A recent study led by researchers from the University of Zurich (UZH) and the University Hospital Zurich (USZ) has uncovered that approximately two percent of the population develop autoantibodies against type 1 interferons, primarily later in life. This makes them more vulnerable to viral infections, such as COVID-19.
Type 1 interferons are crucial proteins produced by immune cells in response to viral infections. They act as early messengers, alerting uninfected cells and tissues to the presence of a virus, enabling them to prepare defenses. However, in individuals with autoantibodies against type 1 interferons, this vital response is compromised.
The study found that severe viral infections, such as COVID-19 and influenza, can be more common in people with a weakened type 1 interferon response. According to the research, between 5 to 15% of those hospitalized with severe COVID-19 or influenza have a type 1 interferon response deficit due to the presence of autoantibodies that neutralize these critical proteins.
“We aimed to uncover why some people’s immune systems turn against themselves and understand the consequences of having autoantibodies against type 1 interferons,” explained Professor Benjamin Hale, the study’s lead researcher from the Institute of Medical Virology at UZH.
The research team utilized a vast collection of frozen blood samples from the Swiss HIV Cohort Study, which included samples from around 2,000 adults collected over several decades. This unique biobank allowed the researchers to analyze the presence and duration of autoantibodies against type 1 interferons.
The analysis revealed that around two percent of individuals develop autoantibodies against type 1 interferons during their lifetime, typically between the ages of 60 and 65. This finding aligns with previous studies suggesting that the prevalence of these autoantibodies increases with age.
Further investigation by researchers at USZ’s Department of Infectious Diseases and Hospital Epidemiology identified factors contributing to the development of these autoantibodies. The study indicated that individuals who developed these autoantibodies were also prone to producing antibodies against other proteins made by their own bodies, a phenomenon known as loss of self-tolerance, which can occur with aging. “These individuals may produce antibodies against their own type 1 interferons due to their propensity to make autoantibodies and exposure to high levels of type 1 interferons from other infections,” noted Hale.
Significantly, the study found that once these autoantibodies developed, they remained detectable in the blood for the individual’s lifetime. Those with autoantibodies dating back to as early as 2008 were more likely to experience severe COVID-19 in 2020. “These autoantibodies have long-term consequences, leading to a compromised type 1 interferon system and reduced immunity against viruses,” Hale emphasized.
Understanding these risk factors could lead to future diagnostic tests to identify older individuals at higher risk of developing this deficiency. This could help implement preventive measures to avoid the development of autoantibodies and prioritize these individuals for vaccines or antivirals to prevent severe viral infections.