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<p>Viral infections often disrupt organelle integrity, causing host DNA to leak into the cytosol. Such mislocalized DNA constitutes a potent damage signal that activates innate immune responses, particularly via the cGAS–STING pathway and subsequent interferon production. Although cytosolic DNA is observed during SARS-CoV-2 infection, interferon responses in patients are typically delayed. We show that the viral nucleocapsid protein directly binds DNA and thereby masks it from recognition by cGAS, providing a potential mechanism for early immune evasion by SARS-CoV-2.</p>

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Wie Viren DNA-Immunerkennung vereiteln: cGAS-Antagonismus durch SARS-CoV-2

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月1日

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  • Theresia Gutmann

摘要

Viral infections often disrupt organelle integrity, causing host DNA to leak into the cytosol. Such mislocalized DNA constitutes a potent damage signal that activates innate immune responses, particularly via the cGAS–STING pathway and subsequent interferon production. Although cytosolic DNA is observed during SARS-CoV-2 infection, interferon responses in patients are typically delayed. We show that the viral nucleocapsid protein directly binds DNA and thereby masks it from recognition by cGAS, providing a potential mechanism for early immune evasion by SARS-CoV-2.