Responding to the COVID crisis

As well as exposing weaknesses in healthcare systems and supply chains, the coronavirus pandemic has underscored the importance of fundamental research and collective effort. During 2020, scientists rose to the challenge of developing new vaccines and effective treatments for Covid-19. Institute immunologists Dr Michelle Linterman and Professor Adrian Liston describe how their labs responded and the lessons we must learn.

In the early days of the coronavirus pandemic, as lockdowns loomed, workplaces closed and travel slowed to a trickle, Dr Michelle Linterman was certain of one thing – she wanted to make her group’s expertise available to the global vaccines effort.

Among those working on a vaccine against SARS-CoV-2 (the coronavirus that causes Covid-19) was Dr Teresa Lambe at the Jenner Institute in Oxford. “I already knew Tess, so once it became clear they had a vaccine candidate, my first instinct was to ask her what we could do to help,” Linterman recalls.

As an immunologist, Linterman’s work focuses on how the immune system responds to vaccines. In particular, she wants to understand why older people respond less well to vaccines, something she studies using human vaccination studies and in aged mice. “I thought the most useful thing was for us to offer something that nobody else could contribute quickly – and that was our ability to use aged mice as a pre-clinical test of how this vaccine is likely to work in an ageing immune system,” she says.

When Lambe said yes, Linterman set up trials to compare immunological responses to the Oxford/AstraZeneca vaccine in young and aged mice, and discovered that although aged mice responded more poorly than young mice to a single dose, after two doses of the vaccine, the immune responses were very good in both groups.

The study helped both institutes. For the Jenner, it showed two doses of the vaccine would give good protection against infection in all adults. For Babraham, it provided new insights into vaccine responses at a cellular and molecular level, expanded research into new vaccine platforms and led to new collaborations. Most importantly, it illustrated the value of publicly-funded research.

“Because we’re funded by the BBSRC – in other words the tax payer – it was incredibly important to use our knowledge and expertise to contribute to vaccine development in the midst of the pandemic,” she says.

Fellow immunologist Professor Adrian Liston also stepped up to the mark, using his research to help clinicians make the best treatment choices for Covid-19 patients and his communication skills to provide accurate information to journalists and the public.

“We need to develop good systems for treating emerging viruses before we know much about them, which is something my lab is working on,” explains Liston. “We are coming up with treatments that are vaccine agnostic, treatments that will work for most viruses with the potential to become pandemic, regardless of the actual virus.”

Liston’s group is also interested in systems immunology – exploring what makes people’s immune systems so different from each other.

 This variation has been graphically illustrated during the pandemic, some people experiencing mild symptoms while others died. “Diversity is intrinsically important to the immune system. It’s the most genetically-diverse system in the human body, and there are other factors at play, such as age, gender and weight,” he explains.

Being so close to events has taught Liston and Linterman many lessons – lessons, they say, that are vital for political leaders to learn. First, zoonoses (diseases spread between animals and humans) with pandemic potential are far from rare events. “They occur every couple of years,” says Liston. “We’ve had coronavirus outbreaks before, like SARS and MERS; they happen like clockwork. In the previous outbreaks we had better luck and better preparation. These are things we must prepare for.”

Secondly, we must guard against complacency. “If we pat each other on the back for a job well done, and then slash science budgets, the next outbreak will be as bad as this one,” he warns. “We must fund surveillance as well as immunology and virology research, because if you scale down this science it takes a decade or more to rebuild that intellectual capital.” This preparation extends to supporting fundamental research in a broad range of areas. “We need to fund fundamental research because you’re never sure which bit of it will save you in the future,” says Linterman.

 Third, a global approach to research, and funding to support this, is essential, because scientific discoveries are not bounded by borders, adds Linterman: “One of the reasons the Oxford vaccine was developed so fast was because of years of work on Ebola and MERS using the same adenoviral vaccine vector.”

