Neuroinflammation in Long Covid

Pyrrhus

Senior Member
Messages
4,171
Likes
12,772
Location
U.S., Earth
Well this is interesting...

Here's a new, fascinating paper that detected inflammatory cells in the eye in Long Covid patients 2-3 months after infection. Since the optic nerve at the back of the eye is part of the nervous system, and the optic nerve is a major route for drainage of brain lymph, inflammatory cells in the eye is sometimes a marker of inflammation in the nervous system:

Subclinical ocular inflammation in persons recovered from ambulatory COVID-19 (Bakhoum et al., September 2020)
https://www.medrxiv.org/content/10.1101/2020.09.22.20128140v2

It's not yet peer-reviewed, but here is an excerpt:
Bakhoum et al 2020 said:
Abstract: Coronavirus disease 2019 (COVID-19) is characterized by striking variability in clinical severity, and a hyperinflammatory response in the lung is associated with high mortality. Little is known about the extent and duration of inflammation in persons recovering from COVID-19. Here, we used spectral domain optical coherence tomography (SD-OCT) to detect the presence of inflammatory cells in the vitreous cavity, an immune-privileged microenvironment, in persons recovered from COVID- 19. Our results provide quasi-histologic evidence that neuroinflammation is present in persons who recovered from COVID-19, only one of whom required hospitalization. Our results also suggest that persons who feel that their recovery is incomplete have evidence of subclinical eye inflammation, which may be a marker of residual inflammation elsewhere as well.
(emphasis added)

NOTE: To understand the difference between Classical Inflammation and Neuroinflammation, see:
https://forums.phoenixrising.me/thr...n-in-me-subcortical-brain.80923/#post-2289868
 
Last edited:

ljimbo423

Senior Member
Messages
4,670
Likes
12,628
Location
United States, New Hampshire
This absract sure makes a lot of sense.


Our results also suggest that persons who feel that their recovery is incomplete have evidence of subclinical eye inflammation, which may be a marker of residual inflammation elsewhere as well.
I'm not sure where they mean by "elsewhere" but I think inflammation in the body is key to understanding brain inflammmation in ME/CFS and probably the Covid 19 "Long Haulers" too.
 

Pyrrhus

Senior Member
Messages
4,171
Likes
12,772
Location
U.S., Earth
There are also discussions on neuroinflammation in other conditions:

Neuroinflammation in ME/CFS:
https://forums.phoenixrising.me/thr...roinflammation-in-me-subcortical-brain.80923/

Neuroinflammation in Fibromyalgia:
https://forums.phoenixrising.me/thr...in-the-brains-of-fibromyalgia-patients.61667/

Neuroinflammation in Post-treatment Lyme Disease:
https://forums.phoenixrising.me/thr...mmation-in-post-treatment-lyme-disease.75319/

Neuroinflammation in Gulf War Illness:
https://forums.phoenixrising.me/thr...n-in-me-subcortical-brain.80923/#post-2289866
 
Last edited:
Messages
11,038
Likes
26,400
Since the optic nerve at the back of the eye is part of the nervous system, and the optic nerve is a major route for drainage of brain lymph, inflammatory cells in the eye is sometimes a marker of inflammation in the nervous system:
I have alot of intense eye inflammation with ME, and my right eye experiences alot of- variation in symptoms...that I notice tracks my overall condition pretty closely. My right side is much more sick than my left.

I thought maybe my going to a real eye doctor would lead to insights into this situation, but alas. Nah.o_O

Really wondering about this whole "main route for lymph drainage"..may mean. Thats Newsworthy here. I figure my right side being more ill is tied to lymph issues, chronic EppsteinB of some type, and the liver is : on that side.
 

Pyrrhus

Senior Member
Messages
4,171
Likes
12,772
Location
U.S., Earth
I have alot of intense eye inflammation with ME, and my right eye experiences alot of- variation in symptoms...that I notice tracks my overall condition pretty closely. My right side is much more sick than my left.
Same here, but with my left eye. And when I'm in a flare I wake up with all this dried gunk in my left eye, but not in my right eye. And only when I'm in a crash.

They used to say that the gunk in the corner of your eyes upon awakening was just "sand" from dried-up tears. (Remember the song "Mr. Sandman"?) We now know that the gunk contains a lot of dried white blood cells.

