Showing: 11 - 20 of 20 RESULTS
Guest Blog

Natural or Nasty? Traditional Chinese Medicine and COVID-19

Written by Heather Darby

COVID-19, caused by SARS-CoV-2, currently has no available cure or vaccine (although not through lack of trying!). At the moment we have to rely on supportive treatments to alleviate symptoms; these can range from taking antipyretics like paracetamol at home to reduce a fever, to mechanical ventilation in intensive care units. It can be scary to face an illness where the only options for patients are to manage symptoms and wait for recovery, so are there any other treatments that could be explored? The Chinese government seem to think so: during the peak of the epidemic in China more than 85% of those treated for COVID-19 in hospitals also received treatment with traditional Chinese medicine (TCM).[1]

What is traditional Chinese medicine?

TCM has been used for thousands of years to treat a whole host of illnesses. It differs a bit from the ‘old wives tales’ you might associate with alternative medicine in that it is based on a theory of ‘syndrome differentiation’; patients are treated according to their individual symptoms, using a holistic approach.[1] This differs from the typical disease-specific treatment offered by conventional medicine, in which the patient’s diagnosis will determine their treatment. TCM can include physical therapies such as acupuncture or targeted exercise, but here we are focusing on herbal medicines, comprised of a mixture of ingredients tailored to an individual’s symptoms. These are usually taken in the form of teas, broths or powders. The Chinese government are currently endorsing a combination of conventional medicine and TCM to treat COVID-19, so could this have any benefit to patients?

Does it actually work?

A huge number of COVID-19 patients in China are receiving TCM. A variety of treatments are in use as each case is taken individually, so there is no standardised “treatment”against COVID-19. One of the more common suggested TCM formulations is Qing Fei Pai Du Tang, a composition of 21 different herbal substances claimed to aid in ‘ventilating the lungs’.[2] This has been widely used in China by COVID-19 patients and is commercially available but contains ingredients which are banned in a number of other countries. The national administration of traditional Chinese medicine claims that after the treatment of a group of 214 patients with this remedy, 60% improved over the course of treatment, with 30% showing stabilisation of their condition.[3] Supporters of TCM claim that remedies can shorten the duration of symptoms by up to 2 days,[4] reduce the chance of illness becoming severe, and provide relief from symptoms such as cough and fever.[5] Usually these claims are supported by anecdotal evidence, for example a bus driver in Wuhan who was admitted to hospital for COVID-19 symptoms. In additional to conventional supportive care he was given a herbal broth, and following a few days of treatment his symptoms subsided.[6] These claims all sound very promising, but how much of this can we believe?

Headline taken from The Economist, 11 April 2020.[6]

TCM makes bold claims about its ability to treat conditions like COVID-19, but how are these claims backed up? As explained above, anecdotal evidence is key in the claims proponents of TCM make. Often individual patients’ recovery after treatment is taken as definite evidence of its efficacy. In the case of COVID-19 in particular, this is suspect as the vast majority of cases resolve quickly and do not progress to severe illness; the patients who are held up as an example of the success of TCM would have likely recovered on their own without intervention. Clinical trials investigating the use of TCM do exist, including those conducted during the 2002-2004 SARS epidemic. However, these trials are frequently funded by those with a vested interest in proving the effectiveness of TCM and are poorly controlled with significant flaws in methodology.[3] While at the time of the SARS epidemic it was claimed that TCM may be beneficial to patients, literature reviews since have shown no difference in mortality between those receiving both TCM and conventional medicine, and conventional medicine only.[3] There are at least 50 ongoing clinical trials examining TCM in China, but again results from these will need to be taken with cation as these are not the double blind, placebo-controlled trails that are the standard in evidence-based medicine.[1]

But it’s just herbs, right? What’s the harm?

Despite the lack of evidence for the efficacy of holistic treatments like TCM, many people are still tempted to try them because they are presumed to be ‘natural’ and therefore safe. Aside from not being proven effective, they can also be harmful. TCM is very poorly regulated in most countries; in the UK, TCM is monitored by the medicines and healthcare products regulatory agency (MHRA) but they aren’t actually tested before being put on the market. Instead, manufacturers are relied upon to accurately declare the contents of their products.[7] One research group in Australia set out to test how reliable this information was. 26 different TCM formulations were purchased over the counter and examined for three key areas of non-compliance to the standards needed for legal sale: presence of undisclosed animal DNA, presence of heavy metals (lead, arsenic or cadmium), and adulteration with pharmaceutical products.[7]

Their results were, frankly, frightening, 92% of the TCM remedies tested contained some form of contamination not disclosed on the ingredients list.[7] Half the tested samples contained DNA of an animal not listed, ranging from snow leopard to rat. Ingredients derived from endangered species like leopard and shark are often added deliberately for their perceived therapeutic benefits, but others such as rat, mouse and cat DNA could indicate serious contamination issues during manufacture.[7] The number of TCM formulations containing heavy metals was also concerning. More than 75% of the 25 tested samples contained at least one heavy metal, with 15 exceeding the recommended daily dose. Several samples even contained more than 10 times the maximum daily dose of lead![7]

