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.
How to Love Someone With Long Covid (Even When It’s Hard)
Let’s talk about something brutal.
When you get sick and stay sick, people disappear. That’s not a flaw in your personality or your worth. That’s human behavior. Animal behavior, actually.
Let me rewind.
Decades ago, I dated someone I loved deeply. She had this deep belief, that if the passion fizzled, it was over. That was the whole rulebook for her: no fireworks, no future. And maybe when you’re young, that feels like truth. But I had already seen what love actually looks like, the kind where your parents argue. and then hold hands shortly after. The kind where frustration turns into listening, and listening, turns back into love, like some weird emotional tide.
So when she asked me, “Is it over?” I was confused. Like… why would she even think that?
Later, I learned something that changed me.
You don’t have to feel love to show it.
Almost always, the showing comes first.
When you do the loving thing as a caregiver, lover, friend, and cook their favorite meal, run the errand, sit through their bad day, something inside shifts. Love grows out of the act in you. It’s a feedback loop. Not a feeling. A practice. Both of my deepest relationships got stronger the moment I stopped chasing emotional proof and just acted out of little acts of me doing loving things. And you know what? The feeling always followed. I loved them more. I was loved back more.
This is where we bring in Long Covid.
Millions of people have been living through something that most of the world pretends isn’t real. Something that doesn’t show up on the surface, but eats through their body, their energy, their memory, their sense of self. And if they are lucky enough to have a partner, or a parent, or a friend who’s still around, chances are, you are also struggling.
Because illness drives people away.
It always has.
It’s not new. Throughout history, when people got sick, they got abandoned. Leprosy. Tuberculosis. Polio. People didn’t just suffer the disease, they suffered being cast out.
We’re no different. Just more polite about it.
And if you’re the one still here, caring for someone who’s chronically ill, let me say this: Your instincts will betray you. There’s a weird effect that illness has on caregivers. It makes you want to retreat. You’ll find yourself pulling away. Not because you’re cruel. But because your brain is screaming for safety. Normalcy. Simplicity. And right now, the sick person you love is the opposite of that.
This is where I remind you: You are an animal.
I listen to this podcast called Tooth and Claw. It’s full of bear attacks and wild animal stories. One of the hosts says something that stuck with me:
“If you see a behavior in animals across a wide population, it’s probably an animal behavior.”
Well guess what? Caregivers disappearing when someone gets sick, and that’s an animal behavior. Human animal behavior. Our biology is hardwired for survival, and that means distancing from perceived danger. Sickness triggers something ancient in us. Something deep. Something hard to override.
But here’s the thing.
You can override it.
It starts with remembering who they are, not who they are now, in bed, groaning, or angry, or falling apart, but who they were. Who you fell in love with. Who made you laugh until you cried. That version of them still exists, even if it’s buried under symptoms and fatigue and grief.
Remember this too: In sickness and in health wasn’t poetic fluff. That vow wasn’t written for fairy tale weddings. It was a survival pact. It came from generations of people who watched their children die of infections. Who lost partners to fevers. Who suffered and stayed. That phrase was carved out of real history, when illness wasn’t rare (Just look up how many children died pre-1930s) it was expected. And now here we are again.
Modern medicine gave us the illusion that we were safe. That sickness was temporary. That suffering was manageable. But Long Covid shattered that illusion. And most people born after 1960 have no emotional blueprint for this.
We’re flying blind.
If you’re the one who’s sick, here’s something you need to hear: You’re not being ignored because you’re annoying or boring or selfish. You’re being ignored because your suffering triggers something ancient and uncomfortable in people. They don’t know how to sit with it. Most weren’t taught how. Their avoidance isn’t always a conscious choice. It’s an emotional reflex.
In the book How Emotions Are Made, Lisa Feldman Barrett explains that emotions come first, and logic comes after. We don’t decide how to feel — we feel, and then decide based on that. So when your loved one shrinks from your pain, or snaps at you, or stops checking in, ask yourself: Are they choosing that? Or is it an emotional response they don’t even recognize?
Think about the last time you stubbed your toe on something, and shouted at an inanimate object. “Damn it!” That wasn’t a planned reaction. That was your animal brain in action.
That’s what we’re dealing with. Not cold indifference. Biology.
So what can you do?
If you’re a caregiver, do one loving thing today. Not because you feel warm and fuzzy. But because it’s the right thing. Make tea. Rub their back. Sit in the room quietly. Do it even if they don’t thank you. Do it even if they’re upset. Because the feedback loop still works. It works on you. You’ll feel more love just from acting in love.
If you’re a patient, and your family member is cold or distant, try this: If you have the energy, think a loving thought toward them. Even if they’re not giving it back. Just thinking it can soften something inside you. Maybe it leaks out. Maybe it doesn’t. But you’ll feel it. And maybe — just maybe — that loop starts to close.
None of us chose this.
But we can choose how we respond.
We’re not just animals.
We’re animals with memory.
With words.
With stories.
I know I tend to make long posts. I’m going to include an audio version for those who can’t read long posts. For future articles, I’m definitely open to suggestions fiture posts. Should they be shorter or should they be broken up with titles?
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.
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.