as it proves the mechanism for the Spike Protein to induce one form of prionopathy - Parkinson’s. The paper shows that proteases, such as Neutrophil Elastase, cleave the Spike Protein into fragments which can stabilize αS-dimer. This can then cause aggregate seeding leading to the development of Parkinson’s. The paper is extremely technical, so I will only quote elements which are more readily understandable.
There is evidence that amyloidogenic segments in SARS-COV-2 proteins can induce aggregation of α-synuclein (αS), the main component of brain-located amyloids whose presence is connected with Parkinson’s Disease (PD). Using molecular dynamic simulations, we could show in earlier work that SARS-COV-2 protein fragments shift the ensemble of αS chains toward more aggregation-prone conformations. However, the mechanism by which these chains assemble into fibrils, the presumed neurotoxic agent in PD, is not clear. The first step on that route are dimers. For this reason, we have now, using again molecular dynamics simulations, studied how the fragment 194FKNIDGYFKI203 (FI10) of the SARS-COV-2 spike protein, and the fragment 54SFYVYSRVK62 (SK9) of the envelope protein, alter the ensemble of α-synuclein dimers.
A hallmark of Parkinson’s Disease (PD) is the presence of amyloids located in the brain of patients that are made mainly of α-synuclein (αS) and appear to be the neurotoxic agent.1, 2 As there have been correlations observed between falling ill with COVID-19 and outbreaks of PD,3 and SARS-COV-2 induced αS amyloid formation has been found in vitro,4 we and other groups5 have proposed that amyloidogenic SARS-COV-2 protein regions can enhance aggregation of αS potentially causing PD. We have speculated that during acute inflammation, as commonly seen in COVID-19, neutrophils release enzymes that cleave SARS-COV-2 proteins into amyloidogenic fragments which in turn cross-seed human proteins. Such cleavage has been shown for the amyloidogenic segment of residues 194FKNIDGYFKI203 (FI10) of the spike protein.
In summary, our results indicate that the two viral protein fragments may stabilize αS-dimer, potentially allowing them to seed neurotoxic aggregates.
The article is extremely keen on what but is very lackadaisical when it comes to when.
We have speculated that during acute inflammation, as commonly seen in COVID-19, neutrophils release enzymes that cleave SARS-COV-2 proteins into amyloidogenic fragments which in turn cross-seed human proteins.
This is where the discussion begins. I do not believe that this mechanism is limited to occurring only during “acute inflammation, as commonly seen in COVID-19.” I will now present evidence that it is most likely occurring in several other instances of Spike Protein presence.
mRNA
Let’s cut right to the chase and start with the eternal elephant in the room. mRNA gene therapies do cause the release of Neutrophil Elastase. The question is, how often and to what extent? Unsurprisingly, in the case of vaccine hypersensitivity it is certainly present.
Main mechanisms of potential COVID-19 vaccine-induced hypersensitivity. The classical mechanism involves specific IgE-dependent mast cell and basophil activation leading to histamine/tryptase release. The alternative or additional mechanism involves specific IgG-dependent neutrophil activation leading to the release of reactive oxygen species (ROS), proteases such as elastase or neutrophil extracellular traps (NETs). Finally, several other mast cell activation mechanisms are suspected to play a role via C3a or C5a fixation to their receptors, or via the direct activation of MRGPRX2 by the vaccine.
Yet even those simply receiving a COVID vaccine experienced elevated NETs, which are responsible for Neutrophil Elastase.
Neutrophil extracellular traps (NETs) play a role in innate pathogen defense and also trigger B-cell response by providing antigens. NETs have been linked to vaccine-induced thrombotic thrombocytopenia. We postulated a potential link between NET biomarkers, NET-promoting autoantibodies, and adverse events (AEs) after COVID-19 vaccine boosters. Healthy donors (HDs) who received ChAdOx1-S (A), mRNA-1273 (M), or recombinant protein (MVC–COV1901) vaccines at the National Taiwan University Hospital between 2021 and 2022 were recruited. We measured serial NET-associated biomarkers, citrullinated-histone3 (citH3), and myeloperoxidase (MPO)-DNA. Serum citH3 and MPO-DNA were significantly or numerically higher in HDs who reported AEs (n = 100, booster Day 0/Day 30, p = 0.01/p = 0.03 and p = 0.30/p = 0.35, respectively). We also observed a positive correlation between rash occurrence in online diaries and elevated citH3. A linear mixed model also revealed significantly higher citH3 levels in mRNA-1273/ChAdOx1-S recipients than MVC-COV1901 recipients. Significant positive correlations were observed between the ratios of anti-heparin platelet factor 4 and citH3 levels on Booster Day 0 and naïve and between the ratios of anti-NET IgM and citH3 on Booster Day 30/Day 0 in the AA-M and MM-M group, respectively. The increased levels of citH3/MPO-DNA accompanied by NET-promoting autoantibodies suggest a potential connection between mRNA-1273/ChAdOx1-S vaccines and cardiovascular complications.
