The race is on to find a cure for Covid-19. Researchers are testing new vaccines, resurrecting old drugs, and repurposing treatments originally developed for other diseases. Things are moving fast; by the time you read this, the situation may have changed (for the better, we hope). So how are scientists thinking they’ll fend off this tiny viral adversary? Here are a few lines of attack.
Lock It Out
Each particle of the new virus, SARS-CoV-2, is studded with spikes, which allow it to attach itself to a human cell, poke a hole, and burrow inside. Like the germ that caused the SARS epidemic in 2003, it sticks to a protein on human cells called ACE2, which is especially prevalent in the lungs and small intestine. (SARS-CoV-2 is at least 10 times stickier than its cousin, which may account for its rapid spread.) One way to stop the invader is to keep it from attaching in the first place. This is what your immune system tries to do—it sends out antibodies that gum up the spikes so the virus can’t stick to ACE2. But there are other ways of achieving the same effect.
1. Make a vaccine. For powerful, long-lasting immunity, a so-called live attenuated vaccine is the gold standard. It contains a defanged version of the virus that your immune system can use for target practice—but it can also cause infection. That’s why many researchers are working on vaccines that contain not the whole virus but just the outer spikes. Mixed with immune-boosting molecules called adjuvants, they’ll elicit a safe antibody response.
2. Take antibody-rich blood plasma from people who have survived Covid-19 and inject it into newly infected or at-risk patients. Plasma won’t teach the body how to fend off the virus, and one injection won’t last forever—but it could be a good way to prepare health workers before they head to a hot spot.
3. Flood the zone with decoys—synthetic molecules that look like ACE2 and trick the virus into binding with them instead, protecting lung cells from damage.
4. Invent drugs that hinder ACE2 from binding with the virus. In theory, these compounds would work on both SARS and Covid-19, stopping the viruses from sticking to cells. But ACE2 plays a number of other roles throughout the body; it helps regulate blood pressure, kidney function, and even fertility. Messing with it could have dangerous consequences.
Kill It on Contact
All viruses wear heavy-duty protein coats to protect their precious genetic material from the elements. The new coronavirus sports an extra outer layer of fatty molecules. That’s great news for humans, because it’s easy to tear open with soap or alcohol-based disinfectants. (Soap works best, and you don’t need to bother with the antibacterial stuff.) Without its fatty layer, the virus dies. Wipe it away or wash it down the drain.
Plus: What it means to “flatten the curve,” and everything else you need to know about the coronavirus.
Sabotage It From the Inside
A virus’s sole purpose in life is to hijack the machinery of its host cell and force it to make viral copies. By changing how that machinery operates, it’s possible to stymie the virus’s attempts. Drugs that were developed to fight other ailments could have off-label applications for Covid-19.
1. Chloroquine phosphate, used for decades to treat malaria, changes the pH level in human cells, making them less acidic—and less hospitable to certain viruses. Researchers are exploring whether SARS-CoV-2 might be one of them. Chloroquine can also reduce the lung inflammation that kills some patients with severe Covid-19 infection. One problem: An overdose can be fatal.
2. A class of drugs called protease inhibitors, long used to treat HIV and hepatitis C, disrupt the viral replication process. Proteases are like molecular scissors; once inside the host cell, SARS-CoV-2 uses them to slice long strands of protein into usable chunks. Without these scissors, the virus’s life cycle can’t continue.
3. Another class of medications targets an enzyme called polymerase, which strings together copies of the virus’s genetic material, RNA, inside the host cell. Two promising candidates in this category—remdesivir, originally developed to treat Ebola, and favipiravir, first deployed against the flu—impersonate the building blocks of RNA and get incorporated into the chain. Once they’re there, the polymerase can’t add new pieces, and replication halts.
This article appears in the May issue. Subscribe now.
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