I Do My Own Research

 

A couple weeks after turning 65 last month, I got a message from CVS suggesting that I get a COVID shot. Now, I hadn't had one since 2021, when I started to become aware of reasons for skepticism about official information on the subject, especially with regard to people like me who were not part of any high-risk group. I'd had two of the AstraZeneca mRNA-based shot in December 2020 as part of a clinical trial which wasn't unblinded until June of 2021, when I learned I had received the vaccine. In the meantime I received two Moderna shots in April and May, also mRNA-based. The worst side effect was a bad headache the day after the second of these.

I've only tested positive for COVID once, in January of 2023. I had no particular symptoms but tests were being administered to everyone at the shelter where I was staying at the time. Because of the positive result I spent six days in a quarantine facility, although I experienced nothing worse than a mild cold. I understand that these test results have often been amplified to such a degree as to guarantee a large number of false positives, so it's likely I actually had nothing at all.

In any case, now I'm officially in an elevated-risk group, so I thought maybe I should consider getting the latest shot. But I'd heard no reason to be any less concerned than before about the mRNA technology, or more specifically the lipid nanoparticle platform, which biologist Bret Weinstein has described as "a promising technology" that's "not ready for prime time." So I was pleased that the CVS webform for scheduling a shot actually gave me a choice in this regard, and I used it to select a more traditional shot (Novavax) which presents you with the spike protein itself rather than genetic material coding for it.

But shortly after this I recalled someone making the argument that most of COVID disease is actually the immune system's response to the spike protein, and that therefore it makes no sense to get a vaccine consisting of the same challenge that causes the disease in the first place. So shortly before my shot was scheduled this afternoon, I asked DuckAI about it:

 

To what extent are the symptoms of COVID-19 disease caused by the immune system's response to the spike protein?

Duck.ai said

The immune response contributes substantially to COVID-19 symptoms, but it is not accurate to attribute them specifically to an immune reaction against the spike protein. COVID-19 symptoms arise from several overlapping processes:

• Viral replication and infected-cell injury. Spike binds ACE2 and enables the virus to enter cells, especially respiratory epithelial cells. The resulting infection and cell damage are important causes of cough, sore throat, loss of smell, and lung disease.
• Innate immune activation. Detection of viral RNA and injured cells triggers interferons, cytokines, prostaglandins, and other inflammatory mediators. This response produces many “sickness” symptoms—fever, fatigue, headache, muscle aches, chills, and malaise.
• Excessive or poorly regulated inflammation. In severe disease, macrophages, neutrophils, complement, platelets, and coagulation pathways can cause lung inflammation, vascular leakage, microclots, and acute respiratory distress. This is an immune-mediated component, but it is driven by the infection as a whole—not by spike alone. Nature1

Spike can contribute in two ways. First, it is the viral component that initiates cell entry and therefore starts the infection. Second, spike or spike-containing viral particles can interact with immune and vascular cells and may amplify inflammation in some circumstances. However, studies using isolated spike protein, cell cultures, or animals do not establish that free spike is responsible for most symptoms in human COVID-19; concentrations, tissue distribution, and exposure conditions differ substantially from natural infection. Nature1

The timing also matters. Early symptoms often reflect the innate response to viral infection. The adaptive response—spike-specific antibodies and T cells—usually helps control the virus and is generally associated with milder disease rather than being the main cause of symptoms. In severe COVID-19, the problem is more often an imbalanced response: inadequate antiviral control alongside damaging inflammation. Frontiers

A practical summary is:

• Mild COVID-19: symptoms are probably a mixture of local viral injury and a normal antiviral inflammatory response.
• Severe COVID-19: tissue damage is substantially immune-mediated, but results from dysregulated responses to ongoing infection, not simply “the immune system attacking spike.”
• Loss of smell: largely relates to infection of support cells in the olfactory lining rather than an isolated anti-spike reaction.
• Long COVID: may involve persistent immune dysregulation, tissue injury, viral remnants, clotting or autonomic abnormalities, and other mechanisms; the specific contribution of spike-directed immunity remains unsettled.

So, in broad terms, the immune response is responsible for many symptoms and much of the damage in severe COVID-19, but spike-specific immunity is only one part of that response and is not the sole—or even necessarily the dominant—cause of most COVID-19 symptoms.

From this I judged that there was little for someone my age to fear from the shot, but I stayed in the CVS for twenty minutes afterward anyway in case there was a reaction. I was fine, however.