I run several science sites and spaces some on my own and some with other colleagues that cover atleast 1,50,000 people daily. I am very strict about what people add/post. I always ask for  evidence, citations, authenticity, validation much to the annoyance  of the members. 'You are running them like science journals and this is not fair' : a complaint I hear day in and day out. I just grin and move on.

Like other genuine people of science I too am fighting a fierce war against pseudo-science, misinformation, junk material and all sorts of nonsense and 'infodemic'.  And I am very proud of my  'providing only genuine science' to the general public legacy. Eventhough several people are asking me to join them to run their sites/spaces, I refuse to get associated with anyone who promote junk science. I have a very clean image till now.

But then this happened yesterday: some scientists accused me of 'inventing science' to make the general public happy. Hmmm!

Did I do that? 'NO' is my firm answer. Then why the accusation?

Well, when you get obsessed with infodemic, everything will look like it!

Tinted glasses: Image source: Lenspick

Let me explain the context. We have an  online group where some people of science meet and discuss things. I added a media report of a scientific paper that deals with the mutations of corona virus along with the link to the original paper published in a peer-reviewed high quality journal.  

This is the link to the paper: https://jvi.asm.org/content/early/2020/04/30/JVI.00711-20

Mutations happen all the while in viruses and for common people they need not be of much importance. But for researchers in the field, especially vaccine developers, they are extremely important. That is why they do research on it and report very often. 

Now this report deals with mutations that happened recently at a site that can have tremendous affect on the virulence factor of the virus. Similar mutations happened earlier to the SARS virus made them weak and less virulent.

This is also important because these less virulent viruses can be used as vaccine candidates. It is significant news for the vaccine developers too. 

We have been expecting such mutations for a long time. When they 're reported, we, the microbiologists, 're elated as our hopes 're realized. We celebrated and posted about the good news on several scientific social networks and people were very happy to hear the morale-boosting news.  We thought a stressed world had relaxed somewhat and their worry had eased to some extent.

Then this shocking accusation came like a bolt from blue. 

"We will see such reports very often. What is the big deal?", the scientists (not from the Microbiology field, otherwise they would have understood the significance of the discovery) asked me."Only when there is empirical evidence of these mutations doing anything, you should celebrate and report," they said.

They even said to make people happy, I 'weaved' a story by inventing 'happy science'. Ufff!

I tried to understand. Analysed it with my Microbiology colleagues. Not only this story but other ones also that caused misunderstanding.

Well, first, scientists from other fields might not understand the significance of this report like we did. So they got irritated when we started celebrating. They failed to understand that it 's the specialists in the field, who know chalk from cheese,  who 're reporting now and not the media people. They started seeing everything through tinted glasses and  failed to see the difference. 

Their obsession with 'more' evidence and data made them  think we 're celebrating prematurely.

But 're we? 

Let me explain.  When a specialist doctor of a particular area sees a critically ill patient of his arena, depending on the symptoms, s/he can diagnose a disease  and atleast can guess correctly to some extent what the disease might be. Other specialists might not be able to clearly see this and if they accuse the doctor of 'misdiagnosis' or not waiting till the test results are out to start the treatment even though the patient is dying? This 's what happened here.

Let me assure you, we are not immune to evidence.

The difference between them and us is .... we can understand the different scenarios in uncertain conditions and can be flexible enough to do our best even in these situations.

So we think ....

Policing is good but over-policing that needlessly interferes with other people's liberty and independence? Eeek! Policing on other law enforcement agencies? NO!

Not only that because of their over emphasis on evidence and data, I realized, the scientists are going into a paralysis mode and are unable to take decisions  quickly. Read this article that depicts how that happens and how I take some bold decisions: science-communication-in-uncertain-times

and sci-com-dilemmas

Moreover, they are sticking with 'old theories' even though the situations are demanding re-look at a few things. Read here how I am fighting it: covid-19-is-not-just-a-respiratory-disease-but-an-illness-that-ca

It is good to demand and depend on evidence. It is good to depend on data to arrive at a conclusion and take a decision. But over-dependence on it and obsession with it  shouldn't paralyse you, make you stagnant and paranoid to the extent that it blinds you and causes  inconvenience to others.

