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Researchers at the Paul-Ehrlich-Institut have conducted a significant study on why some strains of influenza A viruses pose a greater threat than others. The investigation focused on the mechanisms behind the immune response to these viruses, particularly the phenomenon known as cytokine storm, which can lead to severe health complications.
Influenza viruses rank among the most critical pathogens responsible for respiratory illnesses globally. While many infections result in mild symptoms, certain strains can lead to severe pneumonia and acute respiratory failure. Highly pathogenic variants of influenza, especially those originating from avian sources, are often linked to increased mortality rates.
The study, published in Emerging Microbes & Infections, analyzed 11 distinct strains of influenza A to understand their interaction with various human immune cells. The findings reveal that highly pathogenic strains tend to infect specific immune cells, prompting a notable increase in the production of type I interferon, a crucial antiviral messenger.
Professor Zoe Waibler, acting Vice President of the Paul-Ehrlich-Institut, explained that the research indicates that not only the traditional immune cells responsible for type I interferon production are involved, but also other types of immune cells play a critical role in determining whether an influenza infection results in an excessive immune response.
The immune system's reaction to influenza is vital in understanding its danger. Some strains lead to the release of a large quantity of cytokines, which can cause tissue damage and worsen the disease more than the virus itself. This excessive immune response is particularly pronounced in cases involving highly pathogenic strains.
The research team, led by Dr. Martina Anzaghe, aimed to unravel the complexities of the immune response to different influenza strains. Collaborating with the Virology Department at the University Hospital Freiburg, they studied how these viruses infect immune cells and trigger the release of various messenger substances.
One key finding was the role of plasmacytoid dendritic cells, which produce significant amounts of interferon-? upon exposure to influenza viruses. Interestingly, this response occurs irrespective of the virus strain, highlighting a general immune reaction to influenza.
However, the research revealed that not all strains induce the same severity of disease. The team discovered that highly pathogenic viruses infect myeloid dendritic cells and macrophages. This productive infection appears crucial for the production of type I interferon and the subsequent development of a cytokine storm.
These findings shed light on the reasons behind the varying severity of influenza virus infections. The ability of certain strains to replicate within specific immune cells could explain why they trigger a heightened immune response, leading to severe health complications. This knowledge may assist in developing targeted therapies and identifying at-risk populations more effectively.
In summary, understanding the interaction between influenza viruses and the immune system is vital for improving treatment strategies and protective measures against the most dangerous strains.
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