Covid-19 questions answered: an interview with a Senior Lab Research Scientist

Ever since Covid-19 hit our species, unanswered questions about its true origins, our (lack of) immunity to it and how best to tackle the spread have been piling up. Some believe it hailed from space; others still think it’s man-made and a small minority have suspicions it might be something to do with the roll out of 5G telephone networks.

Mad conspiracy theories aside, the truth is often more fascinating than what people can make up. Regardless of what conspiracists think, it’s here – it’s a serious health emergency that’s killed 1,808 people in the UK at the current count (Tues 31 March) – and it poses a threat to our way of life, society and economy.

So what’s the truth and how confident can we be that what we think we know right now, is correct?

Tannice Hemming spoke to Dave Briggs, a Senior Laboratory Research Scientist who works at the Francis Crick Institute, to find out. For the avoidance of doubt, all views expressed are the personal, educated views of Dave and not his employer.

Dave Briggs, Senior Laboratory Research Scientist at Francis Crick Institute
Dave Briggs, Senior Laboratory Research Scientist at Francis Crick Institute

The Francis Crick Institute is a biomedical research centre – a partnership between Cancer Research UK, King’s College London, The Wellcome Trust, the Medical Research Council, University College London and Imperial College London. So, plenty of impressive credentials. Established in 2010, it’s named for Francis Crick, co-discoverer of the structure of DNA with James Watson, Maurice Wilkins (and, arguably, Rosalind Franklin).



Dave’s usual job is working within the Signalling and Structural Biology laboratory on two projects: designing drugs that would target a “specific subset of cancers” and also working on discovering “how neurons tell themselves to stay alive”, which he says is key to understanding neurodegenerative diseases. 

Having been friends with Dave since about 2012 I’ve always been fascinated to read his social media posts about his work, especially so when he moved closer to where I live and started working for the Institute. When he commented on one of my Facebook posts with comments suggesting he was working on Covid-19 research, I couldn’t resist asking him for an interview. 


What follows is an abridged version of our 1 hour discussion on what he’s doing, his personal views and more science than you can shake a 2m long social distancing stick at.

Tannice: “Can you explain what you’re doing currently with Covid-19 research?”

Dave: I usually design drugs for cancer treatments so I’m using that drug design experience, along with data from the Diamond Light Source near Didcot to try and design therapies that will target a weak point in Covid-19. It’s essentially a lot of number-crunching.

More information on the Diamond Light Source

Tannice: “Thanks for explaining that. Can you talk a little bit about the difference between the two types of test that I’ve heard so much about – there’s one to test if you have it right now and we are working on one to test if you’ve had it, is that right?”

Dave: “Yep, so the first one is to test whether you have it right now. That’s called the PCR test or RTPCR and that tests whether you have the genetic material from Covid-19 within your body right now. It’s a swab test from your mucous membranes. The test itself takes 6 hours to run, but around 24-48 hours for the results to come back whether you have it or not. The one that would be really helpful, though, is the serological test. That tests whether your body has made antibodies against Covid-19. It indicates that you have mounted a response against the virus and made antibodies that will identify and kill the virus next time you’re exposed to it. It doesn’t matter whether you got it previously and were asymptomatic or very ill, if you have had it a serological test will show that. It can take about 21 days, on average I’d say, for your body to mount a defence against a virus, typically. In that time you’re susceptible to succumbing to the virus or you can fight it off. 


The medical staff examines patients with suspected coronavirus while in the vehicle. Banner: Gyeongju Public Health Center Corona Virus-19 Drive Thru, Screening Clinic
Gyeongju Public Health Center Corona Virus-19 Drive Thru, Screening Clinic, North Korea

“What happens is your body, when you get a virus, your white blood cells recognise something that needs targeting for destruction. They bind to the virus and flag it for destruction which is the job of a type of white blood cell called a macrophage – and then they basically eat it and it’s gone. That means that if you’ve got antibodies against the virus, the next time you’re exposed to it, the virus never has a chance to get you. We need widespread serological testing, which is likely to be some kind of blood prick test – so people can get back to work and we don’t have people – especially key workers – self-isolating for no reason because they already have those antibodies.

The problem with testing who has it currently is that it’s a snapshot in time of course and someone who doesn’t have it today might have it tomorrow. Serological testing is so important and it’s being developed and tested right now.”

