Many patients with autoimmunity disease contacted us with questions about Coronavirus COVID-19 and worrying if they are at higher risk. As far as I am concerned there are no studies looking directly at the relationship between Coronavisrus COVID-19 and autoimmune diseases. Below I am presenting my personal thoughts on this subject based on some available research.
What is coronavirus?
WHO defines coronaviruses as ‘a large family of viruses which may cause illness in animals or humans. In humans, several coronaviruses are known to cause respiratory infections ranging from the common cold to more severe diseases such as Middle East Respiratory Syndrome (MERS) and Severe Acute Respiratory Syndrome (SARS). The virus that causes COVID-19 and the one that causes Severe Acute Respiratory Syndrome (SARS) are related to each other genetically, but they are different. SARS is more deadly but much less infectious than COVID-19. The most recently discovered coronavirus causes coronavirus disease COVID-19.’
We are all exposed to viruses, some more dangerous than others. Before the recent coronavirus, there were six other HCoVs human coronaviruses found. Few of them are associated with common cold. Thus, there is a chance we have been exposed to a type of coronavirus.
Symptoms of COVID-19 are:
- Dry cough
- Aches and pains
- Nasal congestion
- Runny nose
- Sore throat
These symptoms begin gradually are usually mild. Some people may get infected but don’t develop any symptoms. About 80% of people recover without needing special treatment. Just 1 out of every 6 people who gets COVID-19 becomes seriously ill and develops difficulty breathing. The incubation period (time between catching the virus and beginning to have symptoms) varies from 1-14 days.
How COVID-19 is spread?
People can catch COVID-19 from:
– others who have the virus
– touching the objects or surfaces where respiratory droplets from the nose or mouth of a person with COVID-19 landed and then touching own eyes, nose or mouth
Are there tests for the virus?
- A swab test: sample the inside of the throat or nose
- A nasal aspirate: inject a saline solution into nose and remove the sample with gentle pressure
- A tracheal aspirate: a sample collected from the lungs via a bronchoscope
- A sputum test: Sputum is a variation of mucus from the lungs. This can be coughed out or sampled from the nose with a swab
- A blood test
Who are those in danger?
Older people, and those with underlying medical problems: high blood pressure, heart problems or diabetes
Are people with autoimmune condition at higher risk of Coronavirus COVID-19?
If we look at autoimmune conditions from evolutionary perspective, it seems that physiological responses are a product of long evolutionary processes, and have a function: survival. As Andrea Graham, an evolutionary biologist at Princeton University states: ‘vulnerability to immune-mediated disease is simply the price we must pay for potent and rapid defence against infection.’ From evolutionary perspective, someone with autoimmune condition may be equipped better to fight viruses as COVID-19. Though, this may not be true if this person is on an immunosuppressive therapy.
Inflammation and Gender. Nearly 50% more men than women dying from COVID-19
The production of inﬂammatory markers and the inﬂammatory process are clearly different for females and males. Female predominance is a common characteristic in cases of autoimmune diseases postulated to be due to the combined effects of hormonal influences and genetic factors. The best evidence for hormonal effects on autoimmunity comes from pregnancy studies: when women are pregnant, disease activity subsides, but after delivery, disease exacerbation occurs. It is also well established that major histocompatibility complex alleles are associated with disease susceptibility for most autoimmune diseases. Thus, being a female may be a protective factor by COVID-19, by simply having a different immune response: stringer immune responses than males.
Viruses and thyroid
Several mechanisms of virus-induced initiating or triggering of autoimmune disease have been advocated: 1) ‘Molecular mimicry’ is the most widely proposed mechanism and occurs when a virus antigen mimics a host antigen and activates cross-reactive T cells; 2) ‘Epitope spreading’: Tissue damage resulting from virus-specific T cell activation or direct virus-mediated host tissue destruction causes de novo activation of autoreactive T cells and releases self-antigens into the inflammatory environment; 3) ‘Bystander activation’: the activation of autoreactive T cells as a result of the release of cytokines during a virus-targeted immune response; 4) Encrypted host antigens are released from certain tissues during virus-targeted tissue damage; 5) ‘Superantigens’ activate a wide range of nonspecific T cell clones regardless of their specificity.
Viral infections are frequently cited as a major environmental factor involved in subacute thyroiditis and autoimmune thyroid diseases, as Hashimoto’s. A substantial number of patients with SARS have shown abnormalities in thyroid function. As SARS is a disease known to cause multiple organ injury, it has been supposed that SARS could have a harmful effect on the thyroid gland. However, low serum triiodothyronine and thyroxine levels associated with decreased TSH concentration are in favor of central hypothyroidism induced by hypophysitis or by hypothalamic dysfunction. The exact mechanism by which SARS causes injury to the thyroid gland remains unclear. Further, some studies reveal the association between respiratory viruses and incident of rheumatoid arthritis.
What can we do?
- Keep good hygiene: Studies suggest that coronaviruses may persist on surfaces for a few hours or up to several days. This may vary under different conditions (e.g. type of surface, temperature or humidity of the environment). If you think a surface may be infected, clean it with simple disinfectant to kill the virus and protect yourself and others. Wash your hands with soap and water. Avoid touching your eyes, mouth, nose.
Maintain a balanced immune system by:
- Take care of your gut: A healthy communication between the gut microbiota and the immune system supports defense against pathogens, tolerance to harmless microbes, and support differentiation of what is ours and what is not and not attacking our own tissues or organs
- Make sure that your body detoxes. COVID-19 is sensitive to heat. It might be protective to make regular use of sauna.
- Manage stress: Chronic stress not only increases susceptibility to new viral infections but also renders people more vulnerable to the reactivation of latent viruses within the body. Don’t let the media get under your skin. In China 3% from the patients with COVID-19 virus died states the media. Yet 97 % healed.
I hope this information is useful to you.
Wishing you well.
- Casimir, G. J., & Duchateau, J. (2011). Gender differences in inflammatory processes could explain poorer prognosis for males. Journal of clinical microbiology, 49(1), 478–479. https://doi.org/10.1128/JCM.02096-10
- Joo, Y.B., Lim, Y., Kim, K. et al. Respiratory viral infections and the risk of rheumatoid arthritis. Arthritis Res Ther 21, 199 (2019). https://doi.org/10.1186/s13075-019-1977-9
- Wang W, Ye YX, Yao H: Evaluation and observation of serum thyroid hormone and parathyroid hormone in patients with severe acute respiratory syndrome. J Chin Antituberculous Assoc 2003, 25:232-234.
- Smatti, M. K., Cyprian, F. S., Nasrallah, G. K., Al Thani, A. A., Almishal, R. O., & Yassine, H. M. (2019). Viruses and Autoimmunity: A Review on the Potential Interaction and Molecular Mechanisms. Viruses, 11(8), 762. https://doi.org/10.3390/v11080762
- Lan Wei, Shen Sun, Cai-hong Xu, Jing Zhang, Yun Xu, Hong Zhu, Suat-cheng Peh, Christine Korteweg, Michael A. McNutt, Jiang Gu,
- Pathology of the thyroid in severe acute respiratory syndrome, Human Pathology, Volume 38, Issue 1, 2007, Pages 95-102
- Stress and Susceptibility to Viral Infections II. Sound Stress and Susceptibility to Vesicular Stomatitis Virus Marcus M. Jensen and A. F. Rasmussen J Immunol January 1, 1963, 90 (1) 21-23
- Psychological stress in humans and susceptibility to the common cold. September 1991 New England Journal of Medicine 325(9):606-612 DOI: 10.1056/NEJM199108293250903 Sheldon Cohen Sheldon Cohen David A.J. Tyrrell Andrew P Smith Andrew P Smith