Other research has indicated that up to a quarter of TCM formulations contain undeclared pharmaceuticals, but another  study found that the true number could be closer to half.[7] More than 50% of tested samples contained at least one pharmaceutical adulterant, many of which were at clinically significant doses.[7] One such TCM contained six pharmaceutical products at doses which would normally require a doctor’s prescription, including amoxicillin and warfarin. None of these were mentioned on the label, and the interactions of a medicine containing analgesics, antibiotics, stimulants and antihistamines aren’t certain.[7] As well as proving potentially dangerous to patients, pharmaceutical adulterants can distort the data from any clinical trials of these TCM formulations. It is very likely that any TCM product containing a clinically relevant dose of an undisclosed pharmaceutical would outperform a placebo, so this gives false data about the efficacy of the TCM formulation itself.[7] These pharmaceuticals are often added to give the desired effect without being listed as part of the formulation of the TCM, so it is very difficult for patients to know what they are getting.[7]

Adapted from Coghlan et al, 2015.[7]

Overall, all but two of the 26 formulations tested were non-compliant with standards posed by Australian regulations, which are very similar to UK MHRA standards.[7] It is concerning that these so-called medicines, which could actually pose a serious health risk in some cases, can be commercially available without a transparent ingredients list. Given TCM formulations are being given to patients ill with COVID-19, it is possible for them to cause harm. Holistic treatments marketed as ‘natural’ can have sinister effects or ingredients, so it is extremely important to discuss any alternative therapies with a doctor.

So why are we talking about it?

Although TCM may be ineffective or even dangerous, some ingredients could hold promise for treatments of viral infections including COVID-19. Natural products can be isolated from plant extracts that make up TCM remedies; some of these possess real therapeutic benefit. For example, artemisinin is a current frontline therapy used in the treatment of malaria. In 1971, Chinese scientist Youyou Tu extracted this compound from wormwood, a traditional remedy for fever, and found it was able to cure malaria in mouse and primate models.[8] She later won a Nobel prize for her work. Another example is the finding that an extract from the common TCM ingredient liquorice root, known as glycyrrhizin, showed activity against a strain of coronavirus isolated during the SARS epidemic. When present in very high concentration (4000mg/L), glycyrrhizin was able to fully inhibit viral replication.[9] This seems promising, but the mechanism for this isn’t fully understood and a lot more research is needed before any compound derived from TCM could be used as a treatment for SARS-CoV or indeed COVID-19.

TCM and other holistic therapies are clearly very divisive. Some wholeheartedly believe in their power, having heard anecdotes of miraculous cures. Others write it off completely due to the lack of good science or reliable evidence of its effectiveness. In truth, there is likely to be some benefit to investigating TCM as a potential treatment for COVID-19, just perhaps not in the way it would traditionally be applied. A huge number of potential drug candidates in the form of natural products may be present in the ingredients that make up TCM formulations. For these to be useful as medicines in the fight against COVID-19 and other viral infections, there needs to be rigorous testing, valid and reliable clinical trials, and thorough and transparent regulation of emerging treatments.


[1]- Fung, Y. F. and Linn, Y. C. 2015. Developing Traditional Chinese Medicine in the Era of Evidence-Based Medicine: Current Evidences and Challenges. Evidence-Based Complementary and Alternative Medicine. 2015, article no: 425037 [no pagination].

[2]-Active Herb. 2020. The Official TCM Formula That’s Successfully Treating COVID-19 Patients In China. [Online]. [Accessed 11April 2020]. Available from:

[3]- Yang, Y., Islam, M. S., Wang, J., Li, Y., and Chen, X. 2020. Traditional Chinese Medicine in the Treatment of Patients Infected with 2019-New Coronavirus (SARS-CoV-2): A Review and Perspective. International Journal of Biological Sciences. 16(10), pp1708-1717. 

[4]- Ren, J. L., Zhang, A. H., and Wang, X. J. 2020. Traditional Chinese Medicine for COVID-19 Treatment. Pharmacological Research. 155, article no: 104743 [no. pagination].

[5]- Xu, X. W. et al. 2020. Clinical Findings in a Group of Patients Infected With the 2019 Novel Coronavirus (SARS-CoV-2) Outside of Wuhan, China: Retrospective Case Series. The bmj. 8235, article no:2020;368:m606 [no pagination].

[6]- The Economist. 2020. Fighting it the Chinese Way: China Backs Unproven Treatments for COVID-19. [Online]. [Accessed 14 April 2020]. Available from:

[7]- Coghlan, M. L., Maker, G., Crighton, E. et al. 2015. Combined DNA, Toxicological and Heavy Metal Analysis Provides an Auditing Toolkit to Improve Pharmacovigilance of Traditional Chinese Medicine (TCM). Scientific Reports. 5, article no: 17475 [no pagination].

[8]- Tu, Y. 2011. The Discovery of Artemisinin (Qinghaosu) and Gifts from Chinese Medicine. Nature Medicine. 17, pp1217-1220.

 [9] Cinatl, J. et al. 2003. Glycyrrhizin, an active component of liquorice roots, and replication of SARS-associated coronavirus. The Lancet361, pp2045-2046.

Subscribe for updates:

Any questions and feedback: let us know!

Blog COVID-19

“SARS-COV-2 was already spreading in France in late December 2019” – A Scientific Perspective.

Written by Charlotte Rigby

“SARS-COV-2 was already spreading in France in late December 2019” – A Scientific Perspective.

