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opportunistic infections. The second wave of COVID in India was accompanied by a spike in cases of a gruesome and deadly disease called mucormycosis, also known as "black fungus"-- some people had this fungus in their lungs, but it was held in check until their immune system was suppressed, unleashing it and causing the disease. In most countries, almost no one had this fungus, so the problem was mostly limited to India.. Hoping to find another existing drug that might help, researchers tried other potential treatments that were already at hand. Remdesivir, the antiviral that showed promise in monkey cells, was originally developed to fight off hepatitis C. There are also various ways to take antibodies from the blood of people who have recovered from a disease and give them directly to someone who's still sick, an approach known as convalescent plasma. Unfortunately, neither convalescent plasma nor remdesivir was effective enough to warrant using them broadly for COVID. There was, however, a different approach to giving people antibodies that held more promise. It's called monoclonal antibodies, or mAbs for short, and it worked well enough to be approved for use in COVID cases in November 2020--only a month before the first vaccines became available. Instead of preventing a virus from taking over healthy cells, or from reproducing once it does take over a cell--which is how most antiviral drugs work--mAbs are the same thing your immune system generates to mop up the virus. (Antibodies are a protein with variable regions that allow them to grab onto unique shapes on the surface of the virus.) To make mAbs, scientists either isolate a powerful antibody from a patient's blood or use software modeling to come up with an antibody that grabs the virus. Then they clone it billions of times. (This cloning from a single antibody is why they're called monoclonal.)