Despite the waning public attention to the COVID-19 pandemic, its lingering impact continues to be felt. Researchers at the University of California-Los Angeles believe they are making strides in understanding why COVID-19 can lead to severe outcomes or even death, unlike other common coronaviruses. Their focus is on “zombie” virus fragments that persist and cause inflammation long after the virus has been eliminated.
Professor Gerard Wong explained that these supposedly dead viral fragments can reassemble with double-stranded RNA, commonly found in viral infections. This reassembly triggers a prolonged and intense immune response, deviating from the typical response to viral infections and potentially causing catastrophic outcomes.
Using artificial intelligence, the researchers scanned proteins produced by a SARS-CoV-2 infection and identified specific viral fragments that mimic immune peptides, exacerbating immune responses. This lingering effect could be responsible for fatal results in severe COVID-19 cases.
Wong drew an analogy to consuming croissants, where the impact persists after digestion, potentially affecting health. While some COVID-19 infections result in mild, quickly resolved symptoms, others lead to long COVID, with symptoms lasting for months. Variation in enzymatic activity, the process of breaking down proteins in the human body, may explain why these fragments cause hyper-inflammation in some individuals and not others.
The researchers aim to explore this interaction further to differentiate between harmful and less severe strains of SARS-CoV-2. This understanding could contribute to the development of a surveillance system and better treatment strategies for COVID-19, potentially mitigating severe outcomes.
In essence, the study sheds light on the enduring impact of COVID-19 on the immune system, offering insights that may lead to improved treatment approaches and surveillance measures.