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In a study, recently published in Genomics Medicine, researchers from NDM’s Wellcome Centre for Human Genetics and the CAMS Oxford Institute investigated the long-term impact of COVID-19 on immune cells.

The immune response to COVID-19  has been studied extensively, but less is known about how the infection may hamper the immune system in the long term and its ability to respond to future challenges. In this Genome Medicine study, the researchers from Wellcome Centre for Human Genetics and CAMS Oxford Institute showed that COVID-19 infection causes a prolonged increase in the pro-inflammatory transcriptional status leading to the development of long-term health issues including autoimmune disease, reactivation of other viruses and disruption of the host immune system-microbiome ecosystem.

Since the onset of the pandemic, the breadth of studies dedicated to understanding COVID-19 have facilitated large publicly available single-cell transcriptomics datasets that can help in profiling the immune response to viral infection and disease outcome, in both the acute and post-acute phases of the disease. This has enabled detailed investigation of the long-term effects of the disease.

The team found that COVID-19 leads to a prolonged impact on immune cells in blood for over 2 months after the onset of the clinical symptoms. A key finding was the observation that the transcriptional changes in COVID-19 patients were related to the activation of NF-kB gene signalling pathway, which is consistent with its previously identified role in severe COVID-19 patients.

Their findings shed new light into the recovery period in COVID-19 patients and reveal long-lasting changes to the transcriptional landscape (the pattern of transcription control signals, and the transcripts generated) in circulating immune cells in our blood. These results indicate the automatic alterations triggered by COVID-19 infection need to be further investigated to better understand how to reduce the occurrence of long COVID-19 complications.

The full paper can be accessed here: