Thank you, Emmanuel, for your excellent post! Here is a definition list of the immune cells you talked about, along with their functions. Understanding these immune cells is crucial because they form the basis of how our body defends itself against infections and diseases.
1. Lymphocytes
These are a type of white blood cell that plays a key role in the immune system, and they come in three main forms:
- T Cells: These cells are critical for identifying and attacking infected cells in the body. There are different types of T cells:
- Helper T Cells: Help other immune cells by releasing chemicals (cytokines, which are signaling molecules that help coordinate the immune response) that boost the immune response.
- Cytotoxic T Cells: Directly kill infected cells or cancerous cells.
- Regulatory T Cells: Help to control or "regulate" the immune response, preventing overactivity that could lead to autoimmune diseases.
- B Cells: These cells are responsible for producing antibodies. Antibodies are proteins that bind to foreign invaders like viruses or bacteria, marking them for destruction.
- NK (Natural Killer) Cells: These are part of the innate immune system, meaning they don’t need to recognize a specific invader. The innate immune system provides a general defense against infections, unlike the adaptive immune system, which targets specific pathogens after prior exposure. They are particularly good at detecting and destroying cells that are infected or have become cancerous.
2. Neutrophils
These are the most abundant type of white blood cell and are among the first responders to infection. They primarily attack bacteria and fungi, engulfing and digesting them through a process called phagocytosis (the process by which cells engulf and break down pathogens or particles). They act fast, but they also have a short life span, often dying in the process of defending the body.
3. Macrophages
These are large white blood cells that play a vital role in both the innate and adaptive immune responses. They engulf pathogens (like bacteria, such as Salmonella, or viruses, like influenza) and debris through phagocytosis. Once they’ve digested the invader, macrophages can also present pieces of the invader (antigens) on their surface to other immune cells, helping to stimulate a more specific immune response. Because of their large size, even though they make up a smaller percentage of immune cells by number, they contribute significantly to the overall mass of immune cells.
4. Bone Marrow and Thymus
These are two critical organs for immune cell production. The bone marrow produces most of the immune cells, including all types of lymphocytes, and is the birthplace for neutrophils and macrophages as well. The thymus is a small organ located in the chest, where T cells mature and learn to differentiate between the body’s own cells and foreign invaders.
5. Lymph Nodes and Spleen
These organs serve as hubs where immune cells are stored, activated, and sent out to battle infections. The lymph nodes act like filters, trapping invaders like bacteria or viruses, and giving immune cells the chance to mount an attack. The spleen helps filter blood and also plays a role in housing immune cells, particularly lymphocytes.
6. Changes with Age and Disease
As people age, the bone marrow and thymus produce fewer immune cells, leading to a generally weaker immune system, which increases susceptibility to infections and other diseases. Obesity and infections can also change the distribution and number of immune cells, often causing imbalances that can either weaken the immune response or cause it to become overactive, leading to inflammation and tissue damage.
This detailed understanding of the different immune cells and their roles gives a more complete picture of how our body fights off infections and diseases, including the response to viruses like SARS-CoV-2.
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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.