Temporal changes in biomarkers of neutrophil extracellular traps and NET-promoting autoantibodies following adenovirus-vectored, mRNA, and recombinant protein COVID-19 vaccination https://onlinelibrary.wiley.com/doi/10.1002/jmv.29556
So, it would seem completely logical that post-COVID mRNA there is a very high likelihood that the “ingredients” for developing Parkinson’s are present.
Long COVID
What makes the above concerning is that it may be any exposure to the Spike Protein increases the risk of developing (among many things) Parkinson’s. Let’s look at Long COVID and NETs.
The underlying pathophysiology of long COVID has become a topic of intense research discussion. While chronic inflammation in long COVID has received considerable attention, the role of neutrophils, which are the most abundant of all immune cells and primary responders to inflammation, has been unfortunately overlooked, perhaps due to their short lifespan. In this review, we discuss the emerging role of neutrophil extracellular traps (NETs) in the persistent inflammatory response observed in long COVID patients. We present early evidence linking the persistence of NETs to pulmonary fibrosis, cardiovascular abnormalities, and neurological dysfunction in long COVID. Several uncertainties require investigation in future studies. These include the mechanisms by which SARS-CoV-2 brings about sustained neutrophil activation phenotypes after infection resolution; whether the heterogeneity of neutrophils seen in acute SARS-CoV-2 infection persists into the chronic phase; whether the presence of autoantibodies in long COVID can induce NETs and protect them from degradation; whether NETs exert differential, organ-specific effects; specifically which NET components contribute to organ-specific pathologies, such as pulmonary fibrosis; and whether senescent cells can drive NET formation through their pro-inflammatory secretome in long COVID.
The Spike Protein is present post mRNA. in Long COVID, and simply after mild infection. This shows how any exposure to the Spike Protein may raise the risk of developing Parkinson’s.
Growing research suggests that viral antigens and viral RNA, various proteins or genetic material, remain present and active in the body’s tissues following acute infection. A Harvard study, for example, found that the COVID-19 spike protein—a protein vital in allowing the SARS-CoV-2 virus to infect cells—continues to circulate in some Long COVID patients’ blood up to a year after infection. This protein can also be found in the blood of individuals who had COVID-19 but did not experience lingering symptoms.
The major takeaway from this is, once again, COVID is not a “cold.” The more we look, the more we find so many different kinds of long-term dysregulation after becoming infected with the virus or being exposed to its proteins. Even for those who do not experience Long COVID. Yet the more we understand, the more steps we can take to prevent and treat the various forms of dysregulation. I will continue to seek understanding and to search for therapeutics. Please have a blessed week.
Thank you, as always, for your continued support, dialog and readership. We gained two more paid subscribers since Friday. Each week, between now and Christmas, I am asking if one reader or subscriber would please become a Founding Member of this Substack. Helping make this Substack sustainable keeps the engines running. Please consider becoming a paid subscriber. I will keep working and reporting back to you.
I cannot do this without your support. My research is funded only by Paid Subscription to this Substack and Direct Donation. Currently (9/22/25), of the 14K Subscribers to this Substack, only 359 are Paid Subscribers. Great thanks to the two new Paid Subscribers since Monday. It is an important goal to have a total of 700 Paid Subscribers for sustainability. Please email me for addresses if you would like to donate Crypto. If you are comfortably able to become a Paid Subscriber, please consider doing so. Or, please donate directly at
The Spike Protein’s Presence, Long COVID, COVID Infection and Parkinson’s
Neutrophil Elastase cleaves the Spike Protein into amyloidogenic fragments which may stabilize αS-dimer allowing neurotoxic aggregate seeding.
