Problems with iron levels in the blood and the body’s ability to regulate this important nutrient as a result of SARS-CoV-2 infection could be a key trigger for long COVID, new research has discovered.
Treating those most severely affected by COVID-19 has necessarily taken priority during the pandemic. But could long COVID be the next wave of the crisis?
New research provides important insights into the role played by the immune system in preventing – and in some cases increasing the severity of – COVID-19 symptoms in patients. It also finds clues to why some people experience ‘long COVID’.
In late 2019, a new institute opened on the Cambridge Biomedical Campus. Its timing could not have been better - as the COVID-19 pandemic sent Britain into lockdown several months later, the institute found itself at the heart of the University’s response to this unprecedented challenge.
One of Cambridge’s newest institutes, established to study the relationship between infectious disease and our immune systems, is leading the University of Cambridge’s response to the COVID-19 pandemic, with over 150 scientists and clinicians, the UK’s largest academic Containment Level 3 Facility, and a range of collaborators from across the UK and beyond.
The University of Cambridge is to take a leading role in a major national effort to help understand and control the new coronavirus infection (COVID-19) announced today by the Government and the UK’s Chief Scientific Adviser.
Scientists at the University of Cambridge have developed a new test that can reliably predict the future course of inflammatory bowel disease in individuals, transforming treatments for patients and paving the way for a personalised approach.
Our immune systems are meant to keep us healthy, but sometimes they turn their fire on us, with devastating results. Immunotherapies can help defend against this ‘friendly fire’ – and even weaponise it in our defence.
Researchers have identified a series of genetic variants that affect the severity of Crohn’s disease, an inflammatory bowel disease – but surprisingly, none of these variants appear to be related to an individual’s risk of developing the condition in the first place.
Almost one in four of the world’s cases of tuberculosis (TB) are in India and the disease is constantly adapting itself to outwit our medicines. Could the answer lie in targeting not the bacteria but its host, the patient?
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