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.
• • •
Missing some Tweet in this thread? You can try to
force a refresh
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.