Tannice: “I’ve heard that there is a possibility of a sort of vaccine where people who have had Covid-19 confirmed could donate blood plasma to others to give them their immunity. Would that work?”

Dave: “It would, but it would be pointless really because it wouldn’t work in the long-term. It would be protective for maybe a few days or weeks at the most but you need to make your own antibodies to get any real immunity”

Tannice: “Some people have said that certain blood types might have greater immunity to it and others will be more susceptible. Is there any truth to that?”

ACE-2 Protein ACE-2 Protein By Emw – Own work, CC BY-SA 3.0

Dave: “It’s certainly plausible. The way that blood groups work, at a molecular level means that it could very well be true. Each blood group has a certain structure of sugars on the cell surface and some viruses actually use those as hooks to grab onto and get into the cell. Norovirus is one of those. If you have a mutation on the gene that affects the sugar structure on the cell and it can’t anchor, then you’re likely to be immune to norovirus. Genetic sequencing – like 23&me or other companies who do that kind of DNA genotyping – can actually tell you that.


I am actually immune to some strains of norovirus and I know that because I’ve had my genome sequenced. There are likely other things that would make you more or less susceptible to Covid-19 than your blood sugar structures and the ACE-2 protein that we know is indicated in Covid-19 infections. We don’t currently know for sure about blood types though, but it’s definitely plausible.”

Tannice: “How far away is a vaccine?”

Dave: “Estimates vary but it’s a faster vaccine production model than usual, it’s a huge investment of money so far being ploughed into this project. Of course we know how to make vaccines against viruses but this is so much faster because the entire globe wants to solve it and it’s not about a commercial pressure. Interestingly, because it’s not a commercial endeavour, it’s an ethical and global health emergency it means that pharmaceutical companies and research labs are working together as well as volunteers. We are acting with more urgency because of the global death toll. Pharmaceutical companies are usually pretty risk averse and more interested in drugs for chronic conditions and academic research usually casts the research net wide and then, once they have a model that works in terms of a drug therapy, that’s when they team up with a pharmaceutical company.”

Tannice: “Can you talk to me about vertical transmission, so mother to baby in the womb? As you know, I’m currently just in my second trimester. There was a study released by JAMA Paediatrics that indicated it could be possible. What did you make of that study?”

Ultrasound pictureDave: Currently we think that vertical transmission (while baby is still in utero) is not happening but the JAMA pediatrics article was interesting for a few reasons. Three of the 33 babies in the study had respiratory distress and they tested positive for Covid-19 at 2 and 4 days, yet by 6 days they were negative for Covid-19. So the issue is whether Covid-19 can cross the placenta. Interestingly, none of the amniotic fluid nor the cord blood or placenta of these babies has ever shown positive for Covid-19. The placenta usually does a really good job of filtering out pathogens so you would see it there if that was how it was getting to the baby. So the way that it gets there must happen during the birth and we know that some infections – like Group B Strep – pass to babies on the way through the birth canal. What’s quite confusing about that study is that one of the babies was born via caesarian which would mean its exposure to fluids from mum would be absolutely minimal – they don’t hang about when they’re doing a c-section. That baby was obviously in some distress as they took the decision for it to be born at 31 weeks, it wasn’t a premature labour. So there was a really short window between the waters being broken during the section and it being out of the womb.” – Read the study here

Tannice: “Thanks for that, I guess more data is needed on the case of vertical transmission. Can you talk about the likelihood that once you’ve had it – or the future vaccine –  you will be immune forever?”

Dave: “The trouble is that, because it’s a novel virus, we know very little about exactly how it interacts with our immune system. The worst case scenarios seem not to be coming true – our bodies have seen similar coronaviruses before – that’s why there were all those pictures of Dettol bottles online that people were stunned to see mention coronavirus – one coronavirus causes the common cold. Some strains of virus you never get long-term immunity to. We have really limited results so far but initial studies say we have a really good chance that a vaccine will work. We have had a couple of reports that people are being reinfected but most Chinese data suggests that you are unlikely to get it again. “

Tannice: “Why are men seemingly more susceptible to Covid-19? Why are more men dying of it?”