I thought maybe my going to a real eye doctor would lead to insights into this situation, but alas. Nah.
For years, I had no idea that my vision problems were related to my ME. I would get disappointed at my optometrist when they told me that my prescription had not, in fact, changed. Then why were things blurry!

It wasn't until I got the fully automated LASIK, where a computer maps out your entire eyeball and calculates the exact correction to your vision, that things started to make sense. The computer showed that, after LASIK, there was absolutely nothing wrong with my eyes, so my vision problems had to lie elsewhere...

Really wondering about this whole "main route for lymph drainage"..may mean.
This is currently an active topic of research. Not that many years ago, people thought that the brain had no lymphatic system at all. Then evidence started to accumulate that there was indeed some fluid drainage along the tight spaces surrounding the small veins in the brain that ended up in the lymph nodes at the base of the neck. This quasi-lymphatic system was called a "glymphatic system".

As more evidence accumulated, the quasi-lymphatic system looked more and more like a full lymphatic system, with tight spaces surrounding cranial nerves (such as the optic nerve) providing drainage from the small veins to the lymph nodes. There is also some evidence that some of this drainage along the optic nerve may leak into the eye. However, this is not yet settled science and research is currently ongoing.

Edit: For more information on the brain's lymphatic system, see this post:
https://forums.phoenixrising.me/thr...uses-is-deadly-real.83408/page-2#post-2338931
 
Last edited:

Pyrrhus

Senior Member
Messages
4,171
Likes
12,772
Location
U.S., Earth
I have alot of intense eye inflammation with ME, and my right eye experiences alot of- variation in symptoms...that I notice tracks my overall condition pretty closely. My right side is much more sick than my left.
Just wondering- do you get headaches on mainly one side of your head?
And if so, is it by any chance the left side of your head?
 
Messages
73
Likes
79
Location
Belgium
Viral presence and immunopathology in patients with lethal COVID-19: a prospective autopsy cohort study (Schurink et al., 2020)
https://www.thelancet.com/journals/lanmic/article/PIIS2666-5247(20)30144-0/fulltext

Summary
Background
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) targets multiple organs and causes severe coagulopathy. Histopathological organ changes might not only be attributable to a direct virus-induced effect, but also the immune response. The aims of this study were to assess the duration of viral presence, identify the extent of inflammatory response, and investigate the underlying cause of coagulopathy.
Methods
This prospective autopsy cohort study was done at Amsterdam University Medical Centers (UMC), the Netherlands. With informed consent from relatives, full body autopsy was done on 21 patients with COVID-19 for whom autopsy was requested between March 9 and May 18, 2020. In addition to histopathological evaluation of organ damage, the presence of SARS-CoV-2 nucleocapsid protein and the composition of the immune infiltrate and thrombi were assessed, and all were linked to disease course.
Findings
Our cohort (n=21) included 16 (76%) men, and median age was 68 years (range 41–78). Median disease course (time from onset of symptoms to death) was 22 days (range 5–44 days). In 11 patients tested for SARS-CoV-2 tropism, SARS-CoV-2 infected cells were present in multiple organs, most abundantly in the lungs, but presence in the lungs became sporadic with increased disease course. Other SARS-CoV-2-positive organs included the upper respiratory tract, heart, kidneys, and gastrointestinal tract. In histological analyses of organs (sampled from nine to 21 patients per organ), an extensive inflammatory response was present in the lungs, heart, liver, kidneys, and brain. In the brain, extensive inflammation was seen in the olfactory bulbs and medulla oblongata. Thrombi and neutrophilic plugs were present in the lungs, heart, kidneys, liver, spleen, and brain and were most frequently observed late in the disease course (15 patients with thrombi, median disease course 22 days [5–44]; ten patients with neutrophilic plugs, 21 days [5–44]). Neutrophilic plugs were observed in two forms: solely composed of neutrophils with neutrophil extracellular traps (NETs), or as aggregates of NETs and platelets..
Interpretation
In patients with lethal COVID-19, an extensive systemic inflammatory response was present, with a continued presence of neutrophils and NETs. However, SARS-CoV-2-infected cells were only sporadically present at late stages of COVID-19. This suggests a maladaptive immune response and substantiates the evidence for immunomodulation as a target in the treatment of severe COVID-19.
 

