The Spike Protein, Dorsal Root Ganglions (DRGs) and Autoimmunity: Understanding the Pain of Long COVID A just published study shows autoantibodies attacking DRGs in Long COVID, identifying a source of the condition’s chronic pain. WALTER M CHESNUT NOV 24 The Spike Protein, Dorsal Root Ganglions (DRGs) and Autoimmunity: Understanding the Pain of Long COVID A just published study shows autoantibodies attacking DRGs in Long COVID, identifying a source of the condition’s chronic pain. WALTER M CHESNUT NOV 24
Viral mRNA is visibly detectable in DRGs and SCs by in situ hybridization, but mature virus is not detectable by immunohistochemistry.
(A) Expression pattern of Spike (S) RNA (red) around DAPI (blue) and Rbfox3 (white) in cervical and thoracic DRGs of SARS-CoV-2–infected and mock male hamsters at 1 dpi. Data are representative of n = 2 animals per group. (B) Expression patterns of Spike RNA (red) around DAPI (blue) in cervical and thoracic SCs from SARS-CoV-2–infected and mock-control male hamsters at 1 dpi. Data are representative of n = 2 per group. (C) Nucleocapsid protein expression pattern in thoracic DRGs of SARS-CoV-2–infected and mock-control male hamsters as well as lung tissue of male SARS-CoV-2–infected animals at 1 dpi. Data are representative of n = 2 animals per group. Scale bars, 50 μm; insets, 20 μm.
A study published just days ago shows that autoantibodies from Long COVID patients injected into mice attack dorsal root ganglions. This can help us understand the chronic, and often debilitating pain that those suffering from Long COVID endure.
IgG from LC patients binds to sensory neurons in the lumbar dorsal root ganglia
To identify the cell types targeted by human IgG in the DRG, we performed double immunofluorescence against neuron cell bodies (NeuN) and satellite glial cells (Glutamine Synthetase). As for immunohistochemistry, human IgG from HC subjects were detected in the peri-neuronal network of DRG. Human IgG from LC patients colocalized with NeuN, but not with glutamine synthetase (Fig.6A-C). The percentage of NeuN+/IgG+ cells was significantly higher in DRG from mice injected with LC patient IgG than in DRG transferred with HC IgG (Fig.6B). When characterizing DRG neuron subtypes using fiber-specific markers, we observed that approximately 40% of NF200+ neurons (Aβ and Aδ fibers) colocalized with human IgG, whereas about 18% of peripherin+ neurons (C-fibers) and 12% of cGRP+ neurons (C-fibers and Aδ fibers) showed IgG colocalization (Suppl.Fig.4). The colocalization between human IgG and sensory neurons was no longer observed when mice received IgG-depleted serum or papain-digested IgG compared to mice receiving purified LC IgG (Fig.7).
DRGs modulate our perception of pain. The fact that the Spike Protein induces our body to attack them can explain why doctors are baffled and find “nothing wrong” when confronted with a Long COVID patient’s complaints of chronic pain.
The DRG are highly complex structures located on either side of the spinal cord than span the length of the spinal column. Each ganglion is an enlargement of the dorsal roots given off by the spinal cord. These structures are merely the size of a peanut but are able to house up to 15,000 neurons each. The neurons located within the DRG are responsible for sensory transduction and modulation from the periphery, including pain perception (9). The location of the DRG, which is surrounded by rigid bony structures, leaves little room for expansion of displacement. Herniated disc and osteophytes are common conditions that may cause compression and inflammation at the level of the DRG (10).
The DRG contains clusters of the cell bodies of primary sensory neurons. Each of the axons of these sensory neurons house a variety of fibers with a range of size and excitability. These fibers include the Aβ, Aδ, and C fibers. Compared to the large, myelinated, and high velocity A fibers, the C fibers are unmyelinated, smaller in diameter and have a much slower conduction velocity. Despite these variations, each of these fibers are responsible for conducting sensory signals from the periphery to the DRG and finally the central nervous system (9). Further research demonstrates C fibers, specifically, play an active role in chronic pain. C-fibers nociceptors have been noted to be involved in aberrant pain signaling within the cell bodies of the DRG (11).
How can this happen? It should be of no surprise that the Spike Protein is almost certainly to blame. Though no actual virus was discovered in DRGs, the Spike Protein was.