Cigarette in someone's handDave: “There’s no difference in the amount of protein ACE-2 that the virus binds to in men and women’s lungs as far as I am aware, which suggests that it’s really a cultural phenomenon. I believe most of the data we have on this is from China – most men in China (about 97%) smoke, whereas very few women who do. Add Covid-19 to smoker lungs and they will succumb far more easily than lungs that aren’t affected by the effects of tobacco smoking.”


Tannice: “Can you talk about the possibility that the virus will – or has already – mutated? Would that render any vaccine useless?”

Dave: Covid-19 is actually unusual in that it has quite a large genome. Viruses are usually quite small – they’re compact and they don’t waste anything. Covid-19 has a large genome, much larger than average. Most viruses, when they replicate DNA or RNA, they don’t do any proofreading as such, so there are more errors. Our bodies proofread and error check replication – the simpler an organism is, the less likely it is to error check but Covid-19 does. Data suggests a mutation every 20 transmissions – which is thankfully quite low for a virus, it’s not mutating rapidly which makes antivirals and vaccines far easier to manufacture and far more effective.”

Tannice: “Why is Covid-19 scarier and more easy to transmit than other viruses? If you’re immune to it, could you still carry it and pass it on again?”

Coughs and sneezes public health info posterDave: “This virus has been so successful because of the way that our response to it varies so much. If you did want to make a virus – and I’m not saying this has been made – it would be one like this. You catch it, carry it for quite some time without knowing and then you spread it. If you are however immune to it and pick it up again, the likelihood that you’d pass it on again is really low. It’s spread most often by the symptoms, so coughing usually and if you’re immune it won’t make you cough. There’s never a zero chance but it’s unlikely.”

Tannice: “I’ve read that there is a lag time between the actual zoonotic transfer and the identification of the virus/disease, as it takes a while to identify a new disease in human populations. Do we have any idea how long this lag time is, and therefore how long COVID-19 might actually have been in the UK before the first tests were done?”

Dave: “That’s a hard question to answer. The supposed zoonotic (animal-to-human) transfer was a bush meat market in Wuhan, China, as we know. We think there was a mutation that allowed transfer from an as-yet unidentified creature within the meat market to a human. The first person to get the novel Covid-19 virus may never be identified. We don’t know if they caught it, were ok and spread it to lots of people or whether they caught it and instantly succumbed, transferring it only to a few people around them.”

“We don’t regularly test animal populations at the moment. Until the virus becomes symptomatic, you don’t look for it and you usually won’t just stumble upon it.”

“Once this human pandemic is under better control, you would hope scientists would go into the field around Wuhan and see if they can test bush meat animals for Covid-19. It could have been in them for years and years – some relative of this virus most likely – and then there was a ‘lucky’ mutation that could cross to humans and hit us, the immunologically naive species.”

Pangolins have been suggested as a potential suspect, but the evidence is so far very scant

Tannice: “How can this be compared with SARS which many have talked about when looking at the deadliness of Covid-19 and comparing the higher death rate of SARS? Surely SARS was worse?”

Dave: “When SARS hit in the early 2000s there was a massive burst of funding for us to look at Coronaviruses. SARS was actually less of a big deal than Covid-19 because it just didn’t spread as effectively. The subtle difference is about where in the body – in the respiratory system – that SARS attacks compared with Covid-19. I believe that SARS attacks you deeper within the lungs and it had to get right down in the bottom of the respiratory tract. So it was harder to catch – you had to come in contact with phlegm coughed up right from the deepest parts of the lungs. But if it did get you then it was harder to treat. Some reports say that Covid-19, in very serious cases, sends your immune system totally haywire and it starts attacking your own lung tissue. If you get SARS you’re also less likely to spread it because you’re going to be really ill quickly – so it’s limiting how many people you could effect. Covid-19 means mild symptoms to start with for most so easier to spread. The viruses like Covid-19 are so effective because of the range of effects they have on different populations. It’s far easier to spread something that you can walk about with and feel fine than being quickly incapacitated by SARS.”

So there you have it – there’s a lot we don’t know, but the truth about Covid-19 is, at least to this interviewer, more comforting than a bunch of crackpot theories. Although some of the theories are pretty funny – in this household we’re fans of the idea that nature is getting its own back on us. After all, pigeons in London are purportedly returning to their natural colour, now that pollution levels are down*. Coincidence? I’m not sure.

A picture of some parrots with the caption
*parrots. These are parrots.

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