As vaccines are rolled out, and countries emerge from lockdown, we might usefully reflect on what we would have done without a vaccine. It’s a scenario that frightens Linterman. “There wasn’t another exit strategy,” she says. “The vaccines are great, far better than we expected. But there are pathogens that we don’t have good vaccines for. For me, that’s the scary thing. We’re lucky the vaccines are so effective – but that doesn’t mean the same will be true for the next pandemic.”

This feature was written by Becky Allen for the Annual Research Report 2019-2020.

Covid-19 vaccines: Discussing how they work, the second dose and timing with Babraham Institute immunologist

Vaccination offers by far the best – perhaps only – route out of the Covid-19 crisis.

And, with two vaccines now being rolled out in the UK and a third available in the spring, progress is being made on delivering this vital protection.

Immunologist Prof Adrian Liston, at the Babraham Institute, tells the Cambridge Independent: “Vaccines all work in a fairly similar way. The key outcome we want are antibodies that bind the infecting virus and either block its entry to cells or flag it for destruction."

read the interview with me here

 

As an aside, back in May 2020 I was interviewed on the prospects of a COVID vaccine. Unlike some other experts, I argued that the first COVID vaccines would likely be designed, tested and approved by the end of 2020, and that the regulators would accept a vaccine efficacy rate as low as 50%. Fortunately my optimistic forecast proved true, with the FDA issuing guidence in June that they would accept efficacy rates of 50% and above, and the first approvals occuring in December 2020. Hopefully my optimism on the dosage change proves equally prophetic!

Fact-checking COVID-19 vaccine claims

Anti-vaxxers are out in force with more false claims about the COVID-19 vaccine. I'm mystified about what their endgame is - no vaccines, no masks, no technology, no medicine, cowering in caves like Stone Age humanity?

Anyway, today's false claim is that COVID-19 vaccines can cause heart attacks due to potassium chloride. The truth is, potassium chloride is an essential electrolyte, in every food we eat and every drink we drink. It is recommended that we take in 2000mg of potassium per day, which is about 4000mg of potassium chloride. So how much potassium chloride is in the COVID-19 vaccine? 0.01mg. Yep, that is what the anti-vaxxers want you to be petrified of.

0.01mg is about 1% of the amount of potassium chloride present in a glass of tap water. It is about 50,000 times less than the amount of potassium chloride present in a glass of milk or a banana. It is about the same amount of potassium chloride present in the solitary tear that I wept thinking of those poor anti-vaxxers being given the option to have a life-saving vaccine developed at incredible speed.

The fake excuse anti-vaxxers give for their pseudo-concern is that potassium chloride is used in lethal injections. Yes, at one million times the vaccine dose, and without the balancing sodium that is present in alls foods and vaccines. A small amount of sodium and potassium mixed together in a balanced ratio is good. A vast amount of potassium injected straight into the bloodstream is bad. Pretty simple difference, and I'm not giving anti-vaxxers the benefit of the doubt by assuming they are just ignorant. They are evil, deliberately spreading things they know to be false, resulting in people not taking life-saving medication.

Fact-checking COVID-19 claims

More fact-checking for COVID-19. This time for a claim so false it is down-right criminal.

Claim: The Pfizer COVID-19 vaccine has a strong sequence similarity with syncytin-1, and will cause infertility.

Verdict: False. A complete fabrication. In summary, there is no sequence homology between the Pfizer COVID-19 vaccine and syncytin-1, and there are no associations betwee anti-SARS-CoV-2 antibodies and pregnancy issues. Looking at the history of the people making the claims, their strategy seems to be to throw random mud at any vaccine and hope some of it sticks.

First, on the sequence homology claim. There is essentially no homology between these two proteins. The full protein sequence of both are known. The language of proteins can be considered to be similar to English - there are 20 different amino acids, and each of them is given a letter. In the same way that a paragraph is constructed by 27 letters of the alphabet, a protein is constructed by the 20 "letters" of amino acids. What matters is the order.