A French study has recently made the claim that SARS-CoV-2, the causative agent of COVID-19, was detected in France on December 27th after re-testing samples from patients diagnosed with unknown pneumonias. A single sample, belonging to a French man, tested positive for SARS-CoV-2 DNA multiple times by PCR.

Figure 1: The original paper published in ‘International Journal of Antimicrobial Agents’.

Does this explicitly mean he had COVID-19?

Not necessarily, however, more evidence is required before drawing any final conclusions. The claim is based on a PCR experiment which suggested segments of the SARS-CoV-2 genome were present in this sample. False positives can occur in this type of experiment. The investigators compensate for this by running the PCR twice. Other methods the investigators could have used to further validate this claim include are viral genome sequencing, use of phylogeny to study how closely related this viral genome is to others that the science community have sequenced and finally serology, to detect antibodies that would have been produced by the immune system during infection.

Sequencing is the process of determining the sequence of nucleotides within DNA or RNA. Knowing this can mean the virus can be compared to ‘reference genomes’ of other viruses to see if there is a match. This sequence can also be used to construct phylogenetic trees which show the evolutionary relationships between organisms, including viruses. The more closely related the virus is the more similar it usually is. These methods would show that the virus was present in the sample and also confirm where the virus belonged on the evolutionary tree, allowing scientists to pinpoint whether this virus was closely related to the viruses observed at the beginning of the outbreak.

Finally, serological evidence would prove that infection had occurred. Serological evidence is based on antibodies, a protein produced during the innate immune response to neutralise pathogens. The presence of RNA doesn’t necessarily mean infection (see the recent stir created by RNA being detected in dogs for example), antibody production does as it proves an immune response was mounted. Scientists would require a blood sample from this patient, many different tests can be performed but for SARS-CoV-2 it’s likely a simple colour change test would be used – similar to a pregnancy test(1).

Figure 2: Methods for validating identities of infectious diseases.

So, should we discount the study?

No, we shouldn’t. A result is still a result and knowledge of this is important. However, when information isn’t communicated well, or an incomplete picture is presented a wave of misinformation can occur. It’s important now more than ever to think critically about information and our sources of information. Ultimately, this is what the Science Social is about – communicating science with non-scientists and encouraging critical thinking.

Have any questions about the content covered today? Drop us a message on any of our platforms.


1.        Amanat F, Stadlbauer D, Strohmeier S, Nguyen T, Chromikova V, McMahon M, et al. A serological assay to detect SARS-CoV-2 seroconversion in humans. medRxiv [Internet]. 2020 Jan 1;2020.03.17.20037713. Available from:

Subscribe for updates:

Questions, feedback and comments:
Blog COVID-19

COVID-19: Let’s Talk Vaccines

Grab a coffee, lets do this!

Therapeutic options

We discussed the latest updates on drug therapies as countermeasures for COVID-19 here. Instead of treating diseases, vaccines have the capacity to prevent them.

No, really what is a vaccine and how do they work?

Like natural infections, vaccines work by initiating a first line immune response, known as the innate immune response. In turn this allows the body to remember the pathogen, preparing the body to defend itself on the pathogens next attack, known as an adaptive immune response 1. Each pathogen (or vaccine) contains unique and specific shapes that the body’s immune system is able to recognise. Once the pathogen is dealt with, the adaptive immune response establishes what we call immunological memory, which is essentially the main goal of vaccination 1.

There isn’t just one type of vaccine either, scientists have found different ways of getting your immune system ready and prepared for infectious diseases.  

Two main types of vaccines

Vaccines can be split into two main categories 2:

Live attenuated vaccines

This is when scientists take the causative agent of the disease, i.e. the virus or the bacteria and weaken it so it can no longer cause disease in healthy people. This is not an appropriate vaccination method for those with an immune system that does not work 1,2.

Live attenuated vaccines tend to be produced for viral diseases, as viruses have fewer genes and weakening these pathogens can be achieved more reliably 1.

Examples of Live Attenuated Vaccines used in the UK are as follows:

  • Rotavirus vaccine
  • Measles Mump and Rubella Vaccine
  • Chickenpox vaccine
  • And more….

If you are big on your travelling, you may have had the Yellow Fever Vaccine or the oral typhoid vaccination.

Inactivated vaccines

These types of vaccines contain either; the whole bacteria or virus that have been “killed”. OR, small elements of the disease-causing agents such as associated proteins or sugars. All of which cannot cause disease, even in those with severely weakened immune systems. The immune response produced by these vaccines aren’t always as powerful as those observed in a live attenuated vaccine, and because of this may require boosters 1,2.

Adjuvants are often added to inactivated vaccines to help boost the immune response and thus make them more protective.

Adjuvant… what?

So, an adjuvant is actually an aluminium salt that is added to vaccines to help produce an immune response, such as aluminium hydroxide, aluminium phosphate or potassium aluminium sulphate.

This is not like injecting an aluminium can into your body, by the way. Aluminium is actually a very natural metal found naturally in water, food and the earth itself. The amount used in vaccines is very tiny and is a vital element for these types of vaccines to protect you2.

“Whole killed” vaccines

Some examples of diseases prevented with inactivated “whole killed” vaccines are; poliovirus, hepatitis A, Rabies and Japanese Encephalitis 2.

Subunit vaccines

There are 3 types of subunit vaccines; toxoid, conjugate and recombinant vaccines. All of which essentially take a subunit of the pathogen and turn this into a vaccine 2. When scientists say subunit, they are referring to only a part, or an element of the pathogen as opposed to the whole thing.


