Viral Infections Including COVID-19 And Thyroid Cancer: A New Threat Emerges

Medical News: The thyroid gland, a butterfly-shaped organ at the base of the neck, plays a crucial role in regulating metabolism, energy production, and overall hormonal balance. However, it is increasingly under threat from a variety of factors that can lead to thyroid cancer (TC). Among these factors, recent research by scientists from the The Second Affiliated Hospital, Xi’an Jiaotong University-China, has highlighted the significant role of viral infections in the progression of TC. Viruses such as Epstein-Barr virus (EBV), hepatitis C virus (HCV), human immunodeficiency virus (HIV), and the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have been implicated in the pathogenesis of this disease. This Medical News report explores the potential mechanisms by which these viruses contribute to TC, the latest research findings, and the implications for diagnosis and treatment.


Viral Infections Including COVID-19 And Thyroid Cancer: A New Threat Emerges

The Global Burden of Thyroid Cancer
Thyroid cancer is the most common malignant tumor of the endocrine system, with significant global incidence. According to Global Cancer Statistics 2020, there were approximately 586,000 cases of TC, making it the ninth most common cancer worldwide. In China, the 2022 cancer statistics reported 466,100 new cases, making it the third most common cancer, and 11,600 deaths due to TC. The majority of thyroid cancers are classified as papillary thyroid cancer (PTC) and follicular thyroid cancer (FTC), with rarer forms including medullary thyroid cancer (MTC) and anaplastic thyroid cancer (ATC).
 
Factors Contributing to Thyroid Cancer
The etiology of TC involves a complex interplay of genetic mutations, environmental factors, ionizing radiation, and iodine intake. Recent studies have added viral infections to this list, suggesting that viruses can significantly influence the occurrence, development, and prognosis of TC. Viral DNA from Epstein-Barr virus (EBV) and erythrovirus B19 (EVB19) has been detected in thyroid tumors, and patients with hepatitis C virus (HCV) or human immunodeficiency virus (HIV) have shown higher incidences of TC.
 
The Role of Viral Infections in Thyroid Cancer
-Epstein-Barr Virus (EBV) and Thyroid Cancer
EBV is a ubiquitous virus, with about 95% of adults worldwide being infected. It is known to cause infectious mononucleosis and is associated with several lymphomas and epithelial malignancies, including Hodgkin lymphoma and nasopharyngeal cancer. Recent studies have identified EBV as a potential contributor to the development of thyroid cancer. For instance, a study in Iran found EBV DNA in 27 out of 41 PTC patients, while another study detected EBV DNA in 71.9% of TC patients. These findings suggest a strong correlation between EBV infection and TC, although regional and methodological differences lead to some con tradictory results.
 
-Mechanisms of EBV in Thyroid Cancer
EBV contributes to cancer development through its ability to persist in host cells and evade immune detection. The virus can induce the expression of oncogenic proteins and interfere with normal cellular processes. EBV’s latent infection phase, where it replicates silently within host cells, plays a crucial role in tumor development. The virus's ability to bind to and enter epithelial cells, along with its influence on the tumor microenvironment, further facilitates the progression of TC.
 
-Hepatitis C Virus (HCV) and Thyroid Cancer
HCV is primarily known for causing liver diseases, but it also has significant extrahepatic manifestations, including autoimmune disorders and thyroid diseases. Studies have shown a higher incidence of thyroid disorders, including thyroid cancer, in patients with HCV. A meta-analysis indicated a positive correlation between HCV infection and the risk of TC, particularly through the development of autoimmune thyroid diseases (AITDs) such as Hashimoto's thyroiditis (HT), which is a known risk factor for TC.
 
-Mechanisms of HCV in Thyroid Cancer
HCV may contribute to thyroid cancer through immune system dysregulation. Chronic HCV infection can lead to the upregulation of chemokines and cytokines, creating an inflammatory environment conducive to cancer development. For example, the interaction between HCV proteins and cellular receptors can lead to increased secretion of CXCL10, a chemokine involved in immune responses, which may trigger autoimmune thyroiditis and subsequent cancer development.
 
-Human Immunodeficiency Virus (HIV) and Thyroid Cancer
HIV infection, leading to acquired immune deficiency syndrome (AIDS), significantly increases the risk of various cancers. Non-AIDS-defining cancers (NADCs), including thyroid cancer, have been rising among people living with HIV (PLHIV). Studies indicate that HIV infection may lead to more aggressive forms of thyroid cancer with higher rates of metastasis and poorer outcomes.
 
-Mechanisms of HIV in Thyroid Cancer
HIV-induced immune deficiency allows for unchecked proliferation of cancer cells due to reduced immune surveillance. Additionally, the chronic inflammation and secondary infections common in HIV patients can further promote cancer development. HIV may also disrupt the hypothalamus-pituitary-thyroid axis, leading to hormonal imbalances that can stimulate tumor growth.
 
-SARS-CoV-2 and Thyroid Cancer
The COVID-19 pandemic, caused by SARS-CoV-2, has led to widespread health challenges, including potential impacts on thyroid function. The virus’s ability to bind to the ACE2 receptor, which is highly expressed in the thyroid gland, suggests that the thyroid may be directly affected by SARS-CoV-2. Reports of thyroiditis and other thyroid dysfunctions in COVID-19 patients have raised concerns about long-term impacts on thyroid health, including cancer.
 
-Mechanisms of SARS-CoV-2 in Thyroid Cancer
SARS-CoV-2 can induce a severe inflammatory response and cytokine storm, leading to tissue damage and potential alterations in thyroid function. The virus's interaction with the ACE2 receptor in thyroid cells may directly contribute to thyroid dysfunction and create a pro-tumoral environment. The long-term effects of COVID-19 on thyroid cancer development are still under investigation, but the potential for increased cancer risk cannot be ignored.
 
-Advanced Therapies and Future Directions
The intersection of virology and oncology has opened new avenues for cancer treatment. Antiviral drugs, traditionally used to combat viral infections, have shown promise in treating virus-associated cancers. For instance, ribavirin, an antiviral medication, has demonstrated anticancer properties by inhibiting key signaling pathways involved in cancer cell proliferation. Similarly, nelfinavir, an HIV protease inhibitor, has been found to inhibit growth in thyroid cancer cell lines.
Potential Antiviral Therapies for Thyroid Cancer
-Ribavirin: Inhibits eukaryotic initiation factor 4E (eIF4E), showing potential in reducing thyroid cancer cell viability.
 
-Cidofovir (CDV): Demonstrates apoptosis induction in thyroid cancer cells, suggesting its potential as an antineoplastic agent.
 
-Nelfinavir (NFV): Inhibits PI3K/AKT and MAPK/ERK signaling pathways, showing promise in treating metastatic thyroid cancer.
 
Conclusion
The evidence linking viral infections to thyroid cancer highlights the need for comprehensive research to understand these relationships fully. Viruses such as EBV, HCV, HIV, and SARS-CoV-2 can influence thyroid cancer development through various mechanisms, including immune evasion, chronic inflammation, and hormonal disruptions. Understanding these mechanisms can lead to better diagnostic and therapeutic strategies, potentially incorporating antiviral therapies as part of cancer treatment. As research continues to evolve, it is crucial to explore the long-term impacts of viral infections on thyroid health and develop targeted interventions to improve patient outcomes.
 
The study findings were published in the peer reviewed World Journal of Oncology.
https://www.wjon.org/index.php/wjon/article/view/1830/1576
 
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