Here is the spike protein:

MFVFLVLLPLVSSQCVNLTTRTQLPPAYTNSFTRGVYYPDKVFRSSVLHSTQDLFLPFFSNVTWFHAIHVSGTNGTKRFDNPVLPFNDGVYFASTEKSNIIRGWIFGTTLDSKTQSLLIVNNATNVVIKVCEFQFCNDPFLGVYYHKNNKSWMESEFRVYSSANNCTFEYVSQPFLMDLEGKQGNFKNLREFVFKNIDGYFKIYSKHTPINLVRDLPQGFSALEPLVDLPIGINITRFQTLLALHRSYLTPGDSSSGWTAGAAAYYVGYLQPRTFLLKYNENGTITDAVDCALDPLSETKCTLKSFTVEKGIYQTSNFRVQPTESIVRFPNITNLCPFGEVFNATRFASVYAWNRKRISNCVADYSVLYNSASFSTFKCYGVSPTKLNDLCFTNVYADSFVIRGDEVRQIAPGQTGKIADYNYKLPDDFTGCVIAWNSNNLDSKVGGNYNYLYRLFRKSNLKPFERDISTEIYQAGSTPCNGVEGFNCYFPLQSYGFQPTNGVGYQPYRVVVLSFELLHAPATVCGPKKSTNLVKNKCVNFNFNGLTGTGVLTESNKKFLPFQQFGRDIADTTDAVRDPQTLEILDITPCSFGGVSVITPGTNTSNQVAVLYQDVNCTEVPVAIHADQLTPTWRVYSTGSNVFQTRAGCLIGAEHVNNSYECDIPIGAGICASYQTQTNSPRRARSVASQSIIAYTMSLGAENSVAYSNNSIAIPTNFTISVTTEILPVSMTKTSVDCTMYICGDSTECSNLLLQYGSFCTQLNRALTGIAVEQDKNTQEVFAQVKQIYKTPPIKDFGGFNFSQILPDPSKPSKRSFIEDLLFNKVTLADAGFIKQYGDCLGDIAARDLICAQKFNGLTVLPPLLTDEMIAQYTSALLAGTITSGWTFGAGAALQIPFAMQMAYRFNGIGVTQNVLYENQKLIANQFNSAIGKIQDSLSSTASALGKLQDVVNQNAQALNTLVKQLSSNFGAISSVLNDILSRLDKVEAEVQIDRLITGRLQSLQTYVTQQLIRAAEIRASANLAATKMSECVLGQSKRVDFCGKGYHLMSFPQSAPHGVVFLHVTYVPAQEKNFTTAPAICHDGKAHFPREGVFVSNGTHWFVTQRNFYEPQIITTDNTFVSGNCDVVIGIVNNTVYDPLQPELDSFKEELDKYFKNHTSPDVDLGDISGINASVVNIQKEIDRLNEVAKNLNESLIDLQELGKYEQYIKWPWYIWLGFIAGLIAIVMVTIMLCCMTSCCSCLKGCCSCGSCCKFDEDDSEPVLKGVKLHYT

Here is human syncytin-1:

MALPYHIFLFTVLLPSFTLTAPPPCRCMTSSSPYQEFLWRMQRPGNIDAPSYRSLSKGTPTFTAHTHMPRNCYHSATLCMHANTHYWTGKMINPSCPGGLGVTVCWTYFTQTGMSDGGGVQDQAREKHVKEVISQLTRVHGTSSPYKGLDLSKLHETLRTHTRLVSLFNTTLTGLHEVSAQNPTNCWICLPLNFRPYVSIPVPEQWNNFSTEINTTSVLVGPLVSNLEITHTSNLTCVKFSNTTYTTNSQCIRWVTPPTQIVCLPSGIFFVCGTSAYRCLNGSSESMCFLSFLVPPMTIYTEQDLYSYVISKPRNKRVPILPFVIGAGVLGALGTGIGGITTSTQFYYKLSQELNGDMERVADSLVTLQDQLNSLAAVVLQNRRALDLLTAERGGTCLFLGEECCYYVNQSGIVTEKVKEIRDRIQRRAEELRNTGPWGLLSQWMPWILPFLGPLAAIILLLLFGPCIFNLLVNFVSSRIEAVKLQMEPKMQSKTKIYRRPLDRPASPRSDVNDIKGTPPEEISAAQPLLRPNSAGSS

