Long Covid: ‘Zombie’ Virus Fragments Found to Attack Immune Cells
- While the world has moved past the most acute phases of the COVID-19 pandemic, the long-term effects of the virus continue to impact millions.
- A study led by researchers at UCLA, published in the Proceedings of the National Academy of Sciences, has revealed that when the body’s immune system breaks down the...
- The research demonstrates that these viral fragments don’t attack cells randomly.
While the world has moved past the most acute phases of the COVID-19 pandemic, the long-term effects of the virus continue to impact millions. Recent research is shedding light on a surprising contributor to the persistent symptoms of long COVID: fragments of the virus itself.
A study led by researchers at UCLA, published in the Proceedings of the National Academy of Sciences, has revealed that when the body’s immune system breaks down the spike protein of SARS-CoV-2, some of the resulting fragments can actively target and destroy specific immune cells. This discovery, , offers a potential explanation for why certain populations of immune cells become depleted in patients with severe COVID-19, and may also explain the milder symptoms observed with the Omicron variant.
Viral Fragments Target Immune Cells
The research demonstrates that these viral fragments don’t attack cells randomly. Instead, they target cells based on their shape, specifically those with “spiky” or “star-shaped” membranes. These are often sentinel cells and killer cells – crucial components of the immune system responsible for detecting and fighting off infection. “These fragments target a specific kind of curvature on the membranes of cells. Cells that are spiky, that are star-shaped, or that have lots of tentacles end up getting preferentially suppressed,” explained bioengineer Gerard Wong, according to the UCLA Newsroom.
This process isn’t simply the immune system clearing away debris after defeating the virus. The fragments actively punch holes in the membranes of these immune cells, leading to their destruction. This finding builds upon earlier UCLA research identifying “zombie” coronavirus fragments that can mimic molecules from the body’s own immune system, driving inflammation.
Omicron’s Milder Impact and Viral Fragments
Interestingly, the study also found that fragments from the Omicron variant exhibited less activity against immune cells compared to fragments from other strains. This observation may help explain why Omicron, while highly contagious, generally caused less severe illness. Yue Zhang, a bioengineer at China’s Westlake University, noted that the reduced impact of Omicron fragments suggests a patient’s immune system may not become as depleted with this variant.
The Link to Long COVID
The persistence of these viral fragments could be a key factor in the development of long COVID. Long COVID is characterized by a wide range of ongoing or new symptoms, even after the initial infection has cleared. These symptoms can include severe fatigue, shortness of breath, cognitive dysfunction (“brain fog”), heart palpitations, and more. According to the World Health Network, approximately one in three individuals with a registered COVID-19 infection, and around 50% of those hospitalized, experience long COVID symptoms.
The UCLA study suggests that these lingering viral fragments could be contributing to the chronic inflammation and organ damage seen in long COVID patients. The damage affects the heart, brain, kidney, immune system, and other organs. The fragments may continue to suppress immune function, leaving individuals vulnerable to ongoing symptoms and complications.
Implications for Immunocompromised Individuals
The research also highlights the potential increased vulnerability of individuals with weakened immune systems. Because these fragments target the very cells responsible for detecting and fighting infection, those with compromised immunity may be particularly susceptible to their damaging effects. The study suggests that in these individuals, the depletion of key immune cells could be more pronounced, potentially leading to more severe or prolonged symptoms.
Ongoing Research and Future Directions
The UCLA-led team, comprised of nearly three dozen engineers, microbiologists, immunologists, chemists, physicists, medical researchers, and analytical experts from institutions in the United States, China, Germany, India, and Italy, emphasizes that This represents just the beginning of understanding the complex interplay between SARS-CoV-2 and the immune system. The research was funded in part by the National Science Foundation and the National Institutes of Health.
“Viruses do so many things that we don’t understand,” Wong stated. “We want to understand what all the leftover viral matter does to us, both during COVID and after. With these viral fragments, all of a sudden there’s a whole new range of possibilities to consider.”
This new line of inquiry could pave the way for the development of novel strategies to mitigate the most serious symptoms of COVID-19 and long COVID. Further research is needed to fully elucidate the mechanisms involved and to identify potential therapeutic targets. As of , health officials continue to urge vaccination as a primary means of preventing infection and reducing the risk of long COVID, with one pediatrician stating that “More vaccines should lead to fewer infections, which should lead to less long COVID.”