WALTER M CHESNUT
SEP 22
尖峰蛋白的存在、长新冠肺炎、新冠肺炎感染和帕金森氏症
中性粒细胞弹性酶将尖刺蛋白切割成淀粉样蛋白原片段，可以稳定αS-二聚体，允许神经毒性聚集播种。
沃尔特·M·栗子
9月22日
https://open.substack.com/pub/wmcresearch/p/the-spike-proteins-presence-long
The Spike Protein’s Presence, Long COVID, COVID Infection and Parkinson’s
Neutrophil Elastase cleaves the Spike Protein into amyloidogenic fragments which may stabilize αS-dimer allowing neurotoxic aggregate seeding.
WALTER M CHESNUT
SEP 22
READ IN APP
It has been over three years since I wrote about how I believed Neutrophil Elastase in the presence of the Spike Protein could lead to a new kind of prionopathy – multiple amyloidoses.
ASP: SPIKE PROTEIN AMYLOIDOSIS
https://wmcresearch.substack.com/p/asp-spike-protein-amyloidosis
A paper published in late August of this year shows that this may indeed be the case as it proves the mechanism for the Spike Protein to induce one form of prionopathy - Parkinson’s. The paper shows that proteases, such as Neutrophil Elastase, cleave the Spike Protein into fragments which can stabilize αS-dimer. This can then cause aggregate seeding leading to the development of Parkinson’s. The paper is extremely technical, so I will only quote elements which are more readily understandable.
There is evidence that amyloidogenic segments in SARS-COV-2 proteins can induce aggregation of α-synuclein (αS), the main component of brain-located amyloids whose presence is connected with Parkinson’s Disease (PD). Using molecular dynamic simulations, we could show in earlier work that SARS-COV-2 protein fragments shift the ensemble of αS chains toward more aggregation-prone conformations. However, the mechanism by which these chains assemble into fibrils, the presumed neurotoxic agent in PD, is not clear. The first step on that route are dimers. For this reason, we have now, using again molecular dynamics simulations, studied how the fragment 194FKNIDGYFKI203 (FI10) of the SARS-COV-2 spike protein, and the fragment 54SFYVYSRVK62 (SK9) of the envelope protein, alter the ensemble of α-synuclein dimers.
A hallmark of Parkinson’s Disease (PD) is the presence of amyloids located in the brain of patients that are made mainly of α-synuclein (αS) and appear to be the neurotoxic agent.1, 2 As there have been correlations observed between falling ill with COVID-19 and outbreaks of PD,3 and SARS-COV-2 induced αS amyloid formation has been found in vitro,4 we and other groups5 have proposed that amyloidogenic SARS-COV-2 protein regions can enhance aggregation of αS potentially causing PD. We have speculated that during acute inflammation, as commonly seen in COVID-19, neutrophils release enzymes that cleave SARS-COV-2 proteins into amyloidogenic fragments which in turn cross-seed human proteins. Such cleavage has been shown for the amyloidogenic segment of residues 194FKNIDGYFKI203 (FI10) of the spike protein.
In summary, our results indicate that the two viral protein fragments may stabilize αS-dimer, potentially allowing them to seed neurotoxic aggregates.
The Effect of SARS-COV-2 Protein Fragments on the Dimerization of α-Synuclein
https://www.biorxiv.org/content/10.1101/2025.08.26.672456v1.full
The article is extremely keen on what but is very lackadaisical when it comes to when.
We have speculated that during acute inflammation, as commonly seen in COVID-19, neutrophils release enzymes that cleave SARS-COV-2 proteins into amyloidogenic fragments which in turn cross-seed human proteins.
The Effect of SARS-COV-2 Protein Fragments on the Dimerization of α-Synuclein
https://www.biorxiv.org/content/10.1101/2025.08.26.672456v1.full
This is where the discussion begins. I do not believe that this mechanism is limited to occurring only during “acute inflammation, as commonly seen in COVID-19.” I will now present evidence that it is most likely occurring in several other instances of Spike Protein presence.
mRNA
Let’s cut right to the chase and start with the eternal elephant in the room. mRNA gene therapies do cause the release of Neutrophil Elastase. The question is, how often and to what extent? Unsurprisingly, in the case of vaccine hypersensitivity it is certainly present.