Many bacteria release toxins during an infection. Our bodies are able to recognise these toxins and produce an immune response. Therefore, making these a good target for vaccines. Examples of toxoid vaccines are Diptheria, tetanus and pertussis (whooping cough) 2.


The work “conjugate” means connected or joined. Sometimes, the subunit of a pathogen doesn’t elicit a good enough immune response by itself, so the subunit is joined to something else. Quite often the subunit is joined to the tetanus or diphtheria toxoid. Examples of conjugate vaccines are Haemophilus influenzae B, Meningitis C, Pneumococcal and Meningococcal vaccines 2.

Recombinant vaccines

These types of vaccines take the genetic code (DNA) from the virus or bacteria that we want to protect ourselves from. In the case of the Hepatitis B vaccine, the DNA is inserted into yeast cells, which are able to produce surface proteins of the pathogen. This is then purified and used as the active part of the vaccine. Examples of recombinant vaccines: Hepatitis B, Human Papilloma Virus and Meningitis B vaccines 2.

Vaccine trials are essential

Like we discussed in our article about drugs, all medicines have to go through a robust clinical trial. This is to ensure that the vaccine is not only safe, but to test whether the vaccine works and provide sufficient protection.

Vaccines available

Phase I: a small-scale trial to assess whether the vaccine is safe in health people.

Phase II: more participants are recruited, and the study assess the efficacy of the vaccine, vaccine safety and the immune response is studied.

Phase III: The vaccine is studied under natural disease conditions, hundreds to thousands will be recruited to the study.

If the vaccine retains safety and works well over a defined period of time, the manufacturer of the vaccine is able to apply for a licence to market the product for human use.

Phase IV: The vaccine has been licensed and approved for use, however, data is still collected to monitor adverse effects and to determine the longevity and effectiveness of the vaccine 3,4.

Eradication of disease

In May 1980, the world was declared free of smallpox 5. The last naturally occurring case of this disease was observed in Somalia in 1977 5. Edward Jenner in 1796 observed that those who contracted cowpox, a disease known to be very mild, developed immunity against smallpox 6. This inspired Jenner to prepare a vaccine containing material from cowpox lesions, where he knew “the annihilation of smallpox must be the final result of this practice”. Despite this ground breaking discovery, it took nearly 200 years to eradicate smallpox 5. Smallpox remains the only human infection eradicated by vaccination.

Of course, it is not only humans that are vaccinated against infectious agents, but our pets and our livestock are also vaccinated. Rinderpest is known as the most devastating infectious disease of cattle, associated with a mortality rate more than 70% 7. Rinderpest is a virus belonging to the same virus family as measles. In 1918, the first vaccine was developed in Korea as an inactivated virus. This later got developed into a live attenuated vaccine until 1989 where the first recombinant rinderpest vaccine was developed 7. However, before the recombinant vaccine got to trial, eradication was achieved with the use of Plowright’s live attenuated vaccine 7.

Vaccines will allow us to prevent the disease, protect vulnerable members of our communities through herd immunity and in turn reduce the pressure on healthcare systems.

There is currently no vaccine for any of the known coronaviruses. Despite massive research efforts, it is not expected that a vaccine against SAR-CoV-2 will be available in less than 18 months 8. Keep an eye out for a break down on SARS-CoV-2 vaccines that are going through trial over the next couple of weeks.


1          Vetter, V., Denizer, G., Friedland, L. R., Krishnan, J. & Shapiro, M. Understanding modern-day vaccines: what you need to know. Annals of Medicine 50, 110-120, doi:10.1080/07853890.2017.1407035 (2018).

2          Group, O. V. Types of Vaccines, <> (2020).

3          European Vaccine Initiative. Stages of Vaccine Development, <> (

4          Stern, P. L. Key steps in vaccine development. Annals of Allergy, Asthma and Immunology (2020).

5          Strassburg, M. A. The global eradication of smallpox. American Journal of Infection Control (1982).

6          Jenner, E. History of the Inoculation of the Cow-Pox: Further Observations on the Variolae Vaccinae, or Cow-Pox. The Medical and Physical Journal (1799).

7          Yamanouchi, K. Scientific background to the global eradication of rinderpest. Veterinary Immunology and Immunopathology 148, 12-15, doi: (2012).

8          Grenfell, R., Drew, Trevor. Here’s why the WHO says a coronavirus vaccine is 18 months away, <> (2020).

Blog Personal Blog Post

Psychosis and Me Part I.

Schizophrenia is a mental health disorder that is characterised by repeated psychotic episodes and this blog post is about my own personal experiences of psychotic episodes. You can check out my post about schizophrenia here if you just want to know more about the condition.

This is a long story, so I’ve broken it into three parts:

  1. Building Fictional Worlds: Developing Psychosis
  2. “Think Whatever You Like”: Rebuilding a Mind
  3. Is It All Over?: Returning to Normal Life

I’d like to start with a disclaimer of sorts. This is about my own battles with psychosis and by no means is meant to be a typical account, I doubt if there ever could be such a thing. Psychosis is subjective and variable by its very nature, if you had 100 schizophrenic patients in a room, the way that the disease affects and impacts each one could be completely different. The outcomes for people who are treated in early intervention teams for psychotic disorders vary wildly, and unfortunately, sometimes the interventions don’t work. I was one of the lucky ones.