They both start with "M", like every protein in mammals, but apart from that do you see any similarity? No? Me either. Or any of the protein homology tools that I tested. The closest you get is a run of 2-3 letters being the same. Claiming homology between the two sequences is worse than claiming the US Constitution and Harry Potter are the same, because they both use words like "at" and "the".

How about the second claim? If anti-spike protein antibodies interfered with fertility, you would expect that COVID-19 patients, who almost all make high titres of anti-spike protein antibodies, would have infertility issues. They don't. Multiple studies show no complications with pregnancy or miscarriage in pregnant COVID-19 patients. This is an extreme case - these individuals have an ongoing serious viral infection as well as having the antibody response - and yet there is clear evidence of maintained fertility.

COVID-19 vaccine trial

Today I took part in a COVID-19 vaccine trial (ENSEMBLE2) as a volunteer. It is the Ad26.COV2.S vaccine, an adenovirus-encoded SARS-CoV-2 spike antigen.

Right now, we can use every vaccine we can get. Down the track we can be picky, and use the best ones (if we ever actually find out which are the best! if head-to-head trials aren't done now, they will likely never be done). For now, I'd encourage everyone who is eligible to join a vaccine trial.

As many people possible vaccinated, everyone wearing a mask and eliminate unnecessary contacts. We are so close to beating this virus, every extra death at this stage is an unnecessary trajedy.

Dissecting the immune characteristics of severe COVID-19 responses

• Researchers have analysed immune cell types and numbers from the blood of healthy volunteers, COVID-19 patients experiencing mild-to-moderate effects and patients classified as severe to understand whether particular characteristics of their immune system response can identify treatment targets or indicate disease severity.
• After comparing the T cell immune response, the researchers noted the surprising absence of a strong anti-viral response in the blood of COVID-19 patients.
• The study identified an elevated presence of anti-inflammatory-producing regulatory T cells in the severely affected patients. If confirmed by larger studies, this could be used as a marker for identifying worsening cases and could provide an insight into the mechanism of disease pathology.

A team of immunology experts from Belgium and the UK research organisations have come together to apply their pioneering research methods to put individuals’ COVID-19 response under the microscope. Published today in the journal Clinical and Translational Immunology, their research adds to the developing picture of the immune system response and our understanding of the immunological features associated with the development of severe and life-threatening disease following COVID-19. This understanding is crucial to guide the development of effective healthcare and ‘early-warning’ systems to identify and treat those at risk of a severe response.  

One of the most puzzling questions about the global COVID-19 pandemic is why individuals show such a diverse response. Some people don’t show any symptoms, termed ‘silent spreaders’, whereas some COVID-19 patients require intensive care support as their immune response becomes extreme. Age and underlying health conditions are known to increase the risk of a severe response but the underlying reasons for the hyperactive immune response seen in some individuals is unexplained, although likely to be due to many factors contributing together.

To investigate the immune system variations that might explain the spectrum of responses, teams of researchers from the VIB Centre for Brain and Disease Research and KU Leuven in Belgium and the Babraham Institute in the UK worked with members of the CONTAGIOUS consortium to compare the immune system response to COVID-19 in patients showing mild-moderate or severe effects, using healthy individuals as a control group.

Professor Adrian Liston, senior group leader at the Babraham Institute in the UK, explained: “One of our main motivations for undertaking this research was to understand the complexities of the immune system response occurring in COVID-19 and identify what the hallmarks of severe illness are. We believe that the open sharing of data is key to beating this challenge and so established this data set to allow others to probe and analyse the data independently.”