To gain insight into viral replication within the DRGs, we performed a plaque assay in which combined cervical and tDRGs or SC were collected at 3 dpi and homogenized in PBS. This cell-homogenate solution was then plated with Vero cells, with the number of ensuing plaques representing the number of mature virions present in the harvested tissue. Plaques were observed only in 3-dpi lung homogenates from SARS-CoV-2–infected animals but not in those from mock-treated animals or any DRG or SC (Fig. 1I). This suggested that mature virus was not reaching the peripheral or central sensory nervous systems.
We next sought to determine whether SARS-CoV-2 transcripts were localized to specific cell types in the DRGs, which are predominantly composed of primary sensory neurons and satellite glial cells. Using RNAscope in situ hybridization on 1-dpi cervical and thoracic cell tissue, we observed the presence of RNA (S) puncta around 4′,6-diamidino-2-phenylindole (DAPI)–labeled nuclei, which, in DRGs, are representative of satellite glial cells, and Rbfox3-labeled neuronal spaces in tissues retrieved from SARS-CoV-2–infected animals. S puncta were not present in tissues retrieved from mock-treated animals (Fig. 2A). We also detected S transcript puncta near the DAPI signal throughout SARS-CoV-2–infected cervical and thoracic SC sections at 1 dpi. These puncta were not visible in SCs from mock-infected animals (Fig. 2B).
Early on this was certainly seen as a concern. Yet, at this point (unlike myself and readers of this Substack) only complete viral invasion was being considered as a source of Spike.
Our work highlights neuronal expression of ACE2 in a select subset of nociceptors that express CALCA, P2RX3, MRGPRD, NPPB and SCN10A. While we cannot state with certainty the anatomical projections of these neurons because tracing studies cannot be done in humans, the neurochemical signature of these neurons is consistent with nociceptors that form free nerve endings in the skin [38], luminal organs [12] and meninges [31]. Therefore, one potential consequence of this ACE2 expression could be infection of nociceptors through the nasal passages, cornea, or upper or lower airway. To this end, we noted higher expression of ACE2 in thoracic DRGs, and these DRGs contain nociceptors that innervate the lungs [14; 29], a major site for proliferation of the SARS-CoV-2 virus [36]. It is now clear that many COVID-19 patients have persistent symptoms lasting for months after initial infection. These symptoms include joint and chest pain, cough, headache and dyspnea [7], symptoms that involve activation of nociceptors. Sensory neuronal infection by SARS-CoV-2 may be a causative factor in some of these persistent symptoms.
How is this occurring? Given that we are observing the Spike Protein’s presence in DRGs, it is most likely a combination of molecular mimicry and bystander activation.
Recently, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) raised the concern of autoimmune responses, especially in individuals with genetic backgrounds of autoimmune diseases. Acute manifestations were of particular concern due to fatal respiratory failure90. Moreover, there is a growing concern about COVID-19 being an environmental trigger of autoimmunity through molecular mimicry and bystander cell activation91-97-98. Acute infection with COVID-19 stimulates an innate immune response resulting in a proinflammatory cytokine storm (i.e., IL-1β, TNF-α, and IFNγ) and chemokines as a non-specific anti-viral immune response. The non-specific proinflammatory cytokine response can promote tissue damage and release of hidden self-antigens; APCs uptake the self-antigens and present them to autoreactive T and B cells, triggering polyclonal autoreactive T and B cell activation and autoimmune responses during COVID-19 infection. Specific tissues such as the blood-brain barrier (BBB) and myelin sheath are harmed by the hyperinflammatory response, leading to the development of autoimmune features in COVID-19 infected patients99-102. SARS-CoV-2 viral antigens are also reported to mediate autoimmunity via molecular mimicry92. For instance, polyneuropathies (e.g., myasthenia gravis, GBS, and MS) are associated with human autoantigen production103. Using comparative sequence analysis between SARS-CoV-2 and host factors, viral hexapeptides (i.e., KDKKKK and EIPKEE) showed shared homology with human heat shock proteins (Hsps) (e.g., Hsps 90 and 60), where autoantibodies target Hsps and contribute to autoimmunity 104
The recent paper should provide sufficient evidence to those who thought that Long COVID is not “real,” that is certainly is. My takeaway is that this is clearly happening with many, many other cells. Not just DRGs. I will continue to ask why and to seek therapeutics. Please have a blessed week and Thanksgiving if you are in the States.