Building Fictional Worlds: Developing Psychosis

I had my first psychotic episode when I was 19 years old. This is quite common; most psychotic disorders first develop in late adolescence. My psychosis presented itself in the form of delusional thinking at first, this can be hard to explain to people who’ve never experienced anything like it, but I started to move into another reality with different rules and a different worldview. This would come on suddenly, I would often get a sensation like butterflies in my stomach followed by a sinking feeling and a sense of impending doom. Then the racing thoughts would come, a rush of epiphanies that provided proof and collected evidence for my new, delusional, reality. These thoughts would snowball on top of each other, one leading to the next big epiphany that started the next chain of thinking off. Sometimes this would end with a panic attack and me rushing out of whatever situation I was in. Sometimes it would just stop of its own accord, leaving me shaken and confused about what had happened.

The delusions were often persecutory in nature, but the type of persecution would change. I would be in the middle of a vast conspiracy, like The Truman Show, where everyone around me was keeping up a façade of normal life whilst really they were actors. I’d hear someone talking on the radio and swear they were talking about me or an advertisement on the TV would be referencing the thoughts I was having. Sometimes I would be in a world where I was the only person who existed, everyone else was simply me at another point along my timeline, I would even “remember” being in the shoes of the person I was looking at.

The worst by far were the delusions where I was in Hell. I was being punished for all of my misdeeds in a past life, the people around me were demons and devils, all there to gain my trust, before leading me to ruin and humiliating me, this one was particularly bad because I could use it to explain the transitory nature of the other delusions. OF COURSE! The demons are pretending to be me to trick me! Or, they’ve made me think I’m in the Truman Show, it’s all part of my punishment.

As time went on, I started to collect “evidence” for my theories and figuring out what it all meant. I created a hydra in my mind. Each new episode would be like chopping off the serpent’s head, for each question answered, seven more would grow in its place. I started building a more complex web of coincidences that I had linked together with faulty logic. I spent many an hour in the grips of delusional thought, I felt like my mind was a tumultuous ocean and I was wrestling for something solid to hold on to. Even in my more lucid moments, when the confusing fog had lifted and I was thinking normally (or at least as normally as I was before this had started) I spent a long time, mostly when sitting up alone at night, simply debating the nature of my reality with myself.

All the while that this was going on, I was desperately trying to keep the fact that I was experiencing this from those around me. In the lucid moments I kept it hidden because I feared being labelled as crazy and locked away in some institution. In my delusional moments, well, they were part of the conspiracy, telling them would only let them know I’d seen through their tricks, and then what might happen? What new horrors would they unleash on me if they knew they’d been foiled?

So I tried to keep things together in front of those around me, but people aren’t so easily fooled. In hindsight, I often think back to how strange the conversations I had with my friends must have been. On the surface I’m listening to what they’re saying, but really, I’d be scanning their speech, looking for signs of deception, hidden clues they might be giving me or sly digs they might be making cryptically. This of course would be detected by them, my reactions just weren’t right for the situation. I started to distance myself from those around me, spending more time alone, or if I was in a group, staying quiet and just watching, being there, but not being “there”, so to speak. Those who knew me well could clearly see something was wrong, I had been extroverted and confident, now I was timid and anxious, but I dismissed any attempts to help, I still don’t really know why, I think partly it was because I didn’t want to show anyone how deeply broken I was, partly it was doubt that anything could help.

It stayed like this for a year before things really started deteriorating. The hallucinations started appearing alongside the delusions. I would hear two people discussing my actions as I did them, weighing up the merit of them and how close each action took me to “breaking out” of their trap. Sometimes these were neutral voices, sometimes they were the devil and God himself, fighting over me. Sometimes I would “just know” that everyone around me could read my thoughts, I would then of course start thinking of my most shameful moments, my deepest fears, all the things I wouldn’t want broadcast to everyone around me and I’d have to leave the situation immediately. I once got off a bus, miles away from where I intended to, because I was having such a moment and a man across from me had made eye contact and smiled. He was probably only wondering why the teenager across from him had suddenly started shaking with fear and staring around the bus with an expression of absolute terror on his face, but that eye contact and smile was all the evidence I needed in the grips of my delusion to confirm that I was right. I walked for nearly 3 hours back to my parent’s house, too scared to get back on a bus and too scared to go back to the halls of residence I was living in at the time. This was one of many such occurrences. The episodes had been infrequent at first, now I was in the grips of an episode more than I was lucid. I couldn’t concentrate on anything, my uni work was near impossible, my relationships were becoming strained. I was at breaking point.

What happened next changed the course of my life. I had started attending some local church services. I’d never really been religious in my youth but there were clear religious undertones to some of my delusions and whilst I was in the grips of some of my worst episodes, I’d desperately started praying and made promises to a God I didn’t believe in that if He helped me get a grip on my thoughts, I’d go to church. Plus, in my delusional logic, God was behind all of this, so I thought it best to go and find out more about Him.