The researchers specifically looked at the presence of T cells – immune cells with a diverse set of functions depending on their sub-type, with ‘cytotoxic’ T cells able to kill virus-infected cells directly, while other ‘helper’ T cell types modulate the action of other immune cells. The researchers used flow cytometry to separate out the cells of interest from the participants’ blood, based on T cell identification markers, cell activation markers and cytokine cell signalling molecules.

Surprisingly, the T cell response in the blood of COVID-19 patients classified as severe showed few differences from the healthy volunteers. This is in contrast to what would usually be seen after a viral infection, such as the ‘flu. However, the researchers identified an increase in T cells producing a suppressor of cell inflammation called interleukin 10 (IL-10). IL-10 production is a hallmark of activated regulatory T cells present in tissues such as the lungs. While rare in healthy individuals, the researchers were able to detect a large increase in the number of these cells in severe COVID-19 patients.

Potentially, monitoring the level of IL-10 could provide a warning light of disease progression, but the researchers state that larger-scale studies are required to confirm these findings.

“We’ve made progress in identifying the differences between a helpful and a harmful immune response in COVID-19 patients. The way forward requires an expanded study, looking at much larger numbers of patients, and also a longitudinal study, following up patients after illness. This work is already underway, and the data will be available within months,” says Professor Stephanie Humblet-Baron, at the KU Leuven in Belgium.

“This is part of an unprecedented push to understand the immunology of COVID-19”, concludes Professor Liston. “Our understanding of the immunology of this infection has progressed faster than for any other virus in human history – and it is making a real difference in treatment. Clinical strategies, such as switching to dexamethasone, have arisen from a better understanding of the immune pathology of the virus, and survival rates are increasing because of it”.  

Professor Liston and Professor Humblet-Baron both emphasized the importance of the scientific team that led the study. "This work happened during a period of incredible stress. When much of our laboratory was shut down due to the pandemic, Dr Teresa Prezzemolo and Silke Janssens were in the hospital day-after-day, preparing blood samples that were critical not just for this study but for a whole host of clinical trials on COVID-19 based in Leuven. Julika Neumann and Dr Mathijs Willemsen put their PhD research on hold to run samples, and Dr Carlos Roca and Dr Oliver Burton provided the computational support to turn the data into biological understanding. We are both incredibly proud of the entire team."

Neumann, J., Prezzemolo, T., Vanderbeke, L. & Roca, C.P. et al. Increased IL-10-producing regulatory T cells are characteristic of severe cases of COVID-19. Clinical and Translational Immunology

Fact-checking COVID-19 claims

From a recent interview with a fact-checking journalist:

Claim: Alcohol-based hand sanitiser shouldn't be used day after day as it breaks down the first immune barrier of the body: the lipid bacteria of the skin.

Verdict: Misleading. Alcohol-based gels do reduce the number of skin-resident bacteria and can start to cause some damage to the skin with prolonged use, in some individuals. However, the skin barrier is irrelevant to COVID-19, and alcohol-based gels also eliminate viruses from the skin, preventing transmission to surfaces and your face. Overall there is a clear benefit to use frequent hand-washing, and the negatives can be countered with moisturising.

Claim: We can strengthen our immune system in weeks or even days (for young people), which would mean that if one does contract COVID-19, it's more likely going to be a mild case which does not require hospitalisation.

Verdict: False. First of all, it is misleading to talk about "strengthening" the immune system. The immune system could be considered more like taste. You can increase how spicy food is, or increase how sweet food is - both are "strengthening" the taste but mean different things. Different "flavours" of the immune response are optimal in different circumstances, so there is no such thing as a generic increase in how strong the immune system is. It is also completely unclear as to whether we actually want a "stronger" immune response in COVID-19 - there is good evidence that an excessive immune response of one particular "flavour" is causing the immune pathology. We want to train the immune response in a particular direction (e.g. through vaccines) not generically increase its power (even if that was possible, which it isn't).