Thank you, as always, for your continued support, dialog, and readership. Each week, between now and Christmas, I am asking if at least one reader or subscriber would please become a Founding Member of this Substack. Please consider becoming a paid subscriber, donating crypto, or donating via PayPal.
刺突蛋白、背根神经节（DRGs）与自身免疫：理解长新冠的疼痛机制
一项刚发表的研究显示，在长新冠患者中，自身抗体会攻击背根神经节，这为该疾病的慢性疼痛来源提供了新的线索
The Spike Protein, Dorsal Root Ganglions (DRGs) and Autoimmunity: Understanding the Pain of Long COVID
A just published study shows autoantibodies attacking DRGs in Long COVID, identifying a source of the condition’s chronic pain.
WALTER M CHESNUT
NOV 24
The Spike Protein, Dorsal Root Ganglions (DRGs) and Autoimmunity: Understanding the Pain of Long COVID
A just published study shows autoantibodies attacking DRGs in Long COVID, identifying a source of the condition’s chronic pain.
WALTER M CHESNUT
NOV 24
https://open.substack.com/pub/wmcresearch/p/the-spike-protein-dorsal-root-ganglions
Viral mRNA is visibly detectable in DRGs and SCs by in situ hybridization, but mature virus is not detectable by immunohistochemistry.
(A) Expression pattern of Spike (S) RNA (red) around DAPI (blue) and Rbfox3 (white) in cervical and thoracic DRGs of SARS-CoV-2–infected and mock male hamsters at 1 dpi. Data are representative of n = 2 animals per group. (B) Expression patterns of Spike RNA (red) around DAPI (blue) in cervical and thoracic SCs from SARS-CoV-2–infected and mock-control male hamsters at 1 dpi. Data are representative of n = 2 per group. (C) Nucleocapsid protein expression pattern in thoracic DRGs of SARS-CoV-2–infected and mock-control male hamsters as well as lung tissue of male SARS-CoV-2–infected animals at 1 dpi. Data are representative of n = 2 animals per group. Scale bars, 50 μm; insets, 20 μm.
A study published just days ago shows that autoantibodies from Long COVID patients injected into mice attack dorsal root ganglions. This can help us understand the chronic, and often debilitating pain that those suffering from Long COVID endure.
IgG from LC patients binds to sensory neurons in the lumbar dorsal root ganglia
To identify the cell types targeted by human IgG in the DRG, we performed double immunofluorescence against neuron cell bodies (NeuN) and satellite glial cells (Glutamine Synthetase). As for immunohistochemistry, human IgG from HC subjects were detected in the peri-neuronal network of DRG. Human IgG from LC patients colocalized with NeuN, but not with glutamine synthetase (Fig.6A-C). The percentage of NeuN+/IgG+ cells was significantly higher in DRG from mice injected with LC patient IgG than in DRG transferred with HC IgG (Fig.6B). When characterizing DRG neuron subtypes using fiber-specific markers, we observed that approximately 40% of NF200+ neurons (Aβ and Aδ fibers) colocalized with human IgG, whereas about 18% of peripherin+ neurons (C-fibers) and 12% of cGRP+ neurons (C-fibers and Aδ fibers) showed IgG colocalization (Suppl.Fig.4). The colocalization between human IgG and sensory neurons was no longer observed when mice received IgG-depleted serum or papain-digested IgG compared to mice receiving purified LC IgG (Fig.7).
Pathogenic IgG from long COVID patients with neurological sequelae triggers sensitive but not cognitive impairments upon transfer into mice
https://www.biorxiv.org/content/10.1101/2025.11.20.689423v1.full
DRGs modulate our perception of pain. The fact that the Spike Protein induces our body to attack them can explain why doctors are baffled and find “nothing wrong” when confronted with a Long COVID patient’s complaints of chronic pain.
The DRG are highly complex structures located on either side of the spinal cord than span the length of the spinal column. Each ganglion is an enlargement of the dorsal roots given off by the spinal cord. These structures are merely the size of a peanut but are able to house up to 15,000 neurons each. The neurons located within the DRG are responsible for sensory transduction and modulation from the periphery, including pain perception (9). The location of the DRG, which is surrounded by rigid bony structures, leaves little room for expansion of displacement. Herniated disc and osteophytes are common conditions that may cause compression and inflammation at the level of the DRG (10).
The DRG contains clusters of the cell bodies of primary sensory neurons. Each of the axons of these sensory neurons house a variety of fibers with a range of size and excitability. These fibers include the Aβ, Aδ, and C fibers. Compared to the large, myelinated, and high velocity A fibers, the C fibers are unmyelinated, smaller in diameter and have a much slower conduction velocity. Despite these variations, each of these fibers are responsible for conducting sensory signals from the periphery to the DRG and finally the central nervous system (9). Further research demonstrates C fibers, specifically, play an active role in chronic pain. C-fibers nociceptors have been noted to be involved in aberrant pain signaling within the cell bodies of the DRG (11).
Dorsal Root Ganglion (DRG) and Chronic Pain
https://pmc.ncbi.nlm.nih.gov/articles/PMC8314073/
How can this happen? It should be of no surprise that the Spike Protein is almost certainly to blame. Though no actual virus was discovered in DRGs, the Spike Protein was.
To gain insight into viral replication within the DRGs, we performed a plaque assay in which combined cervical and tDRGs or SC were collected at 3 dpi and homogenized in PBS. This cell-homogenate solution was then plated with Vero cells, with the number of ensuing plaques representing the number of mature virions present in the harvested tissue. Plaques were observed only in 3-dpi lung homogenates from SARS-CoV-2–infected animals but not in those from mock-treated animals or any DRG or SC (Fig. 1I). This suggested that mature virus was not reaching the peripheral or central sensory nervous systems.
We next sought to determine whether SARS-CoV-2 transcripts were localized to specific cell types in the DRGs, which are predominantly composed of primary sensory neurons and satellite glial cells. Using RNAscope in situ hybridization on 1-dpi cervical and thoracic cell tissue, we observed the presence of RNA (S) puncta around 4′,6-diamidino-2-phenylindole (DAPI)–labeled nuclei, which, in DRGs, are representative of satellite glial cells, and Rbfox3-labeled neuronal spaces in tissues retrieved from SARS-CoV-2–infected animals. S puncta were not present in tissues retrieved from mock-treated animals (Fig. 2A). We also detected S transcript puncta near the DAPI signal throughout SARS-CoV-2–infected cervical and thoracic SC sections at 1 dpi. These puncta were not visible in SCs from mock-infected animals (Fig. 2B).
SARS-CoV-2 airway infection results in the development of somatosensory abnormalities in a hamster model
https://www.science.org/doi/10.1126/scisignal.ade4984
Early on this was certainly seen as a concern. Yet, at this point (unlike myself and readers of this Substack) only complete viral invasion was being considered as a source of Spike.
Our work highlights neuronal expression of ACE2 in a select subset of nociceptors that express CALCA, P2RX3, MRGPRD, NPPB and SCN10A. While we cannot state with certainty the anatomical projections of these neurons because tracing studies cannot be done in humans, the neurochemical signature of these neurons is consistent with nociceptors that form free nerve endings in the skin [38], luminal organs [12] and meninges [31]. Therefore, one potential consequence of this ACE2 expression could be infection of nociceptors through the nasal passages, cornea, or upper or lower airway. To this end, we noted higher expression of ACE2 in thoracic DRGs, and these DRGs contain nociceptors that innervate the lungs [14; 29], a major site for proliferation of the SARS-CoV-2 virus [36]. It is now clear that many COVID-19 patients have persistent symptoms lasting for months after initial infection. These symptoms include joint and chest pain, cough, headache and dyspnea [7], symptoms that involve activation of nociceptors. Sensory neuronal infection by SARS-CoV-2 may be a causative factor in some of these persistent symptoms.
ACE2 and SCARF expression in human DRG nociceptors: implications for SARS-CoV-2 virus neurological effects
https://pmc.ncbi.nlm.nih.gov/articles/PMC7572821/
How is this occurring? Given that we are observing the Spike Protein’s presence in DRGs, it is most likely a combination of molecular mimicry and bystander activation.