Main mechanisms of potential COVID-19 vaccine-induced hypersensitivity. The classical mechanism involves specific IgE-dependent mast cell and basophil activation leading to histamine/tryptase release. The alternative or additional mechanism involves specific IgG-dependent neutrophil activation leading to the release of reactive oxygen species (ROS), proteases such as elastase or neutrophil extracellular traps (NETs). Finally, several other mast cell activation mechanisms are suspected to play a role via C3a or C5a fixation to their receptors, or via the direct activation of MRGPRX2 by the vaccine.
Immediate hypersensitivity to COVID-19 vaccines: Focus on biological diagnosis
https://www.frontiersin.org/journals/allergy/articles/10.3389/falgy.2022.1007602/full
Yet even those simply receiving a COVID vaccine experienced elevated NETs, which are responsible for Neutrophil Elastase.
Neutrophil extracellular traps (NETs) play a role in innate pathogen defense and also trigger B-cell response by providing antigens. NETs have been linked to vaccine-induced thrombotic thrombocytopenia. We postulated a potential link between NET biomarkers, NET-promoting autoantibodies, and adverse events (AEs) after COVID-19 vaccine boosters. Healthy donors (HDs) who received ChAdOx1-S (A), mRNA-1273 (M), or recombinant protein (MVC–COV1901) vaccines at the National Taiwan University Hospital between 2021 and 2022 were recruited. We measured serial NET-associated biomarkers, citrullinated-histone3 (citH3), and myeloperoxidase (MPO)-DNA. Serum citH3 and MPO-DNA were significantly or numerically higher in HDs who reported AEs (n = 100, booster Day 0/Day 30, p = 0.01/p = 0.03 and p = 0.30/p = 0.35, respectively). We also observed a positive correlation between rash occurrence in online diaries and elevated citH3. A linear mixed model also revealed significantly higher citH3 levels in mRNA-1273/ChAdOx1-S recipients than MVC-COV1901 recipients. Significant positive correlations were observed between the ratios of anti-heparin platelet factor 4 and citH3 levels on Booster Day 0 and naïve and between the ratios of anti-NET IgM and citH3 on Booster Day 30/Day 0 in the AA-M and MM-M group, respectively. The increased levels of citH3/MPO-DNA accompanied by NET-promoting autoantibodies suggest a potential connection between mRNA-1273/ChAdOx1-S vaccines and cardiovascular complications.
Temporal changes in biomarkers of neutrophil extracellular traps and NET-promoting autoantibodies following adenovirus-vectored, mRNA, and recombinant protein COVID-19 vaccination
https://onlinelibrary.wiley.com/doi/10.1002/jmv.29556
So, it would seem completely logical that post-COVID mRNA there is a very high likelihood that the “ingredients” for developing Parkinson’s are present.
Long COVID
What makes the above concerning is that it may be any exposure to the Spike Protein increases the risk of developing (among many things) Parkinson’s. Let’s look at Long COVID and NETs.
The underlying pathophysiology of long COVID has become a topic of intense research discussion. While chronic inflammation in long COVID has received considerable attention, the role of neutrophils, which are the most abundant of all immune cells and primary responders to inflammation, has been unfortunately overlooked, perhaps due to their short lifespan. In this review, we discuss the emerging role of neutrophil extracellular traps (NETs) in the persistent inflammatory response observed in long COVID patients. We present early evidence linking the persistence of NETs to pulmonary fibrosis, cardiovascular abnormalities, and neurological dysfunction in long COVID. Several uncertainties require investigation in future studies. These include the mechanisms by which SARS-CoV-2 brings about sustained neutrophil activation phenotypes after infection resolution; whether the heterogeneity of neutrophils seen in acute SARS-CoV-2 infection persists into the chronic phase; whether the presence of autoantibodies in long COVID can induce NETs and protect them from degradation; whether NETs exert differential, organ-specific effects; specifically which NET components contribute to organ-specific pathologies, such as pulmonary fibrosis; and whether senescent cells can drive NET formation through their pro-inflammatory secretome in long COVID.
Neutrophil extracellular traps and long COVID
https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2023.1254310/full
And now, COVID infection itself.