 There was a girl at this church who was about my age, and who one day very bravely spoke about her experiences with mental illness in front of an entire congregation. I’d met her a few times before and she seemed nice, I was in a fairly lucid state and her admission that she’d experienced something similar made me less afraid of her judgement, so I did what I hadn’t done with anyone so far. I told her what I was going through, as clearly and as fully as I could. She listened. More than that, she understood. She didn’t discount what I’d experienced or dismiss any of it. She helped me see that I really only had one of two explanations that from my perspective, could be true. Either I was the focal point of a divine conspiracy I didn’t know the full details of and was powerless to escape, or I was mentally ill. At least if it was the latter, I could try to do something about it. The very next day, I was sitting in my GP’s office, with her alongside me. I told my GP what I’d been going through and he booked an appointment with a psychiatrist who would start the process of diagnosis and putting together a treatment plan. The free-falling had stopped, but now I was at the bottom, it was time to start the long climb back out of the depths, it was going to be a long journey…

Part II and Part III (coming soon).

Blog COVID-19

COVID-19: Let’s talk treatments

This is one of our long reads, grab yourself a coffee! 15 min read.

*SPOILER ALERT* At the present time, there is no quick-fix solution to the COVID-19 problem. The good news is, scientists are working on it!

Antibiotics do not work!

Figure 1: Schematic to demonstrate secondary
bacterial infection following initial viral infection.

Antibiotics are not effective against viruses; they are entirely different microorganisms and therefore require different types of intervention. You may however, have heard of antibiotic use in the context of secondary infection. As the name suggests, this term describes when a patient acquires an infection secondary to the original [figure 1]. This is relatively common in patients with an infection of the lung (pneumonia), due to lowered immunity as a result of the original infection. This secondary infection may be viral or bacterial and so, may be treated with antibiotics (1,2).

A brief word on vaccinations…

Whilst there are several drug treatment options under investigation, the best way of protecting the population is through the development and deployment of a vaccination programme. Vaccines work by introducing a weakened version or fragment of the virus or bacteria to an individual’s immune system. This does not cause infection and instead elicits a mild immune response that allows the body to safely generate antibodies against the antigen. As part of this response, special memory cells that are part of the immune system, are trained to recognise and remember. Should you come across the real thing in future, your memory cells will fire into action and enable the production of antibodies to fight against it. As the immune system has already seen the antigen before, the response is more effective and much faster, making it highly efficient at eliminating the intruder and protecting your health (3,4).

Keep an eye out for our future blog post scratching beneath the surface of vaccination.

So, what are the other options?

Whilst vaccinations are in the making, there are a number of options to explore to improve patient outcome. The unprecedented global collaboration has accelerated research into these options, from drugs to vaccinations and beyond but here’s the rub… they still need to go through the clinical trials process. Here we discuss several drugs under the scrutiny of clinical trial to identify their safety and efficacy against SARS-CoV-2.

Drug treatments

The clinical trials process is of vital importance but remains extremely lengthy. It usually takes 10-15 years for a new drug to make it from start to finish, that is, from conception to approval for use. Clinical trials are essential as they serve to filter out the ineffective and unsafe. Just because a drug has made it to first-in-man (phase I) does not mean it’s a sure-fire win. In fact only 10% of medicines that enter phase I ever make it through to approval – at the cost of tens-to-hundreds of millions of pounds (5).

Figure 2: Drug development pipeline workflow. Successful drug candidates progress through pre-clinical to first-in-man and on to the various phases of clinical trial before post-market surveillance at phase IV.

At present, there is tremendous focus on the repurposing of existing medications as opposed to generating new drugs. Drug repurposing is a crucial initiative, as it may greatly reduce the cost and time spent identifying treatment options for COVID-19. There are 4 treatment options under the investigation of the clinical trial named “Solidarity”, which has been launched by the WHO in collaboration with international partners (6).


What is it?

Remdesivir is a rising star in therapeutics against SARS-CoV-2. It is an investigational drug that was originally developed and trialled a treatment strategy against the Ebola virus. However, other treatment options showed greater efficacy against Ebola and remdesivir was subsequently shelved.

Why is it in trial?

Ongoing research has since demonstrated its broad antiviral activity and highlighted its promise in the fight against COVID-19. In in vitro testing, remdesivir was effective at inhibiting the replication of a range of coronaviruses including those that cause severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS). Remdesivir works by targeting and incorporating itself into the genetic material of the virus, so it can no longer replicate (7). Pre-clinical testing has provided strong evidence that intravenous treatment is effective at reducing viral load and preventing progression to severe pneumonia in primates (8).  

Where are we now?

Whilst remdesivir remains unlicensed and has not yet been approved for safe and effective use, it is in clinical trial to determine its utility. A Chinese study concluded that remdesivir afforded no clinically significant benefit to COVID-19 patients and demonstrated adverse events where the treatment was halted in 12% of patients. However, the authors state a key limitation of this study; the number of patients included was not great enough to detect clinical significance (9).

Recent data has shone a more promising light on remdesivir. An international study recruiting over 1000 patients has reported a 30% faster recovery time for remdesivir vs standard care, which was found to be statistically significant. The data also shows a trend towards reduced mortality rate in those receiving remdesivir however, the difference was not great enough to be significant. Although this is good news, we must still be cautious, the safety data has not yet been published and there are some concerns regarding adverse effects (10,11). Whilst it has been touted by leading scientists that remdesivir will become the new standard of care in the United States, there is still work to be done. There are many questions regarding safety, dosing regimen and patient suitability that need answering but so far so good… watch this space and we’ll keep you posted.

Hydroxychloroquine & chloroquine

What is it?