Pyrrhus

Senior Member
Messages
4,171
Likes
12,772
Location
U.S., Earth
Viral presence and immunopathology in patients with lethal COVID-19: a prospective autopsy cohort study (Schurink et al., 2020)
https://www.thelancet.com/journals/lanmic/article/PIIS2666-5247(20)30144-0/fulltext
Wow. Thanks for sharing that great new paper @Legolas !

So we now have some concrete evidence of brain inflammation in acute COVID.

What does this mean for Long Covid? Should we assume that the inflammation just goes away over time? Or could the acute inflammation calm down into a more subtle neuroinflammation?

In the brain, extensive inflammation was seen in the olfactory bulbs and medulla oblongata.
Well, it's certainly easy to see why the olfactory bulb was affected. The olfactory bulb is a part of the brain that directly projects into the nose, and is exposed to the air we breath:
C03D3564-1F38-49E1-9DF9-6C9E1CEABB78.png
In fact, here is a pre-pandemic study that found that the OC43 coronavirus can indeed infect the brain via the olfactory bulb:

Axonal Transport Enables Neuron-to-Neuron Propagation of Human Coronavirus OC43 (Dube et al., 2018)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6096804/
Dube et al. 2018 said:
We describe the route of neuropropagation from the nasal cavity to the olfactory bulb and piriform cortex and then the brain stem. We identified neuron-to-neuron propagation as one underlying mode of virus spreading in cell culture. Our data demonstrate that both passive diffusion of released viral particles and axonal transport are valid propagation strategies used by the virus.
(EDIT: This OC43 coronavirus is also suspected to have caused the 1890 "Russian Flu" pandemic: https://forums.phoenixrising.me/thr...possibly-caused-by-another-coronavirus.86397/ )


And here is a related discussion about other viruses that are known to infect the brain through the olfactory bulb and the olfactory nerve:

Viral entry into the brain through olfactory nerve (CNI)--latency in olfactory bulb? (2018)
https://forums.phoenixrising.me/thr...ry-nerve-cni-latency-in-olfactory-bulb.58695/



But why would the virus target the medulla oblongata in the brainstem?

We know that the polio virus can target the medulla oblongata, resulting in Bulbar Polio:
https://en.m.wikipedia.org/wiki/Polio#Bulbar_polio

The 2014 Japanese ME/CFS PET study found significant neuroinflammation in the brainstem of ME/CFS patients:
https://forums.phoenixrising.me/thr...e-subcortical-brain.80923/page-2#post-2291789

Is the medulla oblongata affected simply because that's where the vagus nerve leads to? Is the vagus nerve a doorway for viruses to enter the brain, like the olfactory nerve?
 
Last edited:

Pyrrhus

Senior Member
Messages
4,171
Likes
12,772
Location
U.S., Earth
The novel coronavirus can directly infect neurons in the brain:
https://yaledailynews.com/blog/2020...ld-invade-the-brain-two-yale-studies-suggest/

Excerpt:
Yale Daily News said:
Yale researchers found that the coronavirus can directly infect brain cells, potentially eliciting neurological symptoms — such as the loss of taste or smell — observed in 40 to 60 percent of COVID-19 patients.

The preprint of a study led by Professor of Immunology Akiko Iwasaki and Director of Yale Center for Genome Analysis Kaya Bilguvar was released on the server bioRxiv earlier this month. In the paper — first-authored by Eric Song MED ‘22 GRD ‘22 and Ce Zhang MED ‘22 GRD ‘22 — they report that several neurological symptoms of COVID-19 could be tied to coronavirus invasion of the central nervous system.

A second study, led by Assistant Professor Shelli Farhadian and also first-authored by Song, was released as a preprint just days after Iwasaki and Bilguvar’s paper. Their findings suggest that immune responses to the coronavirus in the central nervous system could occur independently from the rest of the body.

“The biggest thing about our study is that it has shown people the possibility of neuroinvasion,” Song, who was involved with both projects, said.
[...]
Song and Zhang said that one of their most surprising findings was that infection of specific neurons affected surrounding brain cells, resulting in their death.

