Please sign the petition so I can add COVID data visualization again:
https://www.change.org/p/require-hospitals-to-provide-covid-data-and-bed-utilization-metrics
Contents:
- COVID
- Respiratory Protection
COVID
Coinfection with Influenza A
I will be using SARS-CoV-2 and COVID interchangeably, but SARS-CoV-2 is the virus that causes COVID, which is the disease.
An interesting study came to my attention this week that has me thinking much more about the dynamics of the interaction between influenza A virus (IAV) and the SARS-CoV-2 virus in a way that hadn’t occurred to me before.
The investigators infected a cell culture with IAV and then used spike protein from SARS-CoV-2 attached to a marker to study uptake of the spike protein. They found that “cells became highly sensitive (up to 10,000-fold) to the pseudo-SARS-CoV-2 virus after infection with IAV at different doses.”
They proceeded to repeat the experiment, but instead using live SARS-CoV-2 virus and then measured some of the genetic sequences that were produced as a metric for viral replication. They found that “cells that are inherently susceptible to SARS-CoV-2, IAV preinfection further increased SARS-CoV-2 infectivity by > 5-fold.” This suggests the production of far more of the COVID virus if they are already infected with influenza A, meaning that they will be much sicker but also much more likely to spread COVID because of the higher viral load.
They continued their study in mice. “A significant increase in SARS-CoV-2 viral load was observed in lung homogenates from coinfected mice compared to homogenates from SARS-CoV-2 single-infected mice…The lung histological data further illustrate that IAV and SARS-CoV-2 coinfection induced more severe lung pathologic changes, with massive cell infiltration and obvious alveolar necrosis, compared to SARS-CoV-2 single infection or mock infection.”
They went on to test a few other respiratory viruses to see if the same COVID virus amplification would occur, and it didn’t. This suggests that there is something unique about IAV that enhances COVID infection. In addition, they studied ACE-2 receptor (the binding site for COVID) expression and found that cell cultures infected with IAV expressed THREE TIMES as many ACE-2 receptors. In coinfection of the two viruses, ACE-2 expression increased 5-28x based on the cell culture line used.
My interpretation of the increased ACE-2 expression is that it suggests that someone who is coinfected with both IAV and COVID is MORE susceptible to infections that use the ACE-2 receptor to infect cells.
At this point, you might be wondering why this grabbed my attention since it seems obvious that getting infected with two different viruses simultaneously is bad for someone.
H5N1 is a type of an influenza A virus.
If a H5N1 pandemic starts with rapid human to human transmission, we can expect a massive surge in COVID cases as well based on this evidence. The big problem is that hospitals wouldn’t be able to handle that increased demand. Early in the COVID pandemic, we saw the need for the use of BiPAP and CPAP machines in some areas to help reduce ventilator demand, which I had alluded to in an interview in 2006 (no paywall here). If we have a concurrent H5N1 and COVID pandemic, I don’t think we will be able to stumble through the demand anywhere as easily, and those who were on the front lines at the start of COVID would tell you it wasn’t easy at all.
Caregivers for Future Chronic Disease Pandemics Due to COVID
For those not following me on Twitter, here’s an unroll of a thread that might be of interest.
Respiratory Protection
A really good review of the literature on respiratory protection was just published, prompting me to update two pages on this site. You can read about it and two other review articles in the first link. The second link addresses some of the misinformation about respiratory protection, particularly calling out the Brownstone Institute as well as the Cochrane Review that is often mischaracterized.