Hydroxychloroquine and its cousin chloroquine are also in the running having been publicised early on by the American Government for their effectiveness. They are similar in structure and function however hydroxychloroquine is less toxic and so much safer for a patient (12). Both drugs have already made it through to the clinical trial finish line for use in other applications, where they can be used to prevent and treat malaria. Hydroxychloroquine is also known to have anti-inflammatory action and is often prescribed for the treatment of inflammatory conditions like lupus and rheumatoid arthritis (13,14).

Why is it in trial?

Both drugs have been included in the Solidarity trial as there is a wealth of evidence demonstrating both antiviral and anti-inflammatory properties. Following the SARS epidemic in 2002, pre-clinical research demonstrated that chloroquine inhibited the replication of SARS-CoV in cells (15). More recent work has shown there may be a multitude of mechanisms through which SARS-CoV-2 infection in cells can be prevented (16). Although already approved, they must be tested for safety and efficacy in a COVID-19 setting. There are a number of reported side effects and concerns regarding potential toxicity must be carefully assessed and considered before regarding it as a viable treatment option (15).

Where are we now?

The available data from clinical trials is very mixed. A number of early trials have a small sample size and poor study design (17). One paper available on the preprint server MedRxiv found that patients critically ill with COVID-19 benefitted from administration of hydroxychloroquine. Those that received the drug had a significantly lower mortality rate and level of inflammation. However, the drug treatment group included only a small number of people and inflammation levels were reported to be twice as high as the control group at the beginning of the study (18).

In contrast, an American group found no evidence that use of hydroxychloroquine reduced the risk of need for mechanical ventilation. The authors of this study do also discuss its limitations, in that the study cohort only included men over 65 and the patients were not allocated different treatments at random (19).

It is important to remember these articles are still in preprint and have not yet been accepted for publication. Evidently the answer is not clear cut and the ongoing work is essential to better understand the treatments and outcomes.


What is it?

Lopinavir and ritonavir are antiretroviral drugs that have been approved and are prescribed to treat human immunodeficiency virus (HIV). They are often used in combination as ritonavir helps to boost the efficacy of lopinavir. Although HIV and coronaviruses are very different, the known mechanism of action against HIV has propelled the combination into the Solidarity trial. It is accepted that lopinavir/ritonavir work by blocking essential proteins to prevent replication of the virus (20).

Why is it in trial?

In vitro research has demonstrated that lopinavir has an antiviral effect against several coronaviruses in cells, whilst additional in vitro studies have confirmed the same effect against SARS-CoV-2 (21,22). More advanced pre-clinical study evaluating treatment of MERS in primates, revealed improved clinical outcome when lopinavir/ritonavir was combined with interferon-β1b – more on this next (23).

Where are we now?

Studies conducted early in the epidemic demonstrated no benefit to patients that received lopinavir/ritonavir, compared to those receiving the standard of care. Although less than 200 patients participated, there was no improvement in recovery time or mortality rate (24). Other studies have provided similar evidence, whereby there is no difference in ‘viral clearance’ – the time it takes for the virus to no longer be detectable in a patient (25). Alongside having no benefit, side effects involving the gastrointestinal tract and liver have also been reported in several of these trials (25,26).

At present there just isn’t enough evidence to say if this combination is effective in humans, the current clinical trials will present more data to answer this question in the future.


What is it?

Don’t panic! Interferon-β1a is a subclass of chemical messengers that belongs to a family called type I interferons, broadly speaking they help to regulate the immune system. This β1 subclass refers to specialised signals that are produced by cells in response to infection, particularly viral. Once the signals have been released, they are intercepted and interpreted by other cells, which allows them to increase their antiviral activity. Interferons are naturally produced by the body but have also been manufactured for use in a medical setting. Some of the β1 class, like interferon- β1a, are used as a treatment for the autoimmune condition multiple sclerosis (27).

Why is it in trial?

Interferons have proved promising in in vitro and pre-clinical tests against other coronaviruses. One pre-clinical study demonstrated that administration of interferon-β1b significantly reduced viral load in the lung and severity of disease in MERS (23). There is an ongoing human trial in Saudi Arabia, assessing the utility of interferon-1 and lopinavir/ritonavir against MERS however, no clinical data has yet been published (28). The Solidarity trial is testing interferon-β1a in conjunction with the antiviral drugs lopinavir/ritonavir to see if the combination offers any advantage to patient outcome.

Where are we now?

Interferons are being used in combination with a variety of other antiviral drugs in different trials across the world. There is limited data available to say whether or not this strategy is paying off. In China interferon-B1b is being trialled in an inhaled format for direct administration to the lungs (29). One study has shown that inclusion of interferon therapy accelerated viral clearance compared to treatments that did not include interferon. However, the paper has not yet been accepted for publication and is limited by poor design, a small sample size and disproportionate male-female representation (30).  

Ongoing trials will aim to assess a much larger and more balanced sample population, so we should hope to draw more firm conclusions about this treatment option in the future.

Are there any other therapeutic options?

Convalescent plasma

What is it?