Claim: A well functioning immune system is dependent on the quality of our intestinal flora. This is why we should avoid eating refined "industrial" food.

Verdict: Half true. There is an interaction between the gut bacteria and the immune system, and this is modified by the food we eat. It is not very well understood, and it is likely too early to say whether the net effect of the consequences is generally good or generally bad. It is certainly too early to say whether it makes a positive or negative effect in the case of COVID-19. As general advice, eating fresh and unprocessed foods, high in vegetables and low is red meat is good health advice, regardless of what it does to the immune system.

Claim: Fasting strengthens the immune system in only 3 days.

Verdict: False. Fasting modifies the immune system slightly, which could be advantageous in some circumstances and detrimental in others. It is a minor effect though, and certainly it would not be advised that someone with symptomatic COVID-19 undergoes extensive fasting. The body needs resources to fight an infection.

Claim: Herbal supplements such as echinacea and elderberry strengthen the immune system in a matter of weeks.

Verdict: False. There are active compounds in all plants, which can modify aspects of the immune system if given in high enough doses in a dish. That does not mean that eating a few pills does anything at all. It is very important for people to understand that supplements and medicines are regulated completely differently. "Supplements" are allowed to make essentially any claim, without any evidence, as long as that claim is vague. This is why you get garbage claims about "immune boosting": they are vague enough that they are legally allowed to be made without evidence. Actual medicines, on the other hand, can only make extremely specific claims that are backed up by evidence. All claims about herbal supplements should essentially be treated as advertising material. 

Claim: Vitamins and minerals strengthen the immune system.

Verdict: Misleading. Vitamins and minerals are different from other supplements. They are needed by the body in extremely low quantities, and if they are absent then health problems arise. For people who are actually deficient, taking vitamins and minerals will improve health, including the immune system. However, almost no one in the developed world is actually deficient, and certainly having a balanced diet of fresh food will give you more than enough of every known vitamin and mineral. Unless you have an exceptionally limited diet, taking these tablets doesn't do anything.  

Claim: Fear is a powerful immunodepressant.

Verdict: Half-true. Anxiety can modify the immune system, and can give poorer health outcomes during some types of infection. The effect is weak to moderate, but it is measurable. This should not be used as an excuse not to spread awareness of the COVID-19 pandemic, however: some degree of anxiety is rational and protective, where it supports valid infection-avoidance behaviours (e.g., hand-washing, wearing a mask, avoiding crowded areas).

Claim: Practicing yoga strengthens the immune system.

Verdict: Misleading. There is nothing special about yoga. There are, however, weak to moderate beneficial effects of exercise and the alleviation of anxiety on infection outcomes. For some people, they may get this through yoga. Others may get it through gardening, or a daily run, or the ritual of a cup of tea. We should look after our mental health, which means cultivating habits that make us happy. The idea that one particular solution like yoga or mediation has any special properties beyond this is completely unsupported. Keep it up if you enjoy it, but it doesn't replace medicine and won't work for every person.

Coronavirus is infectious before illness

Coronavirus science simplified: number 6. This article in Nature Medicine looked at the amount of virus present in patients before and after they got symptoms. The data is clear: you can spread COVID19 before you actually get sick, so wear a mask! Read the original paper, or see the illustrated abstract by Tenmai.

What we are doing during the COVID-19 pandemic

This is a strange time for any workplace. People suddenly working from home, large changes in job duties, some people left without much to do while others are expected to manage whole new realms of bureaucracy while also continuing their full-time job. For us, as an immunology lab, this pandemic has an added dimension of peculiarity: our work is directly relevant to the ongoing situation.

