The first HIV vaccine trial launched in 1985 was met with great enthusiasm. In 1985, Margaret Heckler (the U.S. Secretary for Health and Human Services) confidently stated that the first HIV vaccine would be developed within two years. Despite being nearly 40 years since the discovery of HIV/AIDS, no vaccine is available. That doesn’t mean, though, that there is no cure. The grueling and largely thankless work of trialing an HIV/AIDS vaccine has continued steadily over the past four decades (the most recent one launched in January 2022, using Moderna’s mRNA technology), making it the longest-running modern pandemic.
But failure, in the hands of scientists, doesn’t mean the end. It is an excellent foundation for science discovery. Instead of giving up, scientists developed a brand new strategy to stop the AIDS pandemic. Researchers had no way to prevent the disease from spreading without vaccines. And here’s where four decades of scientific failure was transformed into a radical approach to pandemic control, with direct implications for the future of the global effort to end COVID-19.
HIV scientists developed antiviral treatments for HIV to reduce the spread of HIV within human host cells. This would prevent the millions of HIV-infected individuals from getting sick or dying. This is how failure became unfettered success. The combination of HIV therapies known as Highly Active Antiretroviral Therapy (HAART), is so efficient at stopping viral replication it has made HIV infection a chronic condition. What’s more, HAART is so good at disrupting HIV’s ability to replicate that it can reduce the amount of virus in a person’s bloodstream to undetectable levels. It keeps HIV patients alive. But it also prevents HIV from spreading to other people. The best strategy for preventing the spread of the virus is treatment.
That’s a remarkable feat for a retrovirus like HIV, which has the highest recorded mutation rate of any biological entity. The drugs in the HAART combination target several parts of HIV to overcome this inherent advantage. Simply put, the virus can’t mutate its way out of the multiple attacks the drugs make on its ability to replicate. This multi-pronged strategy has made HAART a long-term solution that hasn’t lost its effectiveness over time even as HIV has continued to evolve at a rapid clip. It’s also where HIV prevention intersects neatly with the COVID-19 ‘Test to Treat’ strategy that President Biden announced at the State of the Union. It could not come at a better time, as recent evidence suggests that a post-Omicron wave is steadily rising across Europe and Asia—and that the U.S. is at risk of a renewed surge.
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We now have three antivirals approved for use against COVID-19, all of which target regions of SARS-CoV-2 that are highly conserved, meaning they don’t mutate very much at all. They are far more resistant to variations than the COVID-19 vaccinations that target fast-mutating spike proteins. And that gives us a fighting chance to end this pandemic using weapons we can be confident won’t be obsolete in a year’s time. Only thing we need is to accept the possibility of failure.
The three FDA-approved COVID-19-approved antivirals Remdesivir and Paxlovid target the critical regions that SARS-CoV-2 uses to replicate itself. At their most effective, they nullify the virus’s basic programming feature: replication. The antivirals prevent viruses from entering human host cells as they are made of complex macromolecules. And that’s where effective treatment can become prevention: as the AIDS pandemic taught us, as long as you can stop a virus from replicating, you can stop it from spreading—both through a person’s body, ending their life, and across a population of transmissible hosts, ending an epidemic.
The ‘Test to Treat’ plan is part of a larger containment strategy in which the role of COVID-19 antivirals is only going to become more critical. With ‘Test to Treat’, the Biden administration is looking to rapidly increase access to antivirals (specifically Pfizer’s Paxlovid, which reduces the risk of hospitalization for COVID by nearly 90%) for people who test positive for infection at pharmacies. It’s a smart approach to reducing illness and death from COVID-19, and it may also set the stage for the end of this pandemic. That’s because, even if new variants find a way to escape the vaccines (the U.K. government estimates that a two-dose vaccine regimen is only 10% effective against Omicron), we can be confident that they won’t elude the antivirals, at least not in the short term. That’s why ‘Test to Treat’ should be the first step in a wholesale adoption of the failure playbook to end COVID-19.
It could be advantageous to have a stock of antivirals that can be used strategically in the event of an outbreak. That way, frontline healthcare workers, along with the families and close contacts of infected people, can be given doses to protect them from severe infections even before they’re infected, stamping out the next wave before it starts. That will not be possible without long-term funding. Last week’s congressional vote to cease additional COVID-19 funds has caused the White House to declare that the government would soon no longer cover the cost of vaccines and treatment for those who don’t have insurance.
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That’s shortsighted thinking, because what’s perhaps most impressive about the failure playbook is that it might just spell the end of All Coronavirus pandemics – now and always That’s because the regions that the antivirals target aren’t just similar across SARS-CoV-2 variants: they are remarkably conserved across every one of the hundreds of coronavirus strains discovered, as quintessentially a part of coronaviruses as prehensile hands are to human beings. The antivirals were tested on SARS-CoV-2 and SARS, which is the first known human pathogenic coronavirus. They also worked against MERS (Middle East Respiratory Symdrome) and other coronaviruses. In all cases, they significantly reduced the virus’s replication potential.
And that’s where the failure playbook, starting with Test and Treat, becomes truly great news for our species’s long conflict with coronaviruses. Whatever pathogenic coronavirus is next to emerge, it will still have the same genomic regions of the previous ones, rendering it as vulnerable to the antiviral therapies developed to end SARS-CoV-2. This should reduce our anxiety over a repeat of what happened in the past two years. We might instead look forward to the future and discover that we may, for the first-time in human history, have a way to combat the progeny of our old viral nemesis.