COVID Infection
The Spike Protein is present post mRNA. in Long COVID, and simply after mild infection. This shows how any exposure to the Spike Protein may raise the risk of developing Parkinson’s.
Growing research suggests that viral antigens and viral RNA, various proteins or genetic material, remain present and active in the body’s tissues following acute infection. A Harvard study, for example, found that the COVID-19 spike protein—a protein vital in allowing the SARS-CoV-2 virus to infect cells—continues to circulate in some Long COVID patients’ blood up to a year after infection. This protein can also be found in the blood of individuals who had COVID-19 but did not experience lingering symptoms.
The Long COVID Puzzle: Autoimmunity, Inflammation, and Other Possible Causes
https://www.yalemedicine.org/news/the-long-covid-puzzle-autoimmunity-inflammation-and-other-possible-causes
The major takeaway from this is, once again, COVID is not a “cold.” The more we look, the more we find so many different kinds of long-term dysregulation after becoming infected with the virus or being exposed to its proteins. Even for those who do not experience Long COVID. Yet the more we understand, the more steps we can take to prevent and treat the various forms of dysregulation. I will continue to seek understanding and to search for therapeutics. Please have a blessed week.
Thank you, as always, for your continued support, dialog and readership. We gained two more paid subscribers since Friday. Each week, between now and Christmas, I am asking if one reader or subscriber would please become a Founding Member of this Substack. Helping make this Substack sustainable keeps the engines running. Please consider becoming a paid subscriber. I will keep working and reporting back to you.
I cannot do this without your support. My research is funded only by Paid Subscription to this Substack and Direct Donation. Currently (9/22/25), of the 14K Subscribers to this Substack, only 359 are Paid Subscribers. Great thanks to the two new Paid Subscribers since Monday. It is an important goal to have a total of 700 Paid Subscribers for sustainability. Please email me for addresses if you would like to donate Crypto. If you are comfortably able to become a Paid Subscriber, please consider doing so. Or, please donate directly at
这篇文章主要讨论了中性粒细胞弹性蛋白酶（Neutrophil Elastase）如何通过切割新冠病毒刺突蛋白（Spike Protein）形成淀粉样片段，这些片段可能有助于帕金森病（Parkinson’s Disease）的发生。以下是中文翻译：
⸻
刺突蛋白的存在、长期新冠、COVID-19感染与帕金森病
