{"id":41147,"date":"2026-06-30T11:22:41","date_gmt":"2026-06-30T09:22:41","guid":{"rendered":"https:\/\/www.resist-cluster.de\/?p=41147"},"modified":"2026-06-30T11:27:22","modified_gmt":"2026-06-30T09:27:22","slug":"how-rsv-manipulates-the-immune-response-in-respiratory-cells-twincore-researchers-investigate-gene-activity-in-host-cells","status":"publish","type":"post","link":"https:\/\/www.resist-cluster.de\/en\/how-rsv-manipulates-the-immune-response-in-respiratory-cells-twincore-researchers-investigate-gene-activity-in-host-cells\/","title":{"rendered":"How RSV manipulates the immune response in respiratory cells: TWINCORE researchers investigate gene activity in host cells"},"content":{"rendered":"

Respiratory syncytial virus (RSV) can cause severe lower respiratory tract infections, particularly in newborns and the elderly. How the virus manages to evade the immune system and what changes it triggers in infected cells had not yet been fully understood. Researchers from TWINCORE, Centre for Experimental and Clinical Infection Research, have now, together with interdisciplinary colleagues from W\u00fcrzburg, Regensburg, Braunschweig and Hannover, demonstrated how the virus interferes with the genetic programme of respiratory cells, inhibits the immune response and disrupts cell function. They have published these findings in the journal Science Advances<\/em>.<\/p>\n

According to estimates by the World Health Organisation (WHO), around 3.6 million children worldwide require hospital treatment for RSV each year. For 100,000 of them, the infection is fatal. \u201cHow the virus causes damage in the epithelial cells of the respiratory tract and why the immune response does not keep it better in check has been unclear until now,\u201d says Prof. Thomas Pietschmann<\/strong>, Director of the Institute for Experimental Virology at TWINCORE in Hannover, lead author of the study and a researcher in the RESIST Cluster of Excellence<\/strong>.<\/p>\n

To answer this question, the researchers used a special cell culture model. They cultured respiratory cells from human donors, typically patients receiving a donor lung. \u201cIn the laboratory, these cells then grow together to form a lung-like ciliated epithelium, complete with ciliary beating and mucus production,\u201d explains Prof. Bettina Wiegmann from the Department of Cardiac, Thoracic, Transplant and Vascular Surgery at Hannover Medical School and co-author of the study. They then infected this tissue culture with RSV and subsequently analysed gene activity in every single cell using RNA sequencing. \u201cBy comparing with uninfected cells, we can identify how thousands of genes are regulated by the infection,\u201d says Prof. Emmanuel Saliba, who heads the research group \u201cSingle-Cell Analysis\u201d at the Helmholtz Institute for RNA-based Infection Research (HIRI) in W\u00fcrzburg, a site of the Helmholtz Centre for Infection Research in Braunschweig in cooperation with Julius-Maximilians-Universit\u00e4t W\u00fcrzburg.<\/p>\n

\u201cOur data show that only a fraction of the infected cells even realise they have been infected,\u201d says Dr Sibylle Haid, a researcher at Pietschmann\u2019s institute and, together with Kevin Berg (University of Regensburg), first author of the study. \u201cThis is probably because only some lung cells produce sufficient quantities of virus detectors and thus generate messenger molecules quickly enough to protect themselves and neighbouring cells.\u201d If there are too few of these sensor molecules, the virus gains the upper hand, multiplies and then actively suppresses this protective mechanism. A key messenger substance in the immune system is interferon, which has both a direct antiviral effect and activates the so-called interferon-stimulated genes (ISGs).<\/p>\n

\u201cEven treating the cells with interferon cannot eliminate the virus at this stage,\u201d says Haid. With one exception: the team discovered that the antiviral transcription factor IRF1 is not suppressed by RSV and was then able to demonstrate that artificially activating this factor can suppress the RSV infection \u2013 at least in the simplified model.<\/p>\n

The researchers also found a possible explanation for the cell damage caused by RSV. \u201cIn the infected epithelial cells, the genes that control cilia formation were also inhibited,\u201d says Sibylle Haid. Cilia are the tiny hair-like structures on cells that are responsible, among other things, for clearing mucus. If this function is disrupted by the infection, the typical symptoms of the disease arise.<\/p>\n

\u201cIn this study, we were able to gain important insights into the pathology of RSV infection at the cellular level and also identify IRF1 as a potentially promising candidate for pharmaceutical intervention,\u201d says Thomas Pietschmann. \u201cThis would not have been possible without the interdisciplinary collaboration with our partners.\u201d In addition to the research teams led by Thomas Pietschmann, Emmanuel Saliba and Florian Erhard (University of Regensburg), the Helmholtz Centre for Infection Research in Braunschweig and Hannover Medical School were involved. The research project was funded by the RESIST Cluster of Excellence.<\/strong><\/p>\n

Publikation:<\/strong><\/p>\n

Respiratory syncytial viral load drives ciliated cell dedifferentiation and suppresses antiviral immunity<\/strong>
\nBerg K, Haid S, Vafadarnejad E, Carpentier A, Geffers R, Wiegmann B, Saliba A, Erhard F, Pietschmann T. Science Advances: Volume 12, Issue 25, Page eaed4499
\nDOI: 10.1126\/sciadv.aed4499<\/a><\/em><\/p>\n

Text:\u00a0Twincore<\/a>
\nFoto: Prof. Thomas Pietschmann und Dr. Sibylle Haid im Labor, Copyright Twincore<\/p>\n<\/div>

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