This the third and final article in a three-part series on fading immunity to Covid-19 and the flu—the science behind it, and the implications it has for vaccine development and the pandemic at large. Read the first two articles here and here.
We know that people who are older, obese, immunocompromised, pregnant, or diabetic are at greater risk of developing severe Covid-19. Now evidence has emerged that establishes another determinant of risk—something that isn’t inherited, but acquired over a lifetime. That is the inability to mount a robust interferon response.
Interferons play a critical role in defending our bodies against invading pathogens like SARS-CoV-2, the coronavirus that causes Covid-19. They function as warning signals, alerting the immune system whenever an intruder is on sight. Some people, however, develop what are called autoantibodies against their own interferons—and research shows that they’re more susceptible than most to the more devastating effects of Covid-19, including death.Recommended For You
If antibodies are the defenders our B cells produce to battle oncoming infection, autoantibodies are defectors that do precisely the opposite. Rather than detecting and debilitating viral genetic material, autoantibodies target us. A new study, made available on medRxiv but currently undergoing peer review, examined 52 patients with severe Covid-19 and found that nearly half had autoantibodies of some kind. In those most critically ill—specifically the top 50 percent—that number exceeds 70 percent.
None of the patients who participated in the study reported a history of autoimmune disease, but it may be the case that survivors continue to be prone to severe Covid-19 symptoms upon future encounters with the virus—potentially even worse than the first time around. The flipside is that they might benefit from drug therapies for conditions like lupus. Autoantibodies are more prevalent in older adults than younger, which might explain, at least in part, why Covid-19 is, too.
If the results of this study aren’t momentous enough to impact how we treat Covid-19, at the very least they have bearing on how we diagnose and prevent it. First thing’s first, people who develop serious Covid-19 symptoms, whether they’re hospitalized or not, should be tested for autoantibodies against interferons and other relevant targets. Those who test positive, now that we know they’re more vulnerable to critical illness or death, must receive priority status for vaccinations and be cared for accordingly.
More generally, people aged 65 and older should be routinely tested for anti-interferon antibodies as part of their annual checkup. Again, those who test positive will know to be especially cautious to protect themselves from infection. After all, regardless of whether the tide of the current pandemic is turned by widespread vaccination or any other deterrent, there’s no telling how long we’ll be dealing with Covid-19 in some form—particularly those most vulnerable. Any precautions we can take to prevent further spread, we should, and with haste.
The last two articles in this series—on fading natural immunity to Covid-19 and fading vaccine-mediated immunity to influenza—feature research that puts into perspective the timeframe of infection, disease, and potential protection. For many, all of the above will tend towards the short-term, which has manifold implications for our methods of preventing and vaccinating against Covid-19.
But in the months to come, more studies will be conducted that give us a clearer understanding of the long-termeffects of this disease. These in turn will force us to reconsider our methods once more. The issue of autoantibodies is one to watch, as well as one we should act to address sooner rather than later. If you have autoantibodies against interferon, you may be in it for the long haul.