Having suffered for months from long COVID and made a full recovery, I don't think its accurate to characterize it as a "life destroying" condition.
Sadly, many people suffering from long COVID were persuaded to get mRNA vaccinations which they clearly did not need (on account of having acquired natural immunity), and their recovery from long COVID was either impeded or the vaccines injured them in other ways.
I am glad that you made a relatively full recovery from long COVID. Many others however did not. Some are still suffering, or have been afflicted with permanent damages and won't be making a full recovery. It's also important to appeal to published statistics when making associations or generalizations.
Long COVID is not a single syndrome, but a constellation of possible complications. The variation in individual response to the virus needs to be recognized, we cannot underestimate this. Some individuals show no signs of upper respiratory infection[2], suggesting the virus is affecting them more systemically[1]. Some people continue to have symptoms despite viral clearance (see Yale quote below). The vaccine is not expected to cure cases where the virus has been long cleared and where post-immune inflammation is the primary culprit—but it should help prevent long COVID in the first place[3]. In this regard it is similar to other vaccines. The rabies vaccine has a very short window (1-2 days) after a suspected bite or scratch, after which point it becomes ineffective at stopping the virus' march toward the spinal cord & brain, and death follows invariably. So giving the COVID vaccine long after is likely not going to help, and it could make things worse. The vaccine use needs to be carefully mediated going forward, it's clear if we force it on everyone at exactly the same dose, it can have unwanted effects.
The article I am quoting is here, on the Yale medical blog: https://medicine.yal...ogy-long-covid/
Long COVID refers to the long-term health and cognition effects that some people experience following infection with COVID-19. Patients have reported unrelenting fatigue, brain fog, dysautonomia, shortness of breath, and digestive problems, among over 200 symptoms — in some cases requiring frequent or even long-term hospitalization. The Iwasaki Lab is interested in exploring the biological mechanisms underlying these phenotypes — and how future research can harness this knowledge to engineer more effective and specific biomarkers for long COVID.
As researchers continue to examine how such patterns can provide information indicative of long COVID, Iwasaki proposes four possible hypotheses for the condition’s initiation and progression. They are:
- Persistent viral loads or remnants hidden away in tissue and causing chronic inflammation. These viruses may not be measurable via nasopharyngeal swabs because they might be “hiding” in other internal organs, such as the gut.
- Our body’s own disease-fighting B and T cells triggering an immune response — and subsequent inflammation — in a process called autoimmunity. The problem is: the stimulus that triggers autoimmunity in response to an acute infection is oftentimes occurring continuously in the body, making it difficult to pinpoint and shut down.
- Dormant viruses reactivating, and/or dysbiosis of microbiome disturbing our body’s homeostasis. Humans live with trillions of bacteria and a number of viruses that are latent. When acute infection disturbs the host, these bacteria lose its composition balance and dormant viruses can become reactivated. These viruses and microbes can cause inflammation and throw off body’s homeostasis.
- Macroscopic and microscopic tissue damage resulting from the initial infection. COVID-19 impacts parts of our body that we don’t commonly think about. Whether it’s our lungs or our brains or the endothelial tissue lining our blood vessels and supporting oxygen change, the virus — and the medication used to treat it — can lead to clotting or scarring in places that are difficult to reach and repair. In addition, inflammation that occurs in one tissue can trigger damage in other tissues.
In reality, long COVID is not a single disease. There are likely multiple endotypes of the disease. We are conducting human studies and developing animal models to understand the underlying pathogenesis of long COVID.
References
[1] Chrzan, R., Popiela, T., Małecki, M., Skupień, J., Bryll, A., & Grochowska, A. (2021). COVID-19 Infection Negative in Nasopharyngeal Swabs but Suspected in Computed Tomography and Confirmed in Bronchoalveolar Lavage Material. Case reports in infectious diseases, 2021, 6627207. https://doi.org/10.1155/2021/6627207
[2] Beneš, J., Džupová, O., Poláková, A., & Sojková, N. (2021). Repeatedly negative PCR results in patients with COVID-19 symptoms: Do they have SARS-CoV-2 infection or not?. Opakovaně negativní PCR u pacientů s projevy covid-19: Mají či nemají infekci SARS-CoV-2?. Epidemiologie, mikrobiologie, imunologie : casopis Spolecnosti pro epidemiologii a mikrobiologii Ceske lekarske spolecnosti J.E. Purkyne, 70(1), 3–9. https://pubmed.ncbi....h.gov/33853332/
[3] Watanabe, A., Iwagami, M., Yasuhara, J., Takagi, H., & Kuno, T. (2023). Protective effect of COVID-19 vaccination against long COVID syndrome: A systematic review and meta-analysis. Vaccine, 41(11), 1783–1790. https://doi.org/10.1...ine.2023.02.008