I compiled a list of some significant 'what we know about COVID-19'
articles for myself.
COVID-19 is an RNA VIRUS - that means it mutates, just like the common cold
or flu.
RNA means it only has a single strand that prevents 'proof reading' when it
RNA means it only has a single strand that prevents 'proof reading' when it
reproduces. Reproduction is sloppy.
Those mutations raise serious questions about a VACCINE, just as we have no
vaccine for the common cold and no single vaccine for the flu.
A mutation on the outer shell of COVID-19 might render a vaccine useless.
A mutation on the outer shell of COVID-19 might render a vaccine useless.
Frankly, we don't know.
The ONLY EFFECTIVE treatment is PREVENTION - face masks, social distancing
The ONLY EFFECTIVE treatment is PREVENTION - face masks, social distancing
and STAY AT HOME.
FROM POLITICO NIGHTLY:
STRONG MEDICINE — For weeks doctors and nurses around the country had no real handbook for how to treat the Covid patients that started showing up in their emergency rooms. They had some insight from clinicians in Italy and China and experience treating patients with respiratory ailments, but early treatments included a lot of frantic guesswork.
Now, five months after the first Covid patient walked into a clinic in Everett, Wash., there’s still no FDA-approved therapy or treatment for the virus. In fact, there are two fewer drugs with even a preliminary nod from the agency: The FDA pulled its emergency use authorizations today of chloroquine and hydroxychloroquine, the antimalarial drug touted by President Donald Trump as a Covid treatment.
There are still far more questions than answers when it comes to managing Covid patients. But doctors have made some progress. About 560,000 Covid patients are known to have recovered, according to Johns Hopkins University, though the figure is almost certainly higher because not all states track recoveries and not every infected person goes to the hospital. Here’s a look at what we’ve learned about treating Covid, and what doctors have yet to figure out.
What we got wrong — In the early days of the pandemic, doctors were more willing to try off-label drugs without the usual vetting process, said Daniel Culver, a pulmonary and critical care physician at the Cleveland Clinic who leads a committee that evaluates Covid clinical trial research. That’s partly behind the rise and now fall of hydroxychloroquine. Clinical trials are still ongoing, but the drug’s effectiveness at treating Covid remains questionable.
What we are learning — Evidence is mounting that the antiviral drug remdesivir is effective at helping severely infected Covid patients with low oxygen levels. It’s now the only drug with emergency use authorization from the FDA.
There are hundreds of trials underway for dozens of Covid treatments. Some therapies, like using convalescent plasma from recovered patients to treat the critically ill, are being studied but so far there’s no definitive evidence on whether they are effective.
What we learned not to do — Doctors now believe it’s no longer a good idea to intubate — meaning put on a ventilator — all patients with low oxygen, said Amy Compton-Phillips, chief clinical officer for Providence Health System, which has 51 hospitals including the one that treated the first U.S. Covid patient.
Early on, Compton-Phillips said, her system relied on the advice of doctors in Italy and China to quickly put patients on a ventilator because it was thought to better protect health care workers and because the disease progressed so rapidly. But over time, the health system, which created a registry to track care for Covid patients across its hospitals, realized many patients didn’t need the invasive procedure, which comes with its own risks, right away. Instead the hospital tried other procedures to help patients boost oxygen levels, like proning patients — putting them on their stomachs — to help them inflate their lungs. Over the time, the health system cut its intubations in half, and mortality rates also declined.
What we know now about treating complications — Doctors also began to realize that Covid was more than just a respiratory disease — it can affect all organs and in particular kidneys. Up to 15 percent of patients hospitalized with Covid develop acute kidney injury and many need dialysis.
Intensive-care doctors now pay more attention to how much fluid they are giving patients, being more careful not to flood their lungs and other organs. And they focus more on keeping Covid patients from developing blood clots, which have led to amputations, strokes and other complications.
And hospitals are working on preventing infections by reducing the use of invasive procedures like catheters and better isolating infected patients. “It’s a question of being systematic and careful rather than a eureka thing,” Culver said. “Everyone wants to focus on bells and whistles, but the blocking and tackling part is the most important.”
What we still don’t know — “We’re not even at the end of the beginning for learning about this virus,” Compton-Phillips said. Researchers are trying to figure out answers to the biggest questions including how to intervene early to keep the virus from becoming severe, what are the long-term complications of a Covid infection and why it has been more lethal in black and Hispanic populations.
