Viral attacks on endocrine cells directly or indirectly through other methods can cause temporary or permanent damage to endocrine organs. It causes the host organism’s antiviral immune response to be activated, which can result in systemic or localized inflammation or organ-specific autoimmunity, both of which can cause certain endocrinopathies.
More information on viruses that cause endocrinopathies could lead to novel approaches to treating endocrine disorders. The researchers collected information on how six various viruses affected the human endocrine system.
They gathered information on the endocrine system’s damage caused by human coronaviruses (honors), particularly the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and SARS-CoV. The angiotensin-converting enzyme 2 (ACE2), which is extensively expressed in a number of endocrine glands including the hypothalamus, pituitary, thyroid, and adrenal glands, is how these two viruses, which share 80% similarity, penetrate host cells.
These viruses, particularly SARS-CoV-2, disrupt the human neuroendocrine system’s primary hypothalamic-pituitary-adrenal (HPA) axis, which controls homeostasis by inducing the hypothalamus to release corticotropin-releasing hormone (CRH). Additionally, it causes the anterior pituitary to release adrenocorticotropic hormone (ACTH), which in turn causes the adrenal glands to release cortisol.
The levels of prolactin, growth hormone (GH), luteinizing hormone (LH), and thyroid-stimulating hormone (TSH) are also affected by SARS-CoV-2 infections. Studies have also linked hyponatremia, an electrolyte problem, and elevated interleukin-6 (IL-6) serum levels brought on by SARS-CoV-2 infection. Patients with coronavirus disease 2019 (COVID-19) may also have thyrotoxicosis and low blood TSH due to elevated Il-6 levels.
The potential that SARS-CoV-2, like SARS-CoV, duplicates the amino acid sequences of the host ACTH to cause the formation of antiviral antibodies comparable to anti-ACTH autoantibodies has not been completely ruled out by studies. Studies employing immunohistochemistry on deceased COVID-19 patients discovered SARS-CoV-2 in the pancreas, in both exocrine and endocrine cells.
It’s interesting to note that recent ex vivo research has demonstrated that SARS-CoV-2 can replicate in human pancreatic islets, impairing -cell function, including insulin production induced by glucose. Male sex hormone levels, particularly testosterone, are decreased by COVID-19, which may indicate poor Leydig cell function. Similarly, COVID-19 in women could result in irregular menstruation, abnormally heavy periods, and even postmenopausal bleeding in long COVID cases. It might be due to transient changes in sex hormones during the disease.
Doctors treated patients with severe COVID-19, which in many cases led to hyperglycemia and insulin resistance, using steroids and low-molecular-weight heparin (LMWH). Glucocorticosteroid treatment reduces LH and FSH secretion over time, which causes secondary osteoporosis in females. Similar to how LMWH affects serum-free thyroid hormones, it inhibits hypercoagulability with severe COVID-19. Thus, monitoring COVID-19 patients for endocrinopathies is essential.
Globally, there were more than 38 million HIV-positive individuals in 2021. Testosterone deficiency, euthyroid ill syndrome, and abnormal cortisol response to ACTH have all been linked to HIV. Opportunistic infections brought on by HIV have a negative impact on the pituitary gland or hypothalamus, which results in hypogonadism in males. Loss of weight, inadequate nutrition, and cytokine impacts are further contributing reasons.
An increased incidence of type 2 diabetes is another endocrine condition seen in HIV patients (T2D). Protease inhibitors, one type of drug used to treat HIV infection, also cause insulin resistance and diabetes. Some additional medications, such as ketoconazole, which is used to treat HIV-associated fungus infections, can cause menstrual cycle irregularities in women and hypogonadism in males. They also increase steroid clearance.
Studies have also linked endocrine conditions such as autoimmune thyroiditis, type 2 diabetes, and erectile dysfunction to persistent hepatitis C and B virus infections (ED). In addition, hypothyroidism is more likely with chronic HCV infection. Thyroid follicular cells may be destroyed by the HCV-induced inflammatory process, and autoimmune thyroiditis or thyroid cancer may develop as a result. Similar to chronic HBV infections, free triiodothyronine (FT3) and free thyroxine (FT4) levels are decreased while serum TSH levels are elevated.
Indicating the deleterious impact of HCV on spermatogenesis, patients with chronic HCV infection also have low serum levels of total testosterone and abnormal sperm parameters, such as reduced sperm volume, count, and motility. Interferon (IFN), recognized for having harmful effects on the thyroid gland, is a component of medications used to treat HCV infection.
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The researchers also discussed how ortho hantaviruses affect the endocrine system. It is known that certain viruses, such as the Puumala virus (PUUV), can cause serious illnesses in people, like hemorrhagic fever with renal syndrome (HFRS). Radiographic imaging has shown hypopituitarism and necrotic and hemorrhagic damage to the pituitary gland during the infection cycle in 58 to 72% of HFRS patients.
The common human parvovirus B19 (PVB19) primarily spreads through blood transfusions and the respiratory system, resulting in a variety of endocrine abnormalities in children, such as erythema infectiosum. Studies have also linked the onset of Hashimoto’s thyroiditis to acute PVB19 infection (HT). Its DNA remains in the thyroid of people who have autoimmune thyroid disorders (AITD), most likely starting the inflammatory process inside the thyroid.
Coxsackievirus B (CVB), an enterovirus species, is likely implicated in the pathogenesis of T1D, according to a number of studies. Through molecular mimicry, activation of pre-existing autoreactive T cells, and modification of tolerance to -cell antigens arising from thymus infection, CVB starts autoimmunity against pancreatic cells.
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Furthermore, research has indicated a link between thyroid disorders and EV infection. Neonatal thyroiditis or AITD have both been connected to maternal EV infection. Additionally, research has shown that 60% of kids with antibodies against EV had hypothyroidism.