Neurological damage: Many COVID-19 patients also experience 

neurological damage39-42, the reason for which is not known and has 

to be studied carefully. Interestingly, the template viruses ZC45 and 

ZXC21, upon their discovery, were shown by the PLA scientists to 

cause brain infections and inflammation in suckling rats43. 

Coincidentally or not, the E protein, which is associated to neurotoxicity 

in coronavirus infections44, was kept 100% identical between

ZC45/ZXC21 and SARS-CoV-2.

神經系統損害：許多COVID-19患者也會出現神經系統損害39-42，

其原因尚不清楚，必須仔細研究。有趣的是，模板病毒ZC45和

ZXC21一經發現，就被解放軍科學家證明能引起乳鼠的腦部感染

和炎症43。巧合或不巧合的是，在冠狀病毒感染中與神經毒性

相關的E蛋白44，在ZC45/ZXC21和SARS-CoV-2之間保持100%

的相同。

     引自：

http://file:///C:/Users/Windows/Downloads/Combined_responses_1%20(1).pdf

閆麗夢博士：

So what I want to comment on it, 

對於這一點，我想說的是

I am not neurologist, I just have the medical knowledge about neurology disease. 

我不是神經科醫生，我只是有神經科疾病的醫學知識

But what I have pointed in my third report and also in my first report, I can use it as a smoking gun. 

但正如我在第三份報告和第一份報告中指出的那樣，我可以把它當作確鑿的證據

is envelop protein, E protein, in SARS-Covid 2, 

就是E蛋白，SARS-Covid 2中的E蛋白

it’s hundred percent identical as it as the back born, Zhou Shan Conoravirus

可以100%完全確認SARS-Covid 2使用舟山蝙蝠冠狀病毒作為骨架

First, this is the evidence. It comes from the Zhou Shan bat conoravirus, which is somehow, completely cab into SARS Covid 2. 

首先，這是證據。該E蛋白來自舟山蝙蝠冠狀病毒，不知何故，它完全被發現在SARS Covid 2 病毒里

Because if it is going through the spices that’s a kind of host changing, jump from bat to animal to animal to human

因為如果它經過物種間傳代，那就是一種從蝙蝠到動物再到動物再到人類的宿主

definitely, that we would see the change, because they already observed the change 

當然，我們會看到這種變化，因為他們在人類大流行最早的時候

during the earliest the pandemic in human. 

就已經觀察到了這種變化

And second thing is why do they keep it, because this is a smoking gun, 

第二個問題是，中共為什麼要對此守口如瓶，因為它是確鑿證據

since I write this problem from last year 19^th January, with Youtube. 

因為我在去年1月19日用YouTube寫了這個問題

China had done a quickly get response and later they even locked down. 

中共很快就做出了反應，後來他們甚至封鎖了E蛋白的信息

Because they know someone released the real information of this bio-weapon. 

因為他們知道內部有人泄露了這種生物武器的真實機密

But why until now, no scientist there to touch this E protein issue to argue with me.

但是為什麼到目前為止，還沒有科學家觸及到這個E蛋白的問題，他們也沒有來和我爭論這個E蛋白的問題？

And even Shi Zhengli, and their like the Chinese Military Academy,

就連石正麗, 像那些中國軍事醫學院的學者們

they have developed a lot of novel fabricated too naughty virus, including from bat from Pangolins,

他們已經合成出了很多新奇的病毒，包括從蝙蝠身上，從穿山甲身上，

which all have the identical E protein in those fabricated sequence. 

它們在構建的序列中都有相同的E蛋白。

What do they want to hide? 

他們想隱瞞什麼？

Then lets we back to check E protein’s function. 

然後我們再回來檢查一下E蛋白的功能

Yes it ‘s not clearly investigated , but we know it’s important for virus fabrication 

是的，它還沒有得到明確的調查，但我們知道它對病毒的合成至關重要

as some other important part in the Coronavirus

作為冠狀病毒的其他重要組成部分

But it’s also have another function what 

但是它還有另外一個功能，那就是

discovered and actually my ex-lab in the University of Hong Kong,

在我之前工作的香港大學的實驗室

it’s the lab get involve to discover is E protein can have the virus 

發現這種E蛋白可以幫助病毒

help the virus maintain the neuronal toxicity

幫助病毒保持其神經毒性

https://gnews.org/zh-hans/1166219/

原視頻連接: https://rumble.com/vfy3xf-lethal-deception.html

Neurotropism of SARS-CoV-2

Up to date, many reports have described the association between respiratory viral infections with neurological symptoms. There are several recognized respiratory pathogens that gain access to the central nervous system (CNS), for instance, respiratory syncytial virus, the influenza virus, the human metapneumovirus, and HCoVs (HCoV229E, HCoV-OC43, and SARS-CoV) [39], that induce manifestations such as febrile or afebrile seizures, among other encephalopathies [40, 41].

