A full year into the COVID-19 pandemic, scientists are still searching for answers on how the disease wreaks its devastation and why some people are so much more vulnerable than others. The COVID-19 vaccines have given many people hope, and rightly so. However, danger still lurks, and the more researchers understand, the safer all of us will be.
While most people infected with COVID-19 have mild symptoms, severe COVID-19 can dramatically alter a patient’s immune system, causing inflammation in the heart, lungs, and other organs. Critically ill patients counterintuitively display a strong immune response; in some cases, the patient’s body unleashes a storm of immune factors so severe that it endangers the patient’s life.
With the pandemic raging, doctors and scientists scrambled to find treatments and develop a vaccine. This critical work required access to immune cells and other biological samples from recovering COVID-19 patients.
Cellero COVID-19 immune cell products, including SARS-CoV-2 antigen specific T cells have been, and continue to be, critical research tools for these studies.
PBMC, serum, and plasma from individuals who have recovered from mild versus significant COVID-19 illness can help scientists better understand how differences in immune cell populations, cell phenotype, and genetics impact disease. The history of the donor’s illness is included on the certificate of analysis along with HLA typing and antibody titers.
Studies now suggest severe COVID-19 bears a striking resemblance to autoimmune disease. Many people infected by the coronavirus go on to develop myocarditis, an inflammation of the heart muscle that can cause lasting damage. This symptom has been found even in those patients who initially had mild disease or were asymptomatic. This type of post-COVID inflammation has been observed in other vital organs as well. Along with these observations, evidence shows that treatment with medications for autoimmune disease has a therapeutic effect on patients with severe COVID-19, strengthening the idea that there is a link between the two.
Viruses are known to be capable of triggering autoinflammation and autoimmune disease, so the immunological abnormalities seen with COVID-19 are not without precedent. In October of 2020, a groundbreaking study published in Nature Immunology  reported finding the same changes in immune cells that occur during flare-ups in lupus patients happening in COVID-19 patients. Since then, several more studies [2, 3] have discovered evidence of strong similarities between COVID-19 and autoimmune disease. The latest research suggest that COVID-19 can “evolve” in the body in 4 overlapping phases:
- An initial viral phase, which is asymptomatic or mild in 80% of cases, but more severe in 20% of cases
- Host-virus interactions occur which lead to a hyperresponsive immune response
- A state of hypercoagulation (high chance of blood clot formation), which can lead to stroke or heart attack.
- Intensity autoinflammatory response and/or blood clot sensitivity can result in organ damage.
While researchers are steadily learning more about the long-term effects of COVID-19, there are still many questions that need to be answered. How and why does the disease progress from one phase to the next? What are the risk factors involved? Could other strains of coronavirus be as-yet unidentified triggers for some types of autoimmune disease? Can autoimmune disease therapeutics help stop COVID-19 from progressing?
Research into these questions and many more is ongoing, as is the demand for reliable access to COVID-19 related immune products. At Cellero, we are committed to providing the tools you need to continue this critical research. Please visit our website to learn more.
- Woodruff M. C., et al. Extrafollicular B cell responses correlate with neutralizing antibodies and morbidity in COVID-19. Nature Immunology. 21; 1506-1516. Dec 2020.
- Rodriguez Y., et al. Autoinflammatory and autoimmune conditions at the crossroad of COVID-19. Journal of Autoimmunity. 114. 2020.
- Liu Y., et al. COVID-19 and autoimmune diseases. Current Opinion in Rheumatology: 33(2); 155-162. Mar 2021.