Treatments For Covid-19

𝙒𝙝𝙖𝙩 π™π™šπ™‘π™₯𝙨, 𝙬𝙝𝙖𝙩 π™™π™€π™šπ™¨π™£'𝙩, 𝙖𝙣𝙙 𝙬𝙝𝙖𝙩'𝙨 π™žπ™£ π™©π™π™š π™₯π™žπ™₯π™šπ™‘π™žπ™£π™š.

Most people who become ill with COVID-19 will be able to recover at home. No specific treatments for COVID-19 exist right now. But some of the same things you do to feel better if you have the flu β€” getting enough rest, staying well hydrated, and taking medications to relieve fever and aches and pains β€” also help with COVID-19.

In the meantime, scientists are working hard to develop effective treatments. Therapies that are under investigation include drugs that have been used to treat malaria and autoimmune diseases; antiviral drugs that were developed for other viruses, and antibodies from people who have recovered from COVID-19.

π—œπ—¦ π—§π—›π—˜π—₯π—˜ 𝗔𝗑 π—”π—‘π—§π—œπ—©π—œπ—₯π—”π—Ÿ 𝗧π—₯π—˜π—”π—§π— π—˜π—‘π—§ 𝗙𝗒π—₯ π—–π—’π—©π—œπ——-𝟭𝟡?

Currently there is no specific antiviral treatment for COVID-19.

However, drugs previously developed to treat other viral infections are being tested to see if they might also be effective against the virus that causes COVID-19.

π—ͺ𝗛𝗬 π—œπ—¦ π—œπ—§ 𝗦𝗒 π——π—œπ—™π—™π—œπ—–π—¨π—Ÿπ—§ 𝗧𝗒 π——π—˜π—©π—˜π—Ÿπ—’π—£ 𝗧π—₯π—˜π—”π—§π— π—˜π—‘π—§π—¦ 𝗙𝗒π—₯ π—©π—œπ—₯π—”π—Ÿ π—œπ—Ÿπ—Ÿπ—‘π—˜π—¦π—¦π—˜π—¦ 𝗦𝗨𝗖𝗛 𝗔𝗦 π—–π—’π—©π—œπ——-𝟭𝟡?

An antiviral drug must be able to target the specific part of a virus's life cycle that is necessary for it to reproduce. In addition, an antiviral drug must be able to kill a virus without killing the human cell it occupies. And viruses are highly adaptive. Because they reproduce so rapidly, they have plenty of opportunity to mutate (change their genetic information) with each new generation, potentially developing resistance to whatever drugs or vaccines we develop.

π—ͺ𝗛𝗔𝗧 𝗧π—₯π—˜π—”π—§π— π—˜π—‘π—§π—¦ 𝗔π—₯π—˜ π—”π—©π—”π—œπ—Ÿπ—”π—•π—Ÿπ—˜ 𝗧𝗒 𝗧π—₯π—˜π—”π—§ 𝗖𝗒π—₯π—’π—‘π—”π—©π—œπ—₯𝗨𝗦?

Currently there is no specific antiviral treatment for COVID-19. However, similar to treatment of any viral infection, these measures can help:

βœ…While you don't need to stay in bed, you should get plenty of rest.

βœ…Stay well hydrated.

βœ…To reduce fever and ease aches and pains, take acetaminophen. Be sure to follow directions. If you are taking any combination cold or flu medicine, keep track of all the ingredients and the doses. For acetaminophen, the total daily dose from all products should not exceed 3,000 milligrams.

π—œπ—¦ π—œπ—§ π—¦π—”π—™π—˜ 𝗧𝗒 π—§π—”π—žπ—˜ π—œπ—•π—¨π—£π—₯π—’π—™π—˜π—‘ 𝗧𝗒 𝗧π—₯π—˜π—”π—§ 𝗦𝗬𝗠𝗣𝗧𝗒𝗠𝗦 𝗒𝗙 π—–π—’π—©π—œπ——-𝟭𝟡?

Some French doctors advise against using ibuprofen (Motrin, Advil, many generic versions) for COVID-19 symptoms based on reports of otherwise healthy people with confirmed COVID-19 who were taking an NSAID for symptom relief and developed a severe illness, especially pneumonia. These are only observations and not based on scientific studies.

The WHO initially recommended using acetaminophen instead of ibuprofen to help reduce fever and aches and pains related to this coronavirus infection, but now states that either acetaminophen or ibuprofen can be used. Rapid changes in recommendations create uncertainty. Since some doctors remain concerned about NSAIDs, it still seems prudent to choose acetaminophen first, with a total dose not exceeding 3,000 milligrams per day.

However, if you suspect or know you have COVID-19 and cannot take acetaminophen, or have taken the maximum dose and still need symptom relief, taking over-the-counter ibuprofen does not need to be specifically avoided.