New coronavirus mutation might make it even more infectious
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COVID-19: How many strains of the new coronavirus are there?
Since this is a global pandemic, the US should be leading in global efforts to research and find solutions.
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SARS-CoV-2 is an enveloped RNA virus, which means that its genetic material is encoded in single-stranded RNA. Inside a host cell, it makes its own replication machinery.
RNA viruses have exceptionally high mutations rates because their replications enzymes are prone to errors when making new virus copies.
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Virologist Prof. Jonathan Stoye, a senior group leader at the Francis Crick Institute in London in the United Kingdom, told Medical News Today what makes virus mutations significant.
“A mutation is a change in a genetic sequence,” he said. “The fact of a mutational change is not of primary importance, but the functional consequences are.”
If a particular genetic alteration changes the target of a drug or antibody that acts against the virus, those viral particles with the mutation will outgrow the ones that do not have it.
“A change in a protein to allow virus entry into a cell that carries very low amounts of receptor protein could also provide a growth advantage for the virus,” Prof. Stoye added.
“However, it should be stressed that only a fraction [of] all mutations will be advantageous; most will be neutral or harmful to the virus and will not persist.”
“Mutations in viruses clearly do matter, as evidenced by the need to prepare new vaccines against [the] influenza virus every year for the effective prevention of seasonal flu and the need to treat HIV-1 simultaneously with several drugs to [prevent the] emergence of resistant virus.”
– Prof. Jonathan Stoye
The team studied five nasal swab samples that had a positive SARS-CoV-2 test result. They found that one of these had a deletion, which means that a part of the viral genome was missing. To be precise, 81 nucleotides in the viral genetic code were gone.
Previous research indicated that similar mutations lowered the ability of the SARS virus to replicate.
Another study, this time in the Journal of Translational Medicine, proposed that SARS-CoV-2 had picked up specific mutation patterns in distinct geographical regions.
The researchers, from the University of Maryland in Baltimore and Italian biotech company Ulisse Biomed in Trieste, analyzed eight recurrent mutations in 220 COVID-19 patient samples.
They found three of these exclusively in European samples and another three exclusively in samples from North America.
Another study, which has not yet been through the peer review process, suggests that SARS-CoV-2 mutations have made the virus more transmissible in some cases.
In the paper, Bette Korber — from the Los Alamos National Laboratory in New Mexico — and collaborators describe 13 mutations in the region of the viral genome that encodes the spike protein.
This protein is crucial for infection, as it helps the virus bind to the host cell.
The researchers note that one particular mutation, which changes an amino acid in the spike protein, “may have originated either in China or Europe, but [began] to spread rapidly first in Europe, and then in other parts of the world, and which is now the dominant pandemic form in many countries.”
Prof. Stoye commented that the results of this study are, in some ways, not surprising.
“Viruses are typically finely tuned to their host species. If they jump species, e.g., from bat to human, a degree of retuning is inevitable both to avoid natural host defenses and for optimum interaction with the cells of the new host,” he said.
“Random mutations will occur, and the most fit viruses will come to predominate,” he added. “Therefore, it does not seem surprising that SARS-CoV-2 is evolving following its jump to, and spread through, the human population. Clearly, such changes are currently taking place, as evidenced by the apparent spread of the [mutation] observed by Korber [and colleagues].”
However, Prof. Stoye does not think that it is clear at this point how mutations will drive the behavior of SARS-CoV-2 in the long term.
“Fears about SARS-CoV-2 evolution to resist still-to-be-developed vaccines and drugs are not unreasonable,” he explained. “Nevertheless, it is also possible that we will see evolution to a less harmful version of the virus, as may well have occurred following initial human colonization by the so-called seasonal coronaviruses.”
Opinions remain divided
Earlier this year, researchers from Peking University in Beijing, China, published a paper in National Science Review describing two distinct lineages of SARS-CoV-2, which they termed “S” and “L.”
They analyzed 103 virus sequence samples and wrote that around 70% were of the L lineage.
However, a team at the Center for Virus Research at the University of Glasgow in the U.K. disagreed with the findings and published their critique of the data in the journal Virus Evolution.
