A New Wave of COVID-19 Antivirals
Dr. Adrianne Watson - 18 February 2026
Dr. Tom Hobman
“Unprecedented”
“Social Distancing”
“Lockdown”
These pandemic buzzwords can instantly transport us back to the 2020 Covid-19 pandemic. Thanks to the rapid development of the Covid-19 vaccine, these Covid-19 literal relics now seem like the remnants of a bad dream. Yet, while the worldwide state of emergency caused by the pandemic officially ended in 2023, this doesn’t mean that the virus is no longer a threat to our health.
Since August 2025, there have been almost 50,000 cases of Covid-19 reported in Canada alone, and nearly 800 deaths. Those who are unvaccinated or have pre-existing conditions are more likely than the general population to experience more severe outcomes. In addition, those over 65 (~20% of the population) are the most likely to be hospitalized or die after infection with SARS-CoV-2 virus.
While vaccines have drastically reduced the amount of people hospitalized due to the virus, this flu season alone has seen 12,500 hospitalizations and 200 ICU admissions to date. In an already stressed healthcare system, any additional pressure from viruses like Covid-19 can be detrimental. Unfortunately, we can’t “cure” viral infections. But we can fight them.
Cue the antivirals!
In Canada, there are two approved antivirals to treat high-risk patients with Covid-19: Remdesivir and Paxlovid. The problem is that these medications target the virus directly so, as the virus mutates and new variants emerge, these generic antivirals become less effective. Another approach is to inhibit the machinery that viruses use to spread or replicate inside the body-essentially hitting the emergency stop button.
This is where researcher Dr. Tom Hobman comes in. His recent work, led by recent PhD graduate Dr. Alberto Felix-Lopez, investigates how the SARS-CoV-2 virus infects and replicates inside cells…and more importantly, how to stop this from happening. This behind-the-scenes peek at Covid-19’s toolbox is published in the journal, iScience.
A successful virus must accomplish two key tasks: enter host cells and reproduce. Once the virus finds and attaches to a host cell, many of the tools (proteins) in the host cell become part of their toolbox. Felix-Lopez and the Hobman lab systematically eliminated individual proteins/tools making up the host cell machinery to find out which ones were vital to the virus. If the right tool was broken, the cells would become immune to the virus. This revealed two key players: FGFR1 and NAE1.
The FGFR1 result was relatively straightforward. FGFR1 is the beginning of an assembly line that branches into many different parts, one which affects the cell’s ability to produce interferon which is a critical part of the immune response to viruses. The authors found that SARS-CoV-2 can hijack FGFR1 to block interferon production, allowing the virus to replicate unchecked.
The role of NAE1 in SARS-CoV-2 infection was not as obvious at first. NAE1 adds a particular protein to other tools in the cell to maintain their stability and determine where they should be in the cell. That protein is called, neural precursor cell expressed developmentally downregulated protein 8, but everyone calls it NEDD8. As to the process, it’s appropriately named, neddylation. In viral infections, neddylation helps the virus perform that second task, reproduction.
Here’s the complicated part - it’s not the virus’ proteins like the all too familiar Spike that add the NEDD8. So, while there was a link, Hobman’s team could only say it was indirect. But that wasn’t the end of the story.
That’s because two preclinical cancer drugs, MLN4924 and BGJ398, can block NAE1 and FGFR1, respectively. Using MLN4924, the authors prevented SARS-CoV-2 from entering the cell. Blocking the entire FGFR1 assembly line with BGJ398, or a specific downstream component called “MEK” reduced the ability of SARS-CoV-2 to replicate. In mice with severe Covid-19, both NAE1 and FGFR1 inhibitors reduced viral load in the mice which in turn limited virus-induced lung damage.
“Unprecedented”, “Social Distancing,” and “Lockdown” may be words most of us never want to hear again. But as Covid-19 continues to loom and evolve, it is essential that we continue to work on treatments to define a safer new normal. Work like Felix-Lopez and Hobman’s is key. By understanding how to stop SARS-CoV-2 from using the host’s toolbox, then we can develop treatments that remain effective even as the virus evolves.