𝗔π—₯π—˜ π—–π—›π—Ÿπ—’π—₯π—’π—€π—¨π—œπ—‘π—˜ 𝗔𝗑𝗗 𝗛𝗬𝗗π—₯π—’π—«π—¬π—–π—›π—Ÿπ—’π—₯π—’π—€π—¨π—œπ—‘π—˜ π—˜π—™π—™π—˜π—–π—§π—œπ—©π—˜ 𝗙𝗒π—₯ 𝗧π—₯π—˜π—”π—§π—œπ—‘π—š π—–π—’π—©π—œπ——-𝟭𝟡?

Recently, there has been considerable discussion of whether two related drugs β€” chloroquine and hydroxychloroquine β€” that have been available for decades to treat other illnesses might also be effective in treating COVID-19.

The drugs are primarily used to treat malaria and several inflammatory diseases, including systemic lupus erythematosus (lupus) and rheumatoid arthritis. No drug is perfectly safe, but these drugs are quite safe when used for just the several days they might be needed to treat COVID-19. They are also cheap, already available at our local drug stores, and relatively free of side effects.

The question, of course, is whether they are effective against the coronavirus that causes COVID-19. Are they effective in killing the virus in a laboratory dish? And are they effective in killing the virus in people? If the answer to the first question is "no," there's no point in getting an answer to the second question.

There is strong evidence that both drugs kill the COVID-19 virus in the laboratory dish. The drugs appear to work through two mechanisms. First, they make it harder for the virus to attach itself to the cell, inhibiting the virus from entering the cell and multiplying within it. Second, if the virus does manage to get inside the cell, the drugs kill it before it can multiply.

But do the drugs work in people with COVID-19? Many studies are underway to get an answer to this question, but as of March 24, 2020, only two have issued preliminary results.

One report, published in February 2020, claimed that chloroquine had been used in more than 100 patients in China who had COVID-19. The scientists stated that their results demonstrated that chloroquine is superior to the control treatment in inhibiting the worsening of pneumonia, improving lung imaging findings, eliminating the virus from the body, and shortening the duration of the disease.

These claims are exciting. However, the report provided virtually no evidence in support of the claims. First of all, this was not a randomized, double-blind controlled trial, the gold standard for research studies. Second, no evidence was presented as to how severe the pneumonia was, nor whether findings on lung x-rays or CT scans really improved. Third, although they claim the drug made the virus disappear, they didn't report what the levels of the virus were before versus after the treatment. In short, not much evidence.

Another small study was conducted by a group of scientists in southern France, a region hard hit by COVID-19. This, also, was not a randomized trial. Instead, the scientists compared 26 patients who received hydroxychloroquine to 16 who did not: after six days, the virus was gone from the body in 70% of those given the treatment, compared to only 12.5% of those who weren't. The drug appeared to be as effective in the sickest patients as in the least sick, but the study was too small to be sure about that. The study also was too small to say that people who received the treatment were protected against a prolonged illness or death.

There are many studies underway, and we should have more solid answers within a few months.

π—œπ—¦ π—§π—›π—˜ π—”π—‘π—§π—œπ—©π—œπ—₯π—”π—Ÿ 𝗗π—₯π—¨π—š π—₯π—˜π— π——π—˜π—¦π—œπ—©π—œπ—₯ π—˜π—™π—™π—˜π—–π—§π—œπ—©π—˜ 𝗙𝗒π—₯ 𝗧π—₯π—˜π—”π—§π—œπ—‘π—š π—–π—’π—©π—œπ——-𝟭𝟡?

Scientists all over the world are testing whether drugs previously developed to treat other viral infections might also be effective against the new coronavirus that causes COVID-19.

One drug that has received a lot of attention is the antiviral drug remdesivir. That's because the coronavirus that causes COVID-19 is similar to the coronaviruses that caused the diseases SARS and MERS β€” and evidence from laboratory and animal studies suggests that remdesivir may help limit the reproduction and spread of these viruses in the body. In particular, there is a critical part of all three viruses that can be targeted by drugs. That critical part, which makes an important enzyme that the virus needs to reproduce, is virtually identical in all three coronaviruses; drugs like remdesivir that successfully hit that target in the viruses that cause SARS and MERS are likely to work against the COVID-19 virus.

Remdesivir was developed to treat several other severe viral diseases, including the disease caused by Ebola virus (not a coronavirus). It works by inhibiting the ability of the coronavirus to reproduce and make copies of itself: if it can't reproduce, it can't make copies that spread and infect other cells and other parts of the body.

Remdesivir inhibited the ability of the coronaviruses that cause SARS and MERS to infect cells in a laboratory dish. The drug also was effective in treating these coronaviruses in animals: there was a reduction in the amount of virus in the body, and also an improvement in lung disease caused by the virus.

The drug appears to be effective in the laboratory dish, in protecting cells against infection by the COVID virus (as is true of the SARS and MERS coronaviruses), but more studies are underway to confirm that this is true.

Remdesivir was used in the first case of COVID-19 that occurred in Washington state, in January 2020. The patient was severely ill, but survived. Of course, experience in one patient does not prove the drug is effective.