Looking back on how we dealt with the outbreak, we were ahead of the curve. We put in place strict social distancing and work-from-home measures well before our institutes / government did (and, I would argue as an immunologist, our lab rules were more science-based than those later imposed on us). We also started a public education program on COVID-19, with an interactive Virus Outbreak simulator, an illustrated series translating scientific  articles into lay language and even released a kid's book explaining Coronavirus (with special thanks to lab members Dr Teresa Prezzemolo, Julika Neumann and Dr Mathijs Willemsen for translating this into different languages).

We also had lab members head back to the clinic to help with the capacity issues created by COVID-19. Dr Frederik Staels and Dr Erika Van Nieuwenhove suspended research to increase their clinical duties, and Dr Stephanie Humblet-Baron and Dr Mathijs Willemsen were on-call in case the system was overwhelmed.

Silke Janssen, processing patient blood

Our lab never completely shut-down though - we had important work that needed to be done. I'd like to call out Dr Susan Schlenner, Dr James Dooley and Dr Lubna Kouser who led the unglamorous but key administration on securing the safety of team members who had to be in the lab. Our Leuven lab was central to the processing of clinical COVID-19 samples. We usually think of clinical trials being run by MDs, but the work does not end after the blood is collected. I really want to call out the key contributions of Silke Janssens and Dr Teresa Prezzemolo. Without them, coming in all day, every day to process blood samples, clinical research of COVID-19 would have been crippled.

Dr Teresa Prezzemolo in the L2 labOur team, lead by Dr Stephanie Humblet-Baron, also analysed the samples prepared. We performed an ultra-high parameter analysis (far beyond state-of-the-art hospital diagnostics) of the T cell phenotype of COVID-19 patients: months of work from Dr Teresa Prezzemolo, Silke Janssens, Julika Neumann and Dr Mathijs Willemsen. Data analysis by Julika Neumann, Dr Carlos Roca, Dr Oliver Burton and Dr Stephanie Humblet-Baron identified a novel link between IL-10-producing Tregs and COVID-19 severity. We are now following this up to see if the link is useful as a biomarker or even is mechanistic in disease program. We have made our data an open resource (link), allowing other groups around the work to analyse our work. We are continuing to follow these patients and will soon have more and more information about why some patients remain completely healthy and others develop severe, even fatal, disease.

Dr Dooley and Dr Kouser (pre-COVID-19)We are not just clinical immunologists - we are also basic research immunologists. Mysterious virus triggering immune-mediated destruction of the tissue? We can deal with that. The whole lab contributed to the design of a new potential therapeutic, but I would especially like to call out the contributions of Dr James Dooley, Dr Oliver Burton, Dr Lubna Kouser and Fran Naranjo. Manufacturing is now complete and we are moving to pre-clinical testing. Hopefully we have a vaccine for SARS2 before our treatment is complete, but it is designed to deal with an unknown SARS3 equally well.

Suffice it to say, we have been as busy as we've ever been, and we will likely remain just as busy well after COVID-19 stops making the headlines. Which brings me to my final plea. Don't forget about scientific research. Unsung heroes during the pandemic, our staff are putting in an enormous effort. And yet we face an incredibly uncertain funding situation. Universities and research institutes have taken an enormous financial blow with this pandemic, and unless governments step in with a large financial rescue package, those scientific research staff who got us through the pandemic are going to be laid off in huge numbers. Even if you don't care about the moral imperative of looking after the people who stepped up when we needed them, there will be a SARS3 or novel flu pandemic in the future. We need to secure the research infrastructure to combat them right now. Science is not a factory that can be switched on and off at will - we need to maintain research excellence, scientific equipment and most of all key staff contracts over the long-term.

SARS-CoV-2 is not a bioweapon

Coronavirus science simplified: number 5. This article in Nature Medicine used genetic analysis to test the hypothesis that SARS-CoV-2 was generated in a lab as a bioweapon. Spoiler alert: it wasn't. Clear hallmarks of natural evolution and none of the features of a designed virus. Read the original paper, or see the illustrated abstract by Tenmai.