“We found that once the virus infects the cell, the cell that’s infected actually doesn’t die, [but] rather the neighboring cells around it die,” Zhang said. “We hypothesize that this is because we found that the cell that’s infected with the virus undergoes sort of a hypermetabolic state in which it’s using nutrients that the other cells around it need to survive.”
[...]
Upon examining biological samples from patients and using a mouse model to simulate infection, the group observed that immunological responses in the central nervous system differed from those coursing through the rest of the body — suggesting that brain-specific treatments might be warranted for diseases like COVID-19.
[...]
Overall, Farhadian said that the study is important because it emphasizes that people can’t hope to understand what is happening in the brain simply by studying reactions in the rest of the body.
(emphasis added)

These studies underline two key findings:
  1. The immune system of the brain is quite different from the way that the blood-borne immune system operates in the rest of the body. You simply can not understand neuroinflammation by looking at classical inflammation.
  2. Infected neurons in the brain do not appear to undergo apoptosis or destruction by immune cells. Rather, the infected neurons seem to remain intact, but enter into a hypermetabolic state where it continues to fight the virus from the inside, with intracellular antiviral strategies such as the interferon response. This hypermetabolic state appears to use up key nutrients faster than they can be replenished in the area around the infected neurons.
 
Messages
58
Likes
103
This absract sure makes a lot of sense.




I'm not sure where they mean by "elsewhere" but I think inflammation in the body is key to understanding brain inflammmation in ME/CFS and probably the Covid 19 "Long Haulers" too.

I just came back from my eye doctor appointment and she found inflammation in my right eye and is giving me steroid eye drops.
 
Messages
58
Likes
103

Just to get your attention Pyrrhus! There was a woman, very rich woman, on the Facebook Long Haul Covid groups who was diagnosed with neuroinflammation. Her doctor then sent her to HBOT treatments and she was treated for 35 dives and has fully recovered. She is the only woman of all the support groups I've joined that has done HBOT treatments.
 

Pyrrhus

Senior Member
Messages
4,171
Likes
12,772
Location
U.S., Earth
Early evidence for infection of the brain

Okay, so it looks like I am a bit late to the party. Here are four earlier reports discussing infection of the brain by the novel coronavirus:


A first case of meningitis/encephalitis associated with SARS-Coronavirus-2 (Moriguchi et al., May 2020)
https://doi.org/10.1016/j.ijid.2020.03.062
Moriguchi et al. May 2020 said:
Novel coronavirus (SARS-Coronavirus-2:SARS-CoV-2) which emerged in Wuhan, China, has spread to multiple countries rapidly. We report the first case of meningitis associated with SARS-CoV-2 who was brought in by ambulance due to a convulsion accompanied by unconsciousness. He had never been to any foreign countries. He felt generalized fatigue and fever (day 1). He saw doctors nearby twice (day 2 and 5) and was prescribed Laninamivir and antipyretic agents, His family visited his home and found that he was unconsciousness and lying on the floor in his vomit. He was immediately transported to this hospital by ambulance (day 9). Under emergency transport, he had transient generalized seizures that lasted about a minute. He had obvious neck stiffness. The specific SARS-CoV-2 RNA was not detected in the nasopharyngeal swab but was detected in a CSF. Anti- HSV 1 and varicella-zoster IgM antibodies were not detected in serum samples. A brain MRI showed hyperintensity along the wall of right lateral ventricle and hyperintense signal changes in the right mesial temporal lobe and hippocampus, suggesting the possibility of SARS-CoV-2 meningitis. This case warns the physicians of patients who have CNS symptoms.
(emphasis added)


Multiorgan and Renal Tropism of SARS-CoV-2 (Puelles et al., May 2020)
https://doi.org/10.1056/nejmc2011400
Puelles et al. May 2020 said:
Here, we present data from an autopsy series of 27 patients [...] that show that SARS-CoV-2 can be detected in multiple organs, including the lungs, pharynx, heart, liver, brain, and kidneys. We first quantified the SARS-CoV-2 viral load in autopsy tissue samples obtained from 22 patients who had died from Covid-19. [...] The highest levels of SARS-CoV-2 copies per cell were detected in the respiratory tract, and lower levels were detected the kidneys, liver, heart, brain, and blood.