中性粒细胞弹性蛋白酶将刺突蛋白切割成淀粉样片段，这些片段可能稳定α-突触核蛋白二聚体，从而引发神经毒性聚集物的种子形成。
沃尔特·M·切斯纳特（WALTER M. CHESNUT）
2025年9月22日
⸻
自从三年前我写到我认为中性粒细胞弹性蛋白酶在刺突蛋白存在的情况下，可能会导致一种新的朊毒症——多重淀粉样变病（multiple amyloidoses）以来，已经过去了三年多。
ASP：刺突蛋白淀粉样变病
https://wmcresearch.substack.com/p/asp-spike-protein-amyloidosis
今年8月底发布的一篇论文显示，这一机制确实存在，证明刺突蛋白可以引发一种朊毒症——帕金森病。这篇论文表明，像中性粒细胞弹性蛋白酶（Neutrophil Elastase）这样的蛋白酶会将刺突蛋白切割成片段，这些片段可以稳定αS二聚体，从而导致聚集物种子形成，进而引发帕金森病。这篇文章非常技术性，所以我只会引用一些较为易懂的内容。
有证据表明，SARS-COV-2蛋白中的淀粉样变性片段可以诱导α-突触核蛋白（αS）的聚集，αS是大脑淀粉样蛋白的主要成分，其存在与帕金森病（PD）有关。我们在早期的工作中通过分子动力学模拟表明，SARS-COV-2蛋白片段会将αS链的集合体转变为更易聚集的构象。然而，αS链如何组装成纤维，成为帕金森病中假定的神经毒性物质，机制尚不明确。这个过程的第一步是形成二聚体。因此，我们再次使用分子动力学模拟研究了SARS-COV-2刺突蛋白片段194FKNIDGYFKI203（FI10）和包膜蛋白片段54SFYVYSRVK62（SK9）如何改变α-突触核蛋白二聚体的集合体。
帕金森病的标志是患者大脑中存在由主要由α-突触核蛋白（αS）组成的淀粉样物质，这些物质似乎是神经毒性物质。1, 2 由于观察到COVID-19感染与帕金森病暴发之间的相关性，3 并且在体外发现了SARS-COV-2诱导的αS淀粉样形成，4 我们和其他研究小组5 提出了SARS-COV-2蛋白区域可以增强αS的聚集，可能引发帕金森病。我们推测，在急性炎症期间，如COVID-19中常见的情况，中性粒细胞释放酶类，将SARS-COV-2蛋白切割成淀粉样片段，这些片段反过来会交叉诱导人体蛋白聚集。这种切割已经在刺突蛋白的淀粉样片段194FKNIDGYFKI203（FI10）中得到验证。
总之，我们的研究结果表明，这两个病毒蛋白片段可能通过稳定αS二聚体，进而促进神经毒性聚集物的形成。
SARS-COV-2蛋白片段对α-突触核蛋白二聚体化的影响
https://www.biorxiv.org/content/10.1101/2025.08.26.672456v1.full
这篇文章非常关注“是什么”机制，但对“何时”机制的讨论则较为松散。
我们推测，在急性炎症期间，如COVID-19中常见的情况，中性粒细胞会释放酶类，将SARS-COV-2蛋白切割成淀粉样片段，这些片段会交叉种子人体蛋白。
SARS-COV-2蛋白片段对α-突触核蛋白二聚体化的影响
https://www.biorxiv.org/content/10.1101/2025.08.26.672456v1.full
讨论从这里开始。我不认为这个机制仅限于仅在“急性炎症，如COVID-19中常见”的情况下发生。我将展示证据，证明它很可能在几种刺突蛋白存在的其他情况下也会发生。
⸻
mRNA
让我们直接进入重点，首先讨论一下长期以来的“禁忌话题”。mRNA基因治疗确实会导致中性粒细胞弹性蛋白酶的释放。问题是，它会在多频繁和多大程度上发生？毫不奇怪，在疫苗超敏反应的情况下，它是存在的。
COVID-19疫苗引起的超敏反应的主要机制
经典机制涉及特异性IgE依赖的肥大细胞和嗜碱性粒细胞激活，导致组胺/色氨酸酶的释放。另一个或额外的机制涉及特异性IgG依赖的中性粒细胞激活，导致反应性氧种（ROS）释放，以及弹性蛋白酶或中性粒细胞外陷阱（NETs）的释放。最后，还有一些其他的肥大细胞激活机制通过C3a或C5a固定到其受体，或通过疫苗直接激活MRGPRX2。
COVID-19疫苗的即刻超敏反应：聚焦生物学诊断
https://www.frontiersin.org/journals/allergy/articles/10.3389/falgy.2022.1007602/full
即便是仅接种COVID疫苗的人也出现了NETs水平升高，而NETs正是中性粒细胞弹性蛋白酶的来源。
中性粒细胞外陷阱（NETs）在先天免疫防御中的作用，并触发B细胞反应，提供抗原。NETs已被与疫苗引起的血栓性血小板减少症相关联。我们推测NET生物标志物、NET促进的自身抗体与COVID-19疫苗加强针后的不良事件（AEs）之间可能存在联系。
https://onlinelibrary.wiley.com/doi/10.1002/jmv.29556
因此，看起来非常合乎逻辑的是，在接种COVID-19 mRNA疫苗后，发展帕金森病的“成分”很可能已经出现。
⸻
长期新冠
令人担忧的是，刺突蛋白的任何暴露都可能增加患帕金森病（以及其他许多疾病）的风险。让我们来看一下长期新冠和NETs。
长期新冠的基础病理生理学已成为密集研究讨论的主题。虽然长期新冠中的慢性炎症受到了广泛关注，但作为最丰富的免疫细胞，中性粒细胞在炎症反应中的作用却不幸被忽视了，可能是因为它们的生命周期较短。在这篇综述中，我们讨论了中性粒细胞外陷阱（NETs）在长期新冠患者持续性炎症反应中的新兴作用。我们呈现了早期证据，表明NETs的持续存在与长期新冠中的肺纤维化、心血管异常和神经功能障碍之间存在关联。
https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2023.1254310/full
⸻
COVID感染
刺突蛋白在mRNA疫苗接种后、长期