Dr Monica Kraft Reveals Link Between Preexisting Type 2 Inflammation, PASC Severity

Monica Kraft, MD, ASTF, system chair for the department of medicine at the Icahn School of Medicine at Mount Sinai, spoke about research on the long-term effects of SARS-CoV-2 infection in patients who were previously diagnosed with and/or treated for COVID-19. Kraft also mentions post-acute sequelae of COVID-19 (PASC) symptoms and the impact this has on patients with asthma.

At the American Thoracic Society 2024 International Conference, research Kraft contributed to along with other expert colleagues, emphasized the greater burden some PASC symptoms have depending on the presence or absence of type 2 inflammation.

Transcript:

Your research suggests a link between pre-existing type 2 inflammation and the severity of post-acute sequelae of COVID-19 (PASC) symptoms in asthmatic patients post–COVID-19. Can you elaborate on the potential reasons behind these distinct patterns? Is it possible there's a specific biological mechanism at play?

We have an interesting conundrum when it comes to the role of asthma in acute SARS-CoV-2 infection, and then the post-acute sequelae of COVID, or PASC.

We have data suggesting that type 2 asthma can actually be protective in the acute setting. There's a lot of reasons for that. We think that the kind of inflammation that these asthmatics have decreases the receptor that the virus uses to enter the cells—ACE2 [angiotensin-converting enzyme 2]—and it also inhibits viral entry, and there are a lot of cellular events that the allergic inflammation really helps and protects.

What we're now seeing for those asthmatic patients who then develop SARS-CoV-2 acutely, and then go on to have long COVID or PASC, it seems like they may be a different group of type 2 asthmatics. Because what we're seeing in the data is that they have more severe respiratory symptoms compared to non–type 2 asthma who have PASC, even compared to type 2 asthma with no PASC, and then of course, people without asthma.

There's clearly another layer that we haven't quite identified yet. These data were actually a bit surprising, because what we'd seen in the acute setting was very different. However, we're also seeing while respiratory symptoms are more severe, we're actually seeing some of the physical functioning parameters like ability to exercise and do activities of daily living, social roles in the family, chronic pain, neurocognitive symptoms, are actually better if you happen to have type 2 asthma and PASC.

It looks like there might be a discordance between the kind of symptoms, whereas respiratory seems much more severe in those type 2 asthmatics.

Your study highlights the need for further investigation. What are the key areas you'd like to see future research focus on to better understand the link between asthma, COVID-19, and PASC symptoms?

I'm very interested in why certain kinds of patients with certain kinds of asthma have PASC in the first place. But I actually want to back it up a little bit more and really understand what causes PASC. There's a literature that's forming, a body of literature, on viral persistence after acute SARS-CoV-2 infection. It's been shown in the GI [gastrointestinal] tract that the virus can harbor and replicate. There have been some reports in the lung as well.

Some future work that I'm hoping we're funded for, is to actually look at that in the lung and the GI tract. I'm collaborating with some of my GI colleagues to do this and understand the relationship of viral persistence and the development of PASC. Then if we can really confirm that, then what are the mechanisms driving persistence? How do these other diseases, whether it be asthma, diabetes, obesity, lead to this viral persistence? That's one hypothesis we hope to test.