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Sep 12, 2024 1 tweets 5 min read Read on X
Veins of Ruin: Vascular and Microvascular Damage to the Brain from COVID-19, and a Friend

SARS-CoV-2 (COVID-19) is proven to cause a range of neurological complications, some of which are linked to vascular and microvascular damage in the brain.

For me, vascular damage to anything is probably the scariest of all the things COVID-19 can cause. I have had heart and vascular issues for decades, so anything vascular freaks me out. It caused heart and brain issues that terrified me for decades. My issues were different than my friend's, as mine started for an unknown reason, whereas Dara’s was Covid-19 and caused a stroke.

Mine started as a young husband, almost thirty years ago. My fear is still heart-related, but many are having brain issues, like my friend. That is why today, I want to focus on the brain.

We know that SARS-CoV-2 affects the brain and mind, and we know the underlying mechanisms causing this damage are real.

What is the possible damage?

Endothelial Dysfunction and Blood-Brain Barrier (BBB) Disruption
The endothelial cells, which line the blood vessels, play a critical role in maintaining the integrity of the blood-brain barrier (BBB). SARS-CoV-2 can cause endothelial dysfunction, leading to a compromised BBB. This disruption allows harmful substances, including inflammatory cytokines, to infiltrate the brain, potentially causing neurological damage[1][3][10].
Microvascular Injury

Microvascular injury in the brain has been observed in COVID-19 patients, characterized by fibrinogen leakage, platelet accumulation, and activation of the coagulation system. These changes can lead to occlusion and damage to small blood vessels, contributing to neurological symptoms[8][10]. The resulting microvascular damage can cause ischemia, tissue edema, and inflammation, further exacerbating neurological complications[9].

Neurological and Cognitive Effects

Acute and Long-Term Neurological Symptoms

COVID-19 can lead to a wide range of neurological symptoms, both acute and long-term. Acute symptoms include strokes, encephalopathy, seizures, and encephalitis, while long-term effects may involve chronic neurodegenerative changes, such as those seen in Alzheimer's and Parkinson's diseases[2][4]. The virus's impact on brain regions responsible for cognitive functions can result in symptoms like brain fog, memory loss, and impaired executive function[4][6].

Cognitive Impairment and Dementia

The vascular damage caused by SARS-CoV-2 can lead to vascular cognitive impairment, which may manifest as difficulties in attention, planning, and judgment. These cognitive challenges can progress to vascular dementia, especially in cases where multiple small strokes or significant vascular damage occur[5][6].

Mechanisms of Vascular Damage

Direct and Indirect Mechanisms

SARS-CoV-2 can affect brain vasculature through both direct and indirect mechanisms. While direct infection of endothelial cells by the virus has been debated, the prevailing hypothesis suggests that the virus causes endothelial injury indirectly through an excessive inflammatory response. This inflammation can impair the antithrombogenic properties of the endothelium, leading to thrombosis and vascular occlusion[3][8].

Role of Immune Response

The immune response to SARS-CoV-2 involves the activation of various pathways, including the NF-κB signaling pathway, which can lead to endothelial activation and increased BBB permeability. This immune activation can result in neuroinflammation and contribute to the neurological symptoms observed in COVID-19 patients[9][10].

SARS-CoV-2 has significant implications for brain health, primarily through its impact on the vascular system. The virus can cause both acute and chronic neurological damage, with long-term effects potentially leading to cognitive impairment and dementia. Understanding these mechanisms is crucial for developing strategies to mitigate the neurological impact of COVID-19 and improve patient outcomes. Further research is needed to fully elucidate the pathways involved and to explore potential therapeutic interventions.

Sources

[1] Cerebral microvascular complications associated with SARS-CoV-2 ...
[2] Long-Term Effects of SARS-CoV-2 in the Brain - NCBI
[3] COVID-19 Vasculopathy: Mounting Evidence for an Indirect ... - NCBI
[4] Long-term effects of SARS-CoV-2 infection on human brain ... - Nature
[5] Vascular Cognitive Impairment and Dementia - PMC - NCBI
[6] Vascular Dementia | Symptoms & Treatments |
[7] SARS-CoV-2 deregulates the vascular and immune functions of ...
[8] How COVID-19 affects microvessels in the brain - Oxford Academic
[9] SARS-CoV-2 infection of human brain microvascular endothelial ...
[10] Blood–brain barrier disruption and sustained systemic inflammation ... whereasncbi.nlm.nih.gov/pmc/articles/P…
ncbi.nlm.nih.gov/pmc/articles/P…
ncbi.nlm.nih.gov/pmc/articles/P…
nature.com/articles/s4142…
ncbi.nlm.nih.gov/pmc/articles/P…
alz.org
alz.org/alzheimers-dem…
sciencedirect.com/science/articl…
academic.oup.com/brain/article/…
ncbi.nlm.nih.gov/pmc/articles/P…Image

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More from @Dave_it_up

Jun 23, 2024
Is their evidence for viral persistence in COVID-19?

