The biology of coronavirus COVID-19 - including research and treatments

https://www.statnews.com/2020/04/16...uggests-patients-are-responding-to-treatment/

Early peek at data on Gilead coronavirus drug suggests patients are responding to treatment

Chicago hospital treating severe Covid-19 patients with Gilead Sciences’ antiviral medicine remdesivir in a closely watched clinical trial is seeing rapid recoveries in fever and respiratory symptoms, with nearly all patients discharged in less than a week, STAT has learned.

Remdesivir was one of the first medicines identified as having the potential to impact SARS-CoV-2, the novel coronavirus that causes Covid-19, in lab tests. The entire world has been waiting for results from Gilead’s clinical trials, and positive results would likely lead to fast approvals by the Food and Drug Administration and other regulatory agencies. If safe and effective, it could become the first approved treatment against the disease.

The University of Chicago Medicine recruited 125 people with Covid-19 into Gilead’s two Phase 3 clinical trials. Of those people, 113 had severe disease. All the patients have been treated with daily infusions of remdesivir.

“The best news is that most of our patients have already been discharged, which is great. We’ve only had two patients perish,” said Kathleen Mullane, the University of Chicago infectious disease specialist overseeing the remdesivir studies for the hospital.”

I’m a bit confused though as there wasn’t a placebo? I thought all Phase III trials had a placebo arm? Is it because they have to fast track the drug and it’s not really ethical to give patients placebo?

If the trial shows that people got a lot better, does that mean that this drug will be approved everywhere?

 

COVID-19 therapy, vaccine, epidemiology and policy development research boosted by twenty-one new projects
https://www.ukri.org/news/covid-19-research-boosted-by-new-projects/

 

If there is no placebo this particular trial can tell us nothing about efficacy. It may indicate a level of safety. I think the researchers have tried quite hard to emphasise that no conclusions can be drawn. I assume that a controlled study is being done on earlier cases as well that will give the real results.

 

Convalescent Plasma is likely to be effective, but there is no way they can make enough of it - unless they let a large proportion of the population become infected.

The vaccine projects seem well behind schedule if they are expected to complete human trials in 12-18 months...

 

The WHO now seem to be saying that they're worried that having been infected with coronavirus doesn't necessarily mean that you're immune but if so, how can a vaccine work?

 

I'm skeptical of all these timeframes unless they show a clear planned timeframe of all the procedures involved. Even 18 months requires significant overlapping of the various trial phases and extremely fast decision making by approval authorities.

But unapproved/incomplete evidence vaccines may be rolled out sooner - in developing countries or for at-risk health care workers, given that some authorities can decide not to wait for the evidence.

A am willing to bet however that we will be able to find a vaccine that will be at least as effective as our influenza vaccines and that given the observed spike protein mutation rates, those who seroconvert from an effective vaccine or the virus itself will have protection that lasts at least a few years. I don't suggest buying into the catastrophisation that somehow despite our immune systems working for similar infections, that it will somehow fail for SARS-2. (keep in mind, SARS-2 is not a sophisticated virus like HIV or EBV/CMV that have proteins dedicated to fucking with the immune system.)

 

Clotting issues are also likely due to ACE2 receptor related dysfunction:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4107144/

 

Most of the available antibody tests can say only whether someone has antibodies, not how many they have or how powerful they are at fighting the virus. Many of the tests are also flawed and signal the presence of antibodies even when there are none.

 

https://twitter.com/user/status/1251427343475765249

 

https://twitter.com/user/status/1251950246139133953

 

I agree. Having a very low number of antibodies in the blood doesn't mean much, it is how fast the body can make new ones when there is a new infection.

Antibody tests are used successfully for things like hepatitis, but the kits are tested and quality controlled before they are licensed and that takes a lot of time.

 

https://www.medrxiv.org/content/10.1101/2020.03.30.20048058v1
Interleukin-6 in COVID-19: A Systematic Review and Meta-Analysis
Eric Anthony Coomes, View ORCID ProfileHourmazd Haghbayan
doi: https://doi.org/10.1101/2020.03.30.20048058

Further mechanism might be found here:

 

Coronavirus strains may determine the the optimal treatment :

Coronavirus’s ability to mutate has been vastly underestimated, and mutations affect deadliness of strains, Chinese study finds

https://www.scmp.com/news/china/sci...tions-affect-deadliness-strains-chinese-study

 

To verify the theory, Li and colleagues infected cells with strains carrying different mutations. The most aggressive strains could generate 270 times as much viral load as the weakest type. These strains also killed the cells the fastest.

 

When it multiplies to fast the host will lose the battle.

 

If it kills too fast, the virus will lose the battle because the host will die before the virus can spread.

 

Not if it spreads before the host dies.

Virusses do not want to kill the host, they want to multiply.

Maybe the less virulent strains will get the upperhand.

 

And it even could be enough that the host stays at home in bed and not speaking to anybody else, for getting out of the traffic.

(May this is the reason that common colds do spread only to some percentage of the population?)