Two large randomized clinical trials are underway in China. The two trials will enroll over 700 patients, and are likely to definitively answer the question of whether the drug is effective in treating COVID-19. The results of those studies are expected in April or May 2020. Studies also are underway in the United States, including at several Harvard-affiliated hospitals. It is hard to predict when the drug could be approved for use and produced in large amounts, assuming the clinical trials indicate that it is effective and safe.

I've heard that high-dose vitamin C is being used to treat patients with COVID-19. Does it work? And should I take vitamin C to prevent infection with the COVID-19 virus?

Some critically ill patients with COVID-19 have been treated with high doses of intravenous (IV) vitamin C in the hope that it will hasten recovery. However, there is no clear or convincing scientific evidence that it works for COVID-19 infections, and it is not a standard part of treatment for this new infection. A study is underway in China to determine if this treatment is useful for patients with severe COVID-19; results are expected in the fall.

The idea that high-dose IV vitamin C might help in overwhelming infections is not new. A 2017 study found that high-dose IV vitamin C treatment (along with thiamine and corticosteroids) appeared to prevent deaths among people with sepsis, a form of overwhelming infection causing dangerously low blood pressure and organ failure. Another study published last year assessed the effect of high-dose vitamin C infusions among patients with severe infections who had sepsis and acute respiratory distress syndrome (ARDS), in which the lungs fill with fluid. While the study's main measures of improvement did not improve within the first four days of vitamin C therapy, there was a lower death rate at 28 days among treated patients. Though neither of these studies looked at vitamin C use in patients with COVID-19, the vitamin therapy was specifically given for sepsis and ARDS, and these are the most common conditions leading to intensive care unit admission, ventilator support, or death among those with severe COVID-19 infections.

Regarding prevention, there is no evidence that taking vitamin C will help prevent infection with the coronavirus that causes COVID-19. While standard doses of vitamin C are generally harmless, high doses can cause a number of side effects, including nausea, cramps, and an increased risk of kidney stones.(1)

π—§π—”π—žπ—˜ 𝗖𝗔π—₯π—˜ 𝗒𝗙 𝗬𝗒𝗨π—₯ π—œπ— π— π—¨π—‘π—˜ π—›π—˜π—”π—Ÿπ—§π—›

Melbourne researchers have mapped immune responses from one of Australia's first novel coronavirus (COVID-19) patients, showing the body's ability to fight the virus and recover from the infection.

Researchers at the Peter Doherty Institute for Infection and Immunity (Doherty Institute) -- a joint venture between the University of Melbourne and the Royal Melbourne hospital -- were able to test blood samples at four different time points in an otherwise healthy woman in her 40s, who presented with COVID-19 and had mild-to-moderate symptoms requiring hospital admission.

Published today in Nature Medicine is a detailed report of how the patient's immune system responded to the virus. One of the authors on the paper, research fellow Dr Oanh Nguyen said this was the first time that broad immune responses to COVID-19 have been reported.

"We looked at the whole breadth of the immune response in this patient using the knowledge we have built over many years of looking at immune responses in patients hospitalized with influenza," Dr Nguyen said.

"Three days after the patient was admitted, we saw large populations of several immune cells no, which are often a tell-tale sign of recovery during seasonal influenza infection, so we predicted that the patient would recover in three days, which is what happened."

The research team was able to do this research so rapidly thanks to SETREP-ID (Sentinel Travellers and Research Preparedness for Emerging Infectious Disease), led by Royal Melbourne Hospital Infectious Diseases Physician Dr Irani Thevarajan at the Doherty Institute.

SETREP-ID is a platform that enables a broad range of biological sampling to take place in returned travellers in the event of a new and unexpected infectious disease outbreak, which is exactly how COVID-19 started in Australia.

"When COVID-19 emerged, we already had ethics and protocols in place so we could rapidly start looking at the virus and immune system in great detail," Dr Thevarajan said.

"Already established at a number of Melbourne hospitals, we now plan to roll out SETREP-ID as a national study."

Working together with University of Melbourne Professor Katherine Kedzierska, a laboratory head at the Doherty Institute and a world-leading influenza immunology researcher, the team were able to dissect the immune response leading to successful recovery from COVID-19, which might be the secret to finding an effective vaccine.

"We showed that even though COVID-19 is caused by a new virus, in an otherwise healthy person, a robust immune response across different cell types was associated with clinical recovery, similar to what we see in influenza," Professor Kedzierska said.

"This is an incredible step forward in understanding what drives recovery of COVID-19. People can use our methods to understand the immune responses in larger COVID-19 cohorts, and also understand what's lacking in those who have fatal outcomes."

Dr Thevarajan said that current estimates show more than 80 percent of COVID-19 cases are mild-to-moderate, and understanding the immune response in these mild cases is very important research.

"We hope to now expand our work nationally and internationally to understand why some people die from COVID-19, and build further knowledge to assist in the rapid response of COVID-19 and future emerging viruses," she said.(2)


(1) Harvard Health Publishing. Harvard Medical. March 2020.

(2) University of Melbourne. COVID-19: The immune system can fight back. March 17, 2020

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