Recently, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) raised the concern of autoimmune responses, especially in individuals with genetic backgrounds of autoimmune diseases. Acute manifestations were of particular concern due to fatal respiratory failure90. Moreover, there is a growing concern about COVID-19 being an environmental trigger of autoimmunity through molecular mimicry and bystander cell activation91-97-98. Acute infection with COVID-19 stimulates an innate immune response resulting in a proinflammatory cytokine storm (i.e., IL-1β, TNF-α, and IFNγ) and chemokines as a non-specific anti-viral immune response. The non-specific proinflammatory cytokine response can promote tissue damage and release of hidden self-antigens; APCs uptake the self-antigens and present them to autoreactive T and B cells, triggering polyclonal autoreactive T and B cell activation and autoimmune responses during COVID-19 infection. Specific tissues such as the blood-brain barrier (BBB) and myelin sheath are harmed by the hyperinflammatory response, leading to the development of autoimmune features in COVID-19 infected patients99-102. SARS-CoV-2 viral antigens are also reported to mediate autoimmunity via molecular mimicry92. For instance, polyneuropathies (e.g., myasthenia gravis, GBS, and MS) are associated with human autoantigen production103. Using comparative sequence analysis between SARS-CoV-2 and host factors, viral hexapeptides (i.e., KDKKKK and EIPKEE) showed shared homology with human heat shock proteins (Hsps) (e.g., Hsps 90 and 60), where autoantibodies target Hsps and contribute to autoimmunity 104
Infectious diseases, autoantibodies, and autoimmunity
https://pmc.ncbi.nlm.nih.gov/articles/PMC10235211/
The recent paper should provide sufficient evidence to those who thought that Long COVID is not “real,” that is certainly is. My takeaway is that this is clearly happening with many, many other cells. Not just DRGs. I will continue to ask why and to seek therapeutics. Please have a blessed week and Thanksgiving if you are in the States.
Thank you, as always, for your continued support, dialog, and readership. Each week, between now and Christmas, I am asking if at least one reader or subscriber would please become a Founding Member of this Substack. Please consider becoming a paid subscriber, donating crypto, or donating via PayPal.
通过原位杂交可清晰检测到病毒 mRNA 在背根神经节（DRGs）和脊髓（SC）中的存在，但采用免疫组织化学无法检测到成熟病毒。