There is some exciting research into the usefulness of convalescent plasma. This may sound complicated but the basic premise centres around the plasma of a ‘convalescent’ or recovered individual. Plasma is the liquid part of blood which contains important proteins, salts and crucially, antibodies. It may be isolated through a process called plasmapheresis and for a person donating plasma, it is not dissimilar to giving blood [figure 3]. Instead of donating whole blood, a machine separates it into blood cells and plasma. This allows the plasma to be removed and so returns your blood cells and often a saline solution to replace the lost volume. For patients receiving convalescent plasma, their own will be removed and replaced with the antibody rich plasma of a recovered individual, so conferring passive immunity. This strategy works on the basis that the person donating plasma is now immune and has generated antibodies – which should be around 28 days after recovery. REF.

Why is it in trials?

The concept of convalescent plasma is not new. Use of convalescent blood has been documented as early as 1918 in the prevention and treatment of the Spanish Flu (31). More recent application in several case studies have demonstrated it may be useful against SARS, MERS and even Ebola (32). A study utilising convalescent plasma as a treatment option for SARS reported a clinically significant reduction in mortality rate in those that received it. Early treatment, less than 14 days after symptom onset, also enabled a more positive outcome (33).

Where are we now?

NHS Blood and Transplant is leading a programme to investigate convalescent plasma in clinical trial. The trial will aim to assess if its use can improve patient survival and recovery time. The programme has only just begun but previous case studies are encouraging. A number of these report convalescent plasma use only in severely ill patients but describe clinical improvement and an increase in antibodies against SARS-CoV-2. If you want to more about the convalescent plasma trials and if you could help, click here.

Figure 3: Plasmapheresis

All in all, there is no definite treatment at the moment but there are many options and trials working to gather concrete evidence to make a better judgement.

We hope you enjoyed our first long read! If you need help clarifying some of the jargon or want to know more about the concepts discussed, DM us and we’ll get back to you.

For bite-sized information on clinical trials and convalescent plasma, check out our infographics on social media.  


1.          Hanada S, Pirzadeh M, Carver KY, Deng JC. Respiratory viral infection-induced microbiome alterations and secondary bacterial pneumonia. Vol. 9, Frontiers in Immunology. Frontiers Media S.A.; 2018.

2.          Kim H. Outbreak of novel coronavirus (COVID-19): What is the role of radiologists? European Radiology. Springer; 2020. p. 1–2.

3.          Plotkin S. History of vaccination. Vol. 111, Proceedings of the National Academy of Sciences of the United States of America. National Academy of Sciences; 2014. p. 12283–7.

4.          How Vaccines Work | [Internet]. [cited 2020 May 3]. Available from:

5.          Takebe T, Imai R, Ono S. The Current Status of Drug Discovery and Development as Originated in United States Academia: The Influence of Industrial and Academic Collaboration on Drug Discovery and Development. Clin Transl Sci. 2018 Nov 1;11(6):597–606.

6.          Alpern JD, Gertner E. Off‐Label Therapies for COVID‐19—Are We All In This Together? Clin Pharmacol Ther [Internet]. 2020 Apr 20 [cited 2020 May 3];cpt.1862. Available from:

7.          Yin W, Mao C, Luan X, Shen D-D, Shen Q, Su H, et al. Structural basis for inhibition of the RNA-dependent RNA polymerase from SARS-CoV-2 by remdesivir. Science (80- ) [Internet]. 2020 May 1 [cited 2020 May 5];eabc1560. Available from:

8.          Williamson BN, Feldmann F, Schwarz B, Meade-White K, Porter DP, Schulz J, et al. Clinical benefit of remdesivir in rhesus macaques infected with SARS-CoV-2. bioRxiv. 2020 Apr 15;2020.04.15.043166.

9.          Wang Y, Zhang D, Du G, Du R, Zhao J, Jin Y, et al. Remdesivir in adults with severe COVID-19: a randomised, double-blind, placebo-controlled, multicentre trial. Lancet [Internet]. 2020 [cited 2020 May 2];1–10. Available from:

10.        Ledford H. Hopes rise for coronavirus drug remdesivir. Nature [Internet]. 2020 Apr 29 [cited 2020 May 3]; Available from:

11.        Beasley D, Manas M. Data on Gilead drug raises hopes in pandemic fight, Fauci calls it “highly significant” – Reuters. [cited 2020 May 3]; Available from:

12.        Liu J, Cao R, Xu M, Wang X, Zhang H, Hu H, et al. Hydroxychloroquine, a less toxic derivative of chloroquine, is effective in inhibiting SARS-CoV-2 infection in vitro. Cell Discov. 2020 Dec 1;6(1):1–4.

13.        Sinha S. Hydroxychloroquine Uses, Dosage & Side Effects – [Internet]. [cited 2020 May 3]. Available from:

14.        Multum C. Chloroquine Uses, Side Effects & Warnings – [Internet]. [cited 2020 May 3]. Available from:

15.        Sinha N, Balayla G. Hydroxychloroquine and covid-19. Postgr Med J [Internet]. 2020 [cited 2020 May 2];0:1–6. Available from:

16.        Singh AK, Singh A, Shaikh A, Singh R, Misra A. Chloroquine and hydroxychloroquine in the treatment of COVID-19 with or without diabetes: A systematic search and a narrative review with a special reference to India and other developing countries. Diabetes Metab Syndr Clin Res Rev. 2020 May 1;14(3):241–6.

17.        Ferner RE, Aronson JK. Chloroquine and hydroxychloroquine in covid-19. [cited 2020 May 3]; Available from:

18.        Yu B, Li C, Chen P, Zhou N