From the meticulous work of the PolyBio Research Foundation, in collaboration with the esteemed halls of UC San Francisco and Harvard Medical School, to the robust findings published in Nature and The Lancet, we are presented with compelling evidence of the virus’s tenacity. 

These studies not only confirm the presence of viral proteins and RNA months after the acute phase of infection but also suggest a troubling link to the chronic, debilitating symptoms known as long COVID.

Let’s delve into some of the evidence for the evidence pointing to viral persistence of SARS-CoV-2, 

1. PolyBio Research Foundation Study
A study published by the PolyBio Research Foundation, supported by UC San Francisco and Harvard Medical School, found that viral proteins from SARS-CoV-2 could persist in the body for up to 14 months post-infection. This study used an ultra-sensitive blood test to detect viral proteins in 25% of the 171 participants, indicating that the virus can linger in tissues and organs long after recovery from the acute phase of the infection. The likelihood of detecting these proteins was higher among those who were hospitalized or reported severe symptoms during their initial infection[1].

2. Nature Study on Persistent SARS-CoV-2 RNA Shedding
A cohort study published in *Nature* identified persistent SARS-CoV-2 RNA shedding in individuals for at least 30 days, with some cases extending to 60 days. The study found that individuals with persistent infections had more than 50% higher odds of reporting long COVID symptoms compared to those with non-persistent infections. This suggests that persistent infections could contribute to the pathophysiology of long COVID, although the exact mechanisms remain to be fully understood[3].

3. NCBI Study on Long COVID and Viral Persistence
Research published on NCBI proposed a hypothesis-driven model for long COVID, suggesting that the persistence of SARS-CoV-2 or its components (such as the spike protein) could lead to chronic inflammation and a dysregulated immune response. This model is supported by evidence of viral RNA and antigens being detected in various tissues, including the cerebrospinal fluid and feces, months after the initial infection. The study highlights the potential for viral persistence to trigger long-term health issues[2].

4. Lancet Study on Viral Persistence in Tissues
A study published in *The Lancet* examined the persistence of SARS-CoV-2 in various tissues, including blood, gastrointestinal, and surgical samples. The research found that viral RNA and proteins could be detected in these tissues long after the acute phase of infection, suggesting that the virus can persist in different parts of the body and potentially contribute to ongoing symptoms and health complications[5].

5. NCBI Study on Viral Persistence and Reactivation
Another study on NCBI explored the persistence of viral RNA and antigens in patients with long COVID. It found that viral components could be detected in blood, stool, and urine, and that the presence of these components was associated with persistent symptoms. The study also noted that viral persistence might involve either active replication or the presence of non-replicating viral RNA, which could still trigger immune responses and inflammation[4].

The evidence from these studies collectively supports the notion that SARS-CoV-2 can persist in the body for extended periods, potentially leading to long-term health issues such as long COVID. This persistence can involve both active viral replication and the presence of viral components that continue to stimulate the immune system, leading to chronic inflammation and other symptoms. 

Further research should be done to put to rest this question of viral persistence and to develop effective treatments for long-term COVID.Image
Sources
[1] COVID-19 Virus Can Persist in the Body More Than a Year after ...
[2] Long COVID: A proposed hypothesis-driven model of viral ... - NCBI
[3] Prevalence of persistent SARS-CoV-2 in a large community ... - Nature
[4] Viral persistence, reactivation, and mechanisms of long COVID - NCBI
[5] The persistence of SARS-CoV-2 in tissues and its association with ... biospace.com/article/releas…
ncbi.nlm.nih.gov/pmc/articles/P…
nature.com/articles/s4158…
ncbi.nlm.nih.gov/pmc/articles/P…
thelancet.com/journals/lanin…
Someone just let me know that there are actually two more studies that are important. I will post them as soon as I get a hold of them.
Read 6 tweets
Dec 24, 2023
Similarities of HIV and Covid.

A study reveals that SARS-CoV-2 can infect human CD4+ T helper cells, impacting the immune response in severe COVID-19 cases. The virus uses the CD4 molecule to enter these cells, leading to functional impairment and cell death. This infection results in increased IL-10 production in T cells, associated with viral persistence and severe disease. The findings suggest that SARS-CoV-2 infection of CD4+ T cells contributes to immune dysfunction in COVID-19.

elifesciences.org/articles/84790
From Merk manual for healthcare professionals.
Image
Image
Also thanks for graphic @dbdugger
Read 4 tweets

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