Neuropathological Features of Covid-19 (Solomon et al., June 2020)
https://doi.org/10.1056/nejmc2019373
Solomon et al. June 2020 said:
We report the neuropathological findings from autopsies of 18 consecutive patients with SARS-CoV-2 infection who died in a single teaching hospital between April 14 and April 29, 2020. [...] Testing of brain tissue was performed with quantitative RT-PCR (qRT-PCR) for the SARS-CoV-2 nucleocapsid protein. As shown in Table S3, for 2 patients, all 10 sections were tested, and for the remaining 16 patients, 2 sections were tested (1 from the frontal lobe and olfactory nerve and 1 from the [medulla oblongata]). The results were equivocal (defined as a viral load of <5.0 copies per cubic millimeter) in [the first two patients.] In 32 sections obtained from the remaining 16 patients, 3 sections from the medulla and 3 sections from the frontal lobes and olfactory nerves were positive (5.0 to 59.4 copies per cubic millimeter); the results were equivocal in 20 sections and negative in 6 sections.


Potential neuroinvasive pathways of SARS‐CoV‐2: Deciphering the spectrum of neurological deficit seen in coronavirus disease‐2019 (COVID‐19) (Baig and Sanders, June 2020)
https://onlinelibrary.wiley.com/doi/full/10.1002/jmv.26105
Excerpt:
Baig and Sanders June 2020 said:
Abstract
Coronavirus disease‐2019 (COVID‐19) was declared a global pandemic on 11 March 2020. Scientists and clinicians must acknowledge that severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) has the potential to attack the human body in multiple ways simultaneously and exploit any weaknesses of its host.

A multipronged attack could potentially explain the severity and extensive variety of signs and symptoms observed in patients with COVID‐19. Understanding the diverse tactics of this virus to infect the human body is both critical and incredibly complex.

Although patients diagnosed with COVID‐19 have primarily presented with pulmonary involvement, viral invasion, and injury to diverse end organs is also prevalent and well documented in these patients, but has been largely unheeded. Human organs known for angiotensin‐converting enzyme 2 (ACE2) expression including the gastrointestinal tract, kidneys, heart, adrenals, brain, and testicles are examples of extra pulmonary tissues with confirmed invasion by SARS‐CoV‐2. Initial multiple organ involvement may present with vague signs and symptoms to alert health care professionals early in the course of COVID‐19.

Another example of an ongoing, yet neglected element of the syndromic features of COVID‐19, are the reported findings of loss of smell, altered taste, ataxia, headache, dizziness, and loss of consciousness, which suggest a potential for neural involvement. In this review, we further deliberate on the neuroinvasive potential of SARS‐CoV‐2, the neurologic symptomology observed in COVID‐19, the host‐virus interaction, possible routes of SARS‐CoV‐2 to invade the central nervous system, other neurologic considerations for patients with COVID‐19, and a collective call to action.
(emphasis and spacing added for readability)
 

Pyrrhus

Senior Member
Messages
4,171
Likes
12,772
Location
U.S., Earth
The novel coronavirus was detected inside 53% of the brains of people who died from COVID:

Neuropathology of patients with COVID-19 in Germany: a post-mortem case series (Matschke et al., October 2020)
https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(20)30308-2/fulltext

Matschke et al. 2020 said:
"SARS-CoV-2 could be detected in the brains of 21 (53%) of 40 examined patients, with SARS-CoV-2 viral proteins found in cranial nerves originating from the lower brainstem and in isolated cells of the brainstem."
By "cranial nerves", they mean the glossopharyngeal nerve and the vagus nerve.

The authors also note that:
  • "Diffuse activation of microglia, with occasional microglial nodules, was pronounced in the brainstem and cerebellum."
  • "By immunohistochemistry, SARS-CoV-2 could be mapped to isolated cells within the medulla oblongata and in the cranial nerves (either the glossopharyngeal or vagal nerves) originating from the brainstem (figure 5, appendix p 4)."
  • "There was no evidence of cerebral bleeding or small-vessel thromboses. ... Six (14%) patients had fresh ischaemic infarctions: three in the territory of the posterior cerebral artery, two in the territory of the anterior cerebral artery, and one in the territory of the middle cerebral artery, which were most likely due to thromboembolic events."