“Given the repercussions of these claims and the intense media coverage of these types of articles, we have examined in detail the data presented […] and show that the major conclusions of that paper cannot be substantiated,” the authors write.
Prof. David Robertson, head of Viral Genomics and Bioinformatics at the Centre for Virus Research, was part of the team. MNT asked his views on the possibility of there being more than one strain of SARS-CoV-2.
“Until there is some evidence of a change in virus biology, we cannot say that there are new strains of the virus. It’s important to appreciate that mutations are a normal byproduct of virus replication and that most mutations we observe won’t have any impact on virus biology or function,” he said.
“Some of the reports of, for example, amino acid changes in the spike protein are interesting, but at the moment, these are at best a hypothesis. Their potential impact is currently being tested in a number of labs.”
Prof. Stoye thinks that it is “more a case of semantics rather than anything else” at the moment.
“If we have different sequences, we have different strains. Only when we have a greater understanding of the functional consequences of the evolutionary changes observed does it make sense to reclassify the different isolates,” he said.
“At that point, we can seek to correlate sequence variation with prognostic or therapeutic implications. This may take a number of years.”
Serotypes and future research
So, what kind of evidence are skeptical scientists looking for in the debate around multiple SARS-CoV-2 strains?
MNT asked Prof. Martin Hibberd, from the London School of Hygiene and Tropical Medicine in the U.K., to weigh in on the debate.
“For virologists, ‘strain’ is rather a subjective word that does not always have a clear specific meaning,” he commented.
“More useful in the SARS-CoV-2 situation would be the idea of ‘serotype,’ which is used to describe strains that can be distinguished by the human immune response — an immune response to one serotype will not usually protect against a different serotype. For SARS-CoV-2, there is no conclusive evidence that this has happened yet.”
“To show that the virus has genetically changed sufficiently to create a different immune response, we would need to characterize the immune protection and show that it worked for one serotype and not for another,” he continued.
Prof. Hibberd, who has been researching SARS-CoV-2 mutations, explained that scientists are studying neutralizing antibodies to help them define a serotype for SARS-CoV-2. These antibodies can prevent the virus from infecting a host cell, but they may not be effective against a new strain.
“Several groups around the world have identified a specific mutation in the SARS-CoV-2 spike protein, and they are concerned that this mutation might alter this type of binding, but we cannot be sure it does that at the moment. More likely, this mutation will likely affect the virus binding to its receptor […], which might affect transmissibility.”– Prof. Martin Hibberd
“We ideally need experimental evidence, [such as a] demonstration of a mutation leading to a functional change in the virus in the first instance, and secondly a demonstration that this change will have an impact in [people with the infection],” Prof. Robertson suggested.
He pointed to lessons that experts learned during the 2014–2018 Ebola outbreak in West Africa, where several research groups had suggested that a mutation had resulted in the virus becoming more easily passed between people and more deadly.
Cell culture experiments showed that the mutated virus was able to replicate more rapidly. However, when scientists subsequently studied this in animal models, they found that it did not behave any differently than stains without the mutation.
Scientists around the world continue to search for answers to the many outstanding questions around SARS-CoV-2. No doubt, we will see more research emerge in the coming months and years that will assess the impact of SARS-CoV-2 mutations on the COVID-19 pandemic and the future of this new coronavirus.
For live updates on the latest developments regarding the novel coronavirus and COVID-19, click here
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This tracks the spread:
The world struggled to understand how COVID-19 spread during the pandemic’s first four months, but genetic sequences of the coronavirus reported by laboratories tell the real story—when the virus arrived in each place and where it came from. The sequences, which advance from left to right in the graphic, show that the virus jumped from an animal to humans in China, humans transmitted it to one another within China, then people traveling from there spread it globally person to person. The virus had not mutated significantly as of March 31, 2020; human contact created the pandemic, not a wildly evolving pathogen. Mapping the spread also substantiates actions that could have best mitigated it: faster, wider testing in China; earlier, stricter global travel bans and isolation of infected people; and more immediate social distancing worldwide.
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The WORLD HEALTH ORGANIZATION was the sole source of scientific information from which Daffy Don pulled US FUNDING.
Since this is a global pandemic, the US should be leading in global efforts to research and find solutions.
We've short-changed ourselves in this effort.
We're not. How pathetic!
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