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Recent studies have shown two types of drugs with particular promise. The first are antivirals -- drugs that act on the virus itself and prevent it from replicating. Antivirals generally target either the enzymes a virus needs to copy its genome (polymerases) or those needed to cut larger proteins into smaller functional fragments (proteases). Coronaviruses, in general, are a target-rich environment for antivirals and this coronavirus, SARS-CoV-2, is no different than the others since it uses an active protease, a key protein responsible for the reproduction of the virus, to copy itself.

In a study published last month in Science, researchers announced their discovery of two new drug candidates that inhibit the SARS-CoV-2 protease. In test tube experiments, they found that the chemicals could bind to the protease and prevent replication, with one of them -- a chemical designated 11a -- more promising than the other. Chemical 11a will soon be tested for safety in humans, but early results from this study in dogs and mice suggest that the drug is both effective and non-toxic.

The other set of drugs showing promise are monoclonal antibodies, which are lab-created antibodies that work by blocking SARS-CoV-2 spike proteins from attaching to the ACE2 cell receptors in our body. By blocking the attachment, they prevent infection altogether. In another study published in June in Science, a separate set of scientists discovered two antibodies that each prevented different parts of the SARS2 spike protein from binding to the ACE2 receptor. While each of the antibodies on its own can neutralize the virus, together they are even more effective at preventing infection.

Just this week, late stage trials were announced for another double antibody cocktail that will be tested in 2,000 people across the United States for their ability to prevent infection and treat those in the early stages of Covid-19. With this drug -- and with the other set of monoclonal antibodies already researched -- there is a question of whether they are going to be effective against a virus like SARS-CoV-2 that lives primarily in the nose and the lungs instead of in the blood. That said, monoclonal antibodies have worked against the respiratory syncytial virus, which has many similarities to SARS-CoV-2.

Much like the vaccines that have showed early promise, these drugs too will need more testing before their safety and efficacy can be proven. But the timeline for testing these drugs is much shorter than for a vaccine, in large part due to how quickly and easily their efficacy can be determined. For antivirals and monoclonal antibodies, you know whether the virus works within a matter of days -- either the viral load in the patient goes up or it goes down -- and with very few individuals. Our first effective treatment for HIV, an antiviral, was proven in a group of just 19 patients given the drug.

What this means is that even if our path to a Covid vaccine is much longer and harder than we currently estimate, we can still have drugs in hand as early as the beginning of next year that can keep those most vulnerable from becoming infected and could, potentially, treat those already ill.

Coronavirus: Why surviving the virus may be just the beginning

The first thing Simon Farrell can remember, after being woken from a medically induced coma, is trying to tear off his oxygen mask. He had been in intensive care for 10 days, reliant on a ventilator just to breathe. "I was trying to pull the mask off my face, and the nurse kept putting it back on," he recalls.

When doctors woke him up, his body had fought off the worst of Covid-19 but he still needed oxygen to support his damaged lungs. And the 46-year-old father-of-two was suffering from such severe delirium he was trying to deny himself the oxygen he required.

"Try to stop me," he remembers saying, when nurses at Birmingham's Queen Elizabeth Hospital said they would have to put his hands in boxing glove-sized medical mittens unless he relaxed. "In the end they had to tape my hands up. I was trying to tear the mittens off, I managed to bite through them, and they had to put new mittens on."

It is not an unfamiliar story for anyone working in intensive care. The assault Covid-19 mounts on the most severely ill means patients are ventilated for longer, and require a deeper level of sedation, than the typical ICU patient.

https://www.bbc.com/news/53193835

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thrill wrote: ↑

July 13 20, 1:19 pm

The company I work for works for a district here in Florida which I will not name, other than to tell you it is in the top 10 largest in the nation. We asked a principal if we could donate to their PPE supply to help them re-open and it became apparent to us that the district is not prepared. They don't have the supplies necessary yet. We're like a month away and schools are having to fend for themselves procuring things like masks, plexiglass shielding, sanitizer, etc.

The kids might mostly be fine if they get COVID, but will the staff? If your teacher gets sick, do you have a substitute for 2 weeks (minimum)? Are there actually enough qualified substitute teachers to even step up as teachers inevitably go down with COVID? This is gonna be a constant struggle.