Primary cultures of human astrocytes and microglia and various human neuronal cell lines, such as the neuroblastoma SK-N-SH, the neuroglioma H4, and the oligodendrocytic MO3.13, have potential tropism for HCoV-OC43 [42]. Using an experimental animal model, HCoV-OC-43 infection also showed neuro-invasiveness and neuro-virulence [43]. Therefore, it is not surprising to find brain SARS-positive autopsies. Using in situ hybridization, the SARS genomic sequence has been detected in the cytoplasm of neurons of the hypothalamus and cerebral cortex [44]. Furthermore, Moriguchi et al. [45] confirmed the presence of the new SARS-CoV-2 in cerebral spinal fluid. In accord, epidemiological and clinical research have described neurological, non-common symptoms, and neurological manifestations associated with the SARS-CoV-2 infection (Table 2). These clinical features include neuralgia, confusion, hyposmia, hypogeusia, and altered consciousness, symptoms that evidence the neurotropic invasion by SARS-CoV-2 [19, 41].

Table 2 Neurological manifestations associated with SARS-CoV-2 infection

Full size table

Despite the evidence demonstrating the neurotropism of respiratory viruses, the exact mechanism of neuro-invasion accomplished by viruses remains currently unknown. However, the route of invasion of the CNS has recently been described for HCoV-OC-43. This virus gains access to the CNS through the olfactory bulb, moving along the olfactory nerve. Then, neuro-propagation occurs along the multiple axonal connections expanding through the CNS (e.g., neuron-to-neuron propagation or diffusing particles) [56]. Similar to HCoV-OC-43, a model in vivo of SARS-CoV infection suggested that the virus enters the brain via the olfactory bulb, and then, a transneuronal spread could occurs [57].

Also, some infectious blood-borne viruses primarily targeting peripheral organs have evolved strategies to thwart the blood-brain barrier (BBB). These strategies include direct infection of the brain microvascular endothelial cells that form the BBB, a paracellular entry that involves alteration of the tight junctions, or the “Trojan horse” invasion, via the traffic of infected monocytes/macrophages migrating across the BBB, in a similar manner as the not-respiratory immunodeficiency virus 1 (HIV-1) [58, 59]. Likewise, when human primary monocytes are activated following infection by HCoV-229E and eventually become macrophages, it can invade tissues, including the CNS [60, 61]. Additionally, it has been reported that through activation of the brain microendothelium, the damage caused by the inflammatory response, allows the virus to reach the CNS. In this sense, the neuro-invasion of SARS-CoV-2 could occur through trans-synaptic transfer, via the olfactory nerve, infection of vascular endothelium, or leukocyte migration across the BBB [38].

SARS-CoV-2的神經向性

迄今為止，許多報告已經描述了呼吸道病毒感染與神經系統症狀之間的關係。有幾種公認的呼吸道病原體可以進入中樞神經系統（CNS），例如呼吸道合胞病毒，流感病毒，人間質肺病毒和HCoV（HCoV229E，HCoV-OC43和SARS-CoV）[ 39 ]。 ，誘導表現如發熱或無熱驚厥，其他腦病中[ 40，41 ]。

人類星形膠質細胞和小膠質細胞以及各種人類神經元細胞系（例如神經母細胞瘤SK-N-SH，神經膠質瘤H4和少突膠質細胞MO3.13）的原代培養物具有HCoV-OC43的潛在嗜性[ 42 ]。使用實驗動物模型，HCoV-OC-43感染還表現出神經侵襲性和神經毒力[ 43 ]。因此，發現腦SARS陽性屍檢並不奇怪。使用原位雜交，在下丘腦和大腦皮層神經元的細胞質中檢測到SARS基因組序列[ 44 ]。此外，森口等。[ 45]證實了腦脊髓液中存在新的SARS-CoV-2。相應地，流行病學和臨床研究已經描述了與SARS-CoV-2感染相關的神經系統症狀，非常見症狀和神經系統表現（表2）。這些臨床特徵包括神經痛，精神錯亂，嗅覺減退，味覺減退，和意識改變，症狀的證據由SARS-CoV的-2 [嗜神經侵19，41 ]。

表2與SARS-CoV-2感染相關的神經系統表現

儘管有證據表明呼吸道病毒具有嗜神經性，但目前尚不清楚由病毒完成的神經入侵的確切機制。然而，最近已經針對HCoV-OC-43描述了CNS的入侵途徑。該病毒通過嗅球沿着嗅神經移動，進入中樞神經系統。然後，神經傳播沿着通過中樞神經系統擴展的多個軸突連接發生（例如，神經元到神經元的傳播或擴散粒子）[ 56 ]。與HCoV-OC-43類似，體內SARS-CoV感染的模型表明該病毒通過嗅球進入大腦，然後可能發生跨神經元擴散[ 57 ]。

而且，一些主要針對外圍器官的傳染性血源性病毒已經進化出可以阻止血腦屏障（BBB）的策略。這些策略包括直接感染形成BBB的腦微血管內皮細胞，涉及緊密連接改變的旁細胞進入或“特洛伊木馬”入侵，這是通過在BBB中跨BBB遷移的被感染單核細胞/巨噬細胞的運輸。類似的方式作為不呼吸免疫缺陷病毒1（HIV-1）[ 58，59 ]。同樣，當人的原始單核細胞被激活之後通過冠狀-229E感染，最終成為巨噬細胞，它可侵入組織，包括中樞神經系統[ 60，61]。另外，據報道，通過激活腦微內皮，由炎症反應引起的損害使病毒到達中樞神經系統。從這個意義上說，SARS-CoV-2的神經入侵可能是通過突觸傳遞，嗅覺神經，血管內皮的感染或白細胞在血腦屏障中的遷移而發生的[ 38 ]。

https://link.springer.com/article/10.1007/s12035-020-02134-7