（A） 在感染 SARS-CoV-2 和对照组雄性仓鼠感染后 1 天（1 dpi）的颈段和胸段 DRGs 中，可见刺突蛋白（S）RNA（红色）相对于 DAPI（蓝色）和 Rbfox3（白色）的表达模式。数据代表每组 n = 2 只动物。
（B） 在感染后 1 天，从 SARS-CoV-2 感染和对照组雄性仓鼠获得的颈段和胸段脊髓（SC）组织中，可见刺突蛋白 RNA（红色）相对于 DAPI（蓝色）的表达模式。数据代表每组 n = 2。
（C） 在感染后 1 天，于 SARS-CoV-2 感染与对照组雄性仓鼠的胸段 DRGs 以及感染组肺组织中检测核衣壳蛋白的表达模式。数据代表每组 n = 2 只动物。比例尺：50 μm；插图：20 μm。
⸻
一项刚刚发布的研究显示，将长新冠（Long COVID）患者的自身抗体注射到小鼠体内后，这些抗体会攻击背根神经节。此发现有助于解释长新冠患者所经历的长期且常使人衰弱的慢性疼痛。
⸻
来自长新冠患者的 IgG 会结合腰段 DRGs 中的感觉神经元
为了识别人类 IgG 在 DRG 中的靶细胞，我们进行了双重免疫荧光实验，标记神经元细胞体（NeuN）和卫星胶质细胞（谷氨酰胺合成酶）。与免疫组化类似，来自健康对照（HC）人群的 IgG 在 DRG 的神经元周围网络中被检测到。来自长新冠（LC）患者的 IgG 与 NeuN 共定位，但与谷氨酰胺合成酶无共定位（Fig.6A–C）。
NeuN+/IgG+ 细胞的比例在注射 LC IgG 的小鼠 DRG 中显著高于注射 HC IgG 的小鼠（Fig.6B）。
使用纤维特异性标记物进一步区分 DRG 神经元亚型后，我们观察到：
• 约 40% 的 NF200+ 神经元（Aβ 和 Aδ 纤维）与人类 IgG 共定位
• 约 18% 的 peripherin+ 神经元（C 纤维）出现共定位
• 约 12% 的 cGRP+ 神经元（C 纤维及 Aδ 纤维）出现共定位（Suppl. Fig.4）
当向小鼠注射去除 IgG 的血清或木瓜蛋白酶消化后的 IgG 时，不再观察到人类 IgG 与感觉神经元之间的共定位；而纯化的 LC IgG 则能产生共定位（Fig.7）。
⸻
来自具有神经系统后遗症的长新冠患者的致病性 IgG 在转移至小鼠后可引发敏感性受损，而不会引起认知障碍
论文链接（预印本）：
https://www.biorxiv.org/content/10.1101/2025.11.20.689423v1.full
⸻
DRGs 调节我们对疼痛的感知。刺突蛋白诱导机体攻击 DRG 的事实，可以解释为何医生常常找不到“器质性原因”，却需要面对长新冠患者的长期疼痛抱怨。
⸻
DRG 的结构与功能
背根神经节是高度复杂的结构，位于脊髓两侧，沿整个脊柱分布。每个神经节是脊髓背根的膨大结构，虽然仅有花生大小，却可容纳多达 15,000 个神经元。
DRG 内的神经元负责来自身体周边的感觉传导与调节，包括疼痛感知（9）。由于 DRG 被坚硬骨性结构包围，其位置几乎没有扩张或移动的空间。因此，椎间盘突出和骨赘是常见的可导致 DRG 受压和炎症的原因（10）。
DRG 内含有初级感觉神经元的胞体，其中轴突携带多种神经纤维：
• Aβ、Aδ：有髓鞘、大直径、高传导速度
• C 纤维：无髓鞘、小直径、传导速度低
尽管不同纤维性质不同，它们均负责将外周信号传导至 DRG，再进入中枢神经系统（9）。研究表明 C 纤维在慢性疼痛中尤为重要，它们的伤害感受器常参与 DRG 内的异常疼痛信号（11）。
来源：
《背根神经节（DRG）与慢性疼痛》
https://pmc.ncbi.nlm.nih.gov/articles/PMC8314073/
⸻
这是如何发生的？关键在于刺突蛋白。虽然没有在 DRG 中发现完整病毒，但发现了刺突蛋白。
为了了解 DRG 内的病毒复制情况，研究者进行了斑块实验，收集感染后第 3 天的颈段与胸段 DRGs 和脊髓组织均质化后接种 Vero 细胞。结果：
• 只有肺组织出现病毒斑块
• DRG 与脊髓均未见斑块
说明 成熟病毒未到达外周或中枢感觉神经系统。
随后进行 RNAscope 原位杂交：
• 在感染 1 天的 DRG 中可看见刺突蛋白 RNA（S）信号
• 在对照组织中则不存在
• 在脊髓组织中同样能观察到 S RNA 信号
来源：
《SARS-CoV-2 气道感染在仓鼠模型中导致体感异常》
https://www.science.org/doi/10.1126/scisignal.ade4984
⸻
早期研究曾担心这种情况。然而，当时（与本文作者和读者不同）科学界主要关注的是病毒完整入侵作为刺突蛋白的来源。
研究显示人类 DRG 中某些伤害感受器神经元表达 ACE2，理论上允许病毒从：
• 鼻腔
• 角膜
• 上下呼吸道
进入神经系统。这些神经元与皮肤、内脏和脑膜的伤害感受器一致。
来源：
《ACE2 与 SCARF 在 DRG 伤害感受器中的表达：对 SARS-CoV-2 神经影响的启示》
https://pmc.ncbi.nlm.nih.gov/articles/PMC7572821/
⸻
机制是什么？最可能是分子模拟与旁观者激活共同导致。
新冠感染会引发强烈的炎症风暴：
• IL-1β
• TNF-α
• IFNγ
• 各种趋化因子
这些炎症反应可：
• 损伤组织
• 释放自体抗原
• 被 APC 摄取并呈递
• 激活原本无害的自反应 T/B 细胞
• 触发自动免疫
此外，SARS-CoV-2 的蛋白与人体蛋白存在 分子模拟，如病毒序列与人类 Hsp90/60 具有同源片段，可诱发表自身抗体（104）。
来源：
《感染性疾病、自身抗体与自体免疫》
https://pmc.ncbi.nlm.nih.gov/articles/PMC10235211/
⸻
总结
这篇最新研究为仍怀疑“长新冠不是真的”的人提供了足够证据。
作者的观点是：这种现象显然发生在 多个组织，远不止 DRG。