Home Medizin Hormone und Viren beeinflussen sich gegenseitig

Hormone und Viren beeinflussen sich gegenseitig

von NFI Redaktion

During a press conference at the 67th Congress of the German Society of Endocrinology (DGE), Stefan Bornstein, MD, PhD, Professor, emphasized that there is more than one interaction between them. Nowadays, one could almost speak of an „endocrine virology and even of the virome as an additional, hormonally metabolically active gland,“ said Bornstein, who will receive the Berthold Medal from the DGE in 2024.

Many questions remain unanswered: „We need a better understanding of the interaction of hormonal systems with infectious agents – from basics to therapeutic applications,“ emphasized the Director of the Medical Clinic and Polyclinic III and the Center for Internal Medicine at Carl Gustav Carus University Hospital, Dresden, Germany.

If infectious diseases could trigger diabetes and other metabolic disorders, this means that „we may be able to prevent the occurrence of more common metabolic diseases like diabetes through vaccination programs,“ said Bornstein. He emphasized that many people who became seriously ill or died from COVID-19 during the pandemic had diabetes or a pre-metabolic syndrome.

„SARS-CoV-2 has utilized an endocrine signaling pathway to enter our cells and cause damage in organ systems and inflammation,“ said Bornstein. Conversely, it is now known that infections with coronaviruses or other infectious agents like influenza can significantly worsen the metabolic status, diabetes, and other endocrine disorders.

SARS-CoV-2 infects beta cells

Data from the COVID-19 pandemic showed that the likelihood of developing type 1 diabetes increases significantly with a SARS-CoV-2 infection. Researchers led by Bornstein demonstrated in 2021 that SARS-CoV-2 can infect the insulin-producing cells of the organ. They examined pancreatic tissue from 20 COVID-19 deceased patients using immunofluorescence, immunohistochemistry, RNA in situ hybridization, and electron microscopy.

They found viral SARS-CoV-2 infiltration of the beta cells in all patients. In 11 patients with COVID-19, the expression of ACE2, TMPRSS, and other receptors and factors such as DPP4, HMGB1, and NRP1 that can facilitate viral entry was investigated. They found that necrotic cell death, infiltration of immune cells, and SARS-CoV-2 infection of the pancreatic beta cells can contribute to varying degrees of metabolic disturbances in COVID-19 patients even without overtly newly onset diabetes.

In a report published in October 2020, Tim Hollstein, MD, from the Institute for Diabetology and Clinical Metabolic Research at UKSH in Kiel, Germany, and colleagues described the case of a 19-year-old man who developed symptoms of insulin-dependent diabetes following a SARS-CoV-2 infection, without the presence of the typical autoantibodies for type 1 diabetes.

The man presented in the emergency room with diabetic ketoacidosis, a C-peptide level of 0.62 µg/L, a blood glucose concentration of 30.6 mmol/L (552 mg/dL), and an HbA1c level of 16.8%. The patient’s history revealed a probable SARS-CoV-2 infection 5-7 weeks before admission, based on a positive antibody test against SARS-CoV-2.

Some viruses produce insulin-like proteins

Recent studies have shown that some viruses can produce insulin-like proteins or hormones that interfere with the metabolism of the affected organism, reported Bornstein. Besides metabolic regulation, these „viral hormones“ also seem to have an impact on cell turnover and cell death.

Bornstein pointed out that antiviral medications can delay the onset of type 1 diabetes by preserving the function of insulin-producing beta cells. It has also been shown that conventional medications for treating hormone disorders can reduce the organism’s susceptibility to infections – such as antidiabetic agents like DPP-4 inhibitors or metformin.

In a review published in 2023, Nikolaos Perakakis, MD, Professor and Research Group Leader at the Paul-Langerhans Institute Dresden, Dresden, Germany, Bornstein, and colleagues discussed scientific evidence for a close mutual dependence between various virus infections and metabolic disorders. They discussed how viruses can lead to the development or progression of metabolic disorders and vice versa, and how metabolic disorders can increase the severity of a virus infection.

Viruses favor metabolic diseases…

Viruses can favor metabolic diseases by affecting the regulation of cell survival and specific signaling pathways relevant for cell death, cell proliferation, or dedifferentiation in important endocrine and metabolic organs. Viruses are also capable of controlling cellular glucose metabolism by modulating glucose transporters, altering glucose uptake, regulating pathways, and stimulating glycolysis in infected cells.

Enteroviruses, as well as the mumps virus, parainfluenza virus, or human herpesvirus 6, have been associated with the development of diabetes by destroying beta cells. The time of infection often precedes or coincides with the peak of development of islet autoantibodies. The fact that only a small fraction of patients actually develop type 1 diabetes suggests that genetic background and likely the timing of infection play a significant role.

…and metabolic diseases influence the course of infection

Infection with the hepatitis C virus (HCV), on the other hand, is associated with an increased risk of type 2 diabetes, with older people with diabetes in the family history having a higher risk. The negative effects of HCV on glucose metabolism are mainly attributed to increased insulin resistance in the liver. HCV reduces glucose uptake in the liver by downregulating the expression of glucose transporters and additionally impairs insulin signal transduction by inhibiting the PI3K/Akt signaling pathway.

People with obesity, diabetes, or insulin resistance show significant changes in the innate and adaptive functions of the immune system. Regarding the innate immune system, disturbances in chemotaxis and phagocytosis of neutrophils have been observed in patients with type 2 diabetes.

In obesity, the number of natural killer T cells decreases in adipose tissue, while B cells accumulate in adipose tissue and secrete more pro-inflammatory cytokines. Longitudinal multiomics analyses of various biopsies from individuals with insulin resistance showed a delayed immune response to respiratory virus infections compared to individuals with normal insulin sensitivity.

This story was translated from Medscape Germany. Throughout the process, several editorial tools, including AI, were used. Human editors reviewed this content before publication.

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