Viruses and Hashimoto’s

How infection affects the thyroid?

Viral infections are some of the most common triggers of thyroid problems and Hashimoto’s (1).

Some viruses have actually been shown to be cause Hashimoto’s: rubella or German measles, mumpsEpstein Barr Virus (EBV)parvovirus and enterovirus.

How does it all start?

1. Viruses attack the thyroid gland

Most commonly this happens when viruses attack the throat, nose, and upper respiratory area (sore throat), but also enteroviruses (2–4). Why doesn’t everyone who gets a cold get thyroid problems? Because viruses work together with genetic predisposition (5). Viruses migrate from the throat into the thyroid gland, invade the thyroid cells and start multiplying there. This causes an inflammation of the thyroid.

2. Thyroid autoimmune disease starts

Infection and inflammation cause many different immune cells to move to the thyroid to fight viruses (6,7).

How does this happen? When viruses attack thyroid cells and immune cells come to fight them, the end result is a destroyed thyroid cell, which is chopped in fragments in the process of cell death, called apoptosis. When cells die several things happen: they produce specific molecules and attract immune cells. Immune cells might get confused and recognize parts of the destroyed cell as an enemy. They memorize how these cell parts look like and transfer this knowledge to more immune cells. This is how immune memory works (8).

3. Thyroid becomes (mildly) underactive

This process damages the thyroid. At first the thyroid becomes mildly underactive, but subsequently more and more. This might take a few weeks to months, or be as long as 5 or more years. By this time viruses will be long gone from the body, and may not be detected during a routine lab test.

4. A too-clean environment doesn’t help either

Even though infections trigger autoimmune thyroid problems, having a too-clean environment is not the best solution.

Every time we have a viral infection, our immune system gets smarter, and starts to memorize and better distinguish between the virus and our own body (9,10).

References

  1. Prummel M, et al. The environment and autoimmune thyroid diseases, 2004
  2. Volpe R. Thyroiditis: current views of pathogenesis, 1975
  3. Martino E, et al. High prevalence of subacute thyroiditis during summer season in Italy, 1987
  4. de Bruin TW, et al. An outbreak of thyrotoxicosis due to atypical subacute thyroiditis, 1990
  5. Kacprzak-Bergman I, et al. Influence of genetic factors on the susceptibility to HBV infection, its clinical pictures, and responsiveness to HBV vaccination, 2005
  6. Tomer Y, et al. Infection, thyroid disease, and autoimmunity, 1993
  7. Davies TF. Infection and Autoimmune Thyroid Disease, 2008
  8. Harii N, et al. Thyrocytes express a functional toll-like receptor 3: overexpression can be induced by viral infection and reversed by phenylmethimazole and is associated with Hashimoto’s autoimmune thyroiditis, 2005
  9. Bach JF. Infections and autoimmunity, 2005
  10. Kondrashova A, et al. Serological evidence of thyroid autoimmunity among schoolchildren in two different socioeconomic environments, 2008