Health
Determinants of persistent and severe COVID-19 revealed — ScienceDaily
As COVID-19 wreaks havoc around the world, one aspect of the infection has not gone unnoticed. The disease is heterogeneous in nature, with a wide range of symptoms and severity of the condition. The medical community now believes this is due to differences in human host biology and has little to do with the virus itself. This conundrum is being shed light on by Associate Professor Sei Sumitomo of Okayama University’s Research Institute for Interdisciplinary Sciences (RIIS) and Associate Professor Koji Harada of the Center for Information and Technology Education (CITE) at Toyohashi University of Technology. The duo recently reported their findings regarding host immune system imbalances that drive persistent or severe forms of disease in some patients.
Researchers have begun a computer simulation study using a model based on the host’s immune system and its natural response to SARS-CoV-2 exposure. We plugged in a mathematical expression for the dynamics of cells infected with SARS-CoV-2 to predict their behavior. The immune system now has messenger cells known as dendritic cells (DC). These cells report information about the invader (in the form of antigens) to the immune system’s warriors (T cells). This model showed that at the onset of infection, DCs in infected tissues are activated and then gradually begin to build antibodies that neutralize SARS-CoV-2.
To investigate long-term infection with COVID-19, we evaluated the behavior of DCs 7 months after infection by computer simulation. Baseline model simulations revealed a large decrease in DCs at the peak of infection and a slow increase again. However, they tended to fall below pre-infection levels. These observations were similar to those seen in clinical patient samples. Low DC levels appeared to be associated with persistent long-term infection.
The next step was to understand whether DC function contributes to disease severity. Deficiencies in the antigen-reporting function of DCs and reduced levels of chemicals known as interferons released by DCs were found to be associated with severe symptoms. When both of these functions are impaired, the viral load in the blood increases (viral load). The researchers also discovered the presence of two factors that influence the ability of the virus to replicate within the host: antigen-reporting DCs and antibodies to the virus. Abnormalities in these functions can impede virus clearance and allow it to remain in the body longer than expected, whereas these high capabilities of immune function suppress viral replication and result in rapid viral clearance.
This study uncovers components of immune signaling that directly influence the outcome of COVID-19 infection. “Our mathematical model predicts sustained DC decline, indicating that certain patients with severe and mild symptoms fail to effectively clear the virus and may develop prolonged COVID. A better understanding of these immune responses may help shape COVID-19 prognosis and therapeutic interventions.
Background
Dendritic Cells and the Immune System: Dendritic cells (DCs) are part of the body’s innate immune system and are present in areas in close contact with pathogens such as the skin, respiratory tract, and gastrointestinal tract. When these tissues are infected, DCs collate and display information about pathogens. DCs are now activated and converted into antigen-presenting cells (APCs). APCs then migrate to lymph nodes where T cells reside and report this information. The T cells then migrate to and kill invading pathogens. DCs also play a role in the body’s protective mechanism, inflammation, by releasing interferons. Interferons are chemical messengers that alert neighboring cells to viral infection.
Although the number of DCs does not change with age, their function is known to be impaired. Because older patients are more likely to develop severe her COVID-19, patterns of her DC function in severe infections were investigated by computer simulation experiments.
Story source:
material provided by Okayama University. Note: Content may be edited for style and length.
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