People of science, beware of this obsessive-compulsive disorder (OCD).

Vaccines

All viral vaccines contain material that resembles the virus they are trying to protect against. This fools the immune system into mounting a response and producing antibodies ready to be used should it ever encounter the real thing. In the case of the coronavirus, the immune system produces antibodies that target the spike protein – the part of the virus that is used to invade our cells.

One concern is that the virus will mutate to form “escape mutants”. These are mutated versions of the virus that the vaccine-induced antibodies won’t recognise. We see this with other viruses, such as influenza. The flu vaccine has to be altered each year to counter changes to circulating strains.

Luckily, the novel coronavirus has a lower mutation rate than influenza. And while the LSTHM study identified changes in the S gene (the gene that makes the spike) of the various virus strains, mutations in this gene were comparatively rare. Mutations in the epitope regions (the sites in the spike protein the antibodies attach to) were also infrequent.

Antiviral drugs

Initial searches for an effective treatment have focused on existing drugs, as seen in recent reports of the success of dexamethasone. While this drug prevents a hyperactive immune reaction to the virus, other promising drugs, such as remdesivir, directly target the virus itself. Remdesivir specifically targets the enzyme the virus needs to replicate.

Previous studies found two mutations in the enzyme gene that confer resistance to remdesivir, but the LSHTM study didn’t find many instances of these mutations. Wide use of the drug, however, will put selective pressure on the virus (environmental factors that contribute to evolutionary change), so monitoring these mutations will be important.

Tests

To diagnose a current infection, diagnostic tests look for certain genes from the virus. The accuracy of these tests depends on the target areas of the genome being as expected.

The first published diagnostic method, released shortly after the first viral genome was sequenced, screened for more than one viral gene considered to be “well conserved” across viral strains. (Well-conserved genes are important for the virus to function and so tend not to change as the organism evolves.) Most diagnostic tests since have continued to screen for two or more coronavirus genes, although the genes they test for often vary.

The authors of the LSHTM study looked for variations in regions of the genome screened for in common diagnostic tests and found several mutations that could result in “false negatives”, where a person has the disease but the test says they don’t. These mutations had a strong geographical distribution, so clinical scientists need to be aware of locally circulating strains when considering which tests to use.

Similarly, once restrictions on international travel are relaxed, scientists will need to be wary of possible false negatives among imported cases of the disease.

More or less lethal?

Some viruses that cross the species barrier into humans are ill-equipped to replicate in their human host and fail to sustain a presence in the human population. However, the coronavirus has already achieved sustained human-to-human transmission, but will this presence be maintained? And if so, will the virus evolve to become more or less lethal?

Like mutations in any organism, for a viral mutation to prevail, it must provide an evolutionary advantage. There is no evolutionary advantage to a virus if it kills its host, particularly if it kills the host before transmitting to a new one. But evoking symptoms in the infected person, such as coughing and sneezing, can help the virus transmit to a new host and this does offer an evolutionary advantage.

To identify which mutations may help the virus survive, the authors of the LSHTM study set out to identify “convergent mutations” – mutations that occurred in different parts of the world and at a higher than random rate, suggesting that these mutations benefit the survival of the virus.

Although scientists have analysed many genomes, the study of the genome-disease relationship is still a work in progress. Unfortunately, there is a bias in the database of genome sequences because samples from patients with more severe symptoms are more likely to be sequenced, making it difficult to associate particular mutations to how severe the disease is.

Of course, disease outcomes are affected by other factors, too, such as how old or sick the host is. The effect of interventions also has to be considered. Until a large dataset of genome data from mild or non-symptomatic patients from a diverse population is available, it will be difficult to deduce how the convergent mutations identified translate to severity of disease.