Abstract:
Lancet Neurology 5 October 2020 said:
Background
Prominent clinical symptoms of COVID-19 include CNS manifestations. However, it is unclear whether severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of COVID-19, gains access to the CNS and whether it causes neuropathological changes. We investigated the brain tissue of patients who died from COVID-19 for glial responses, inflammatory changes, and the presence of SARS-CoV-2 in the CNS.

Methods
In this post-mortem case series, we investigated the neuropathological features in the brains of patients who died between March 13 and April 24, 2020, in Hamburg, Germany. Inclusion criteria comprised a positive test for SARS-CoV-2 by quantitative RT-PCR (qRT-PCR) and availability of adequate samples. We did a neuropathological workup including histological staining and immunohistochemical staining for activated astrocytes, activated microglia, and cytotoxic T lymphocytes in the olfactory bulb, basal ganglia, brainstem, and cerebellum. Additionally, we investigated the presence and localisation of SARS-CoV-2 by qRT-PCR and by immunohistochemistry in selected patients and brain regions.

Findings
43 patients were included in our study. Patients died in hospitals, nursing homes, or at home, and were aged between 51 years and 94 years (median 76 years [IQR 70–86]). We detected fresh territorial ischaemic lesions in six (14%) patients. 37 (86%) patients had astrogliosis in all assessed regions. Activation of microglia and infiltration by cytotoxic T lymphocytes was most pronounced in the brainstem and cerebellum, and meningeal cytotoxic T lymphocyte infiltration was seen in 34 (79%) patients. SARS-CoV-2 could be detected in the brains of 21 (53%) of 40 examined patients, with SARS-CoV-2 viral proteins found in cranial nerves originating from the lower brainstem and in isolated cells of the brainstem. The presence of SARS-CoV-2 in the CNS was not associated with the severity of neuropathological changes.

Interpretation
In general, neuropathological changes in patients with COVID-19 seem to be mild, with pronounced neuroinflammatory changes in the brainstem being the most common finding. There was no evidence for CNS damage directly caused by SARS-CoV-2. The generalisability of these findings needs to be validated in future studies as the number of cases and availability of clinical data were low and no age-matched and sex-matched controls were included.
 
Last edited:
Messages
58
Likes
103
The novel coronavirus was detected inside 53% of the brains of people who died from COVID:
https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(20)30308-2/fulltext

"SARS-CoV-2 could be detected in the brains of 21 (53%) of 40 examined patients, with SARS-CoV-2 viral proteins found in cranial nerves originating from the lower brainstem and in isolated cells of the brainstem."

Excerpt:

I've got neuro covid for sure. I just hope it goes away haha. The inflammation really sucks though.
 

Pyrrhus

Senior Member
Messages
4,171
Likes
12,772
Location
U.S., Earth
This interesting website by a non-scientist has also been compiling a list of research on how the novel coronavirus might infect the brain:

Infection of the Brain by Covid-19 Explains Long Covid (Conte, 2020)
https://covid.us.org/2020/10/08/infection-of-the-brain-by-covid-19-explains-longcovid/


EDIT: Here's a newer preprint that also found coronavirus infection of the brain in acute COVID:

Mapping of SARS-CoV-2 Brain Invasion and Histopathology in COVID-19 Disease (Serrano et al., February 2021)
https://www.medrxiv.org/content/10.1101/2021.02.15.21251511v1
Serrano et al. 2021 said:
As [SARS-CoV-2 (SCV2)] is related to previously-studied coronaviruses that have been shown to have the capability for brain invasion, it seems likely that SCV2 may be able to do so as well. [...] We conducted an extensive neuroanatomical survey of RT-PCR-detected SCV2 in 16 brain regions from 20 subjects who died of COVID-19 disease. [...] Two subjects had severe neuropathology, one with a large acute cerebral infarction and one with hemorrhagic encephalitis, that was unequivocally related to their COVID-19 disease while most of the 18 other subjects had non-specific histopathology including focal β-amyloid precursor protein white matter immunoreactivity and sparse perivascular mononuclear cell cuffing. Four subjects (20%) had SCV2 RNA in one or more brain regions including the olfactory bulb, amygdala, entorhinal area, temporal and frontal neocortex, dorsal medulla and leptomeninges. The subject with encephalitis was SCV2-positive in a histopathologically-affected area, the entorhinal cortex, while the subject with the large acute cerebral infarct was SCV2-negative in all brain regions.
 
Last edited: