Epstein-Barr Virus Latency

 

Epstein-Barr Virus (EBV), best known for causing glandular fever, infects over 90% of the world’s population. After the initial infection, EBV remains in the body in a dormant (latent) state, hiding inside immune cells. While dormant, it doesn't produce new viruses but continues to express certain viral proteins that can subtly influence the immune system.

 

Research shows a strong link between this latent EBV activity and the development of Hashimoto’s thyroiditis. In tissue samples from patients with Hashimoto’s, EBV was detected in over 80% of cases using a marker called EBER, which confirms the virus's presence in its latent form. Additionally, another EBV protein, LMP1, was found in about 34% of cases, further supporting its activity within thyroid tissue.

Furthermore, blood tests comparing 60 people with Hashimoto’s to 60 healthy individuals revealed that while all had signs of past EBV infection, about one-third of Hashimoto’s patients had elevated levels of EA IgG, a marker of viral reactivation. This was rare in the healthy group. 

 

This suggests that not just past infection, but ongoing low-level reactivation of EBV may contribute to triggering or worsening Hashimoto’s. Interestingly, higher levels of EBNA-1 IgG, which is a marker of long-term viral latency, were linked to lower T3 thyroid hormone levels in patients, implying that more viral activity might suppress thyroid function.[4][5]

 

Treg Dysfunction

 

In Hashimoto’s thyroiditis, a specific part of immune protection, known as regulatory T cells (Tregs), which are essential for maintaining immune tolerance, often exhibit impaired function. This dysfunction permits self-reactive immune responses to continue unchecked, leading to the destruction of thyroid tissue and the production of autoantibodies such as anti-TPO and anti-Tg.[6]

 

Infections 

A central underlying factor contributing to the immune imbalance, including Treg Dysfunction which correlates to the pathogenesis of Hashimoto's, is the presence of chronic infections, which serve as persistent immunological triggers. These include:

 

• SIBO

• Candiadiasis

• Helminth infection

• Protozoa Infection

• Herpes Simplex Virus

• Epstein Barr Virus

• Mycotoxicosis

 

These infections drive the chronic elevation of interleukin-6 (IL-6) which plays a central role in immune dysregulation. IL-6 is a pro-inflammatory cytokine, and within the thyroid elevated IL-6 promotes the conversion of regulatory T cells (Tregs), which normally suppress inappropriate immune responses into pro-inflammatory Th17 cells, which contributes directly to the development and sustainment of Hashimoto's.[6]

 

Oxidative Stress 

 

Oxidative stress plays a central role in the pathophysiology of Hashimoto’s. Excessive production of reactive oxygen species (ROS) leads to fat peroxidation, protein oxidation, and DNA damage within thyroid follicular cells. These oxidative insults compromise cellular membranes and mitochondrial function, ultimately resulting in thyrocyte damage and death.

 

It has been demonstrated in individuals with HT, antioxidant defense mechanisms are notably impaired. Studies have demonstrated reduced activity of key antioxidant enzymes, including superoxide dismutase (SOD) and glutathione peroxidase (GPx), alongside a decline in total antioxidant capacity. Moreover, patients who test positive for thyroid peroxidase antibodies (TPOAb) exhibit significantly elevated oxidative stress markers, highlighting a strong association between autoimmune activity and antioxidant capacity [30].

 

Heavy Metal Toxicity

 

Cadmium 

 

Cadmium, commonly released from industrial pollution and cigarette smoke, accumulates in various tissues including the thyroid gland. It induces oxidative stress and impairs the biosynthesis of thyroid hormones. 

 

Cadmium has the strongest evidence linking it to Hashimoto’s. Several human studies have found a positive correlation between blood or urinary cadmium levels and elevated TPOAb and TgAb. The underlying mechanisms include oxidative stress, damage to thyroid follicular cells, and suppression of antioxidant enzyme production, which leads to immune dysregulation. Cadmium can also impair the function of thyroid-specific enzymes, increasing their antigenicity and promoting autoimmune reactivity.[8]

 

Lead 

 

Lead is commonly found in old paints, gasoline, contaminated soil near older buildings, It can also be present in imported spices, and traditional cosmetics.

 

Lead exposure is also significantly associated with autoimmune thyroid activity. Research has shown that women with higher blood lead levels have an increased risk of developing thyroid autoimmunity, including higher TPOAb levels and a greater likelihood of hypothyroid symptoms. Lead disrupts thyroid hormone synthesis, alters immune tolerance, and may compromise the blood-thyroid barrier, which allows immune cells to access thyroid antigens, triggering antibody formation.[8]

 

Arsenic 

 

Exposure to Arsenic  can take place from contaminated ground water and imported foods such as rice and seafood. Studies have reported elevated thyroid antibodies, particularly TgAb in relation to arsenic exposure, which affect gene regulation through epigenetic mechanisms, and cause structural damage to thyroid tissue. Additionally, arsenic often acts antagonistically with selenium, a key nutrient for thyroid protection, potentially increasing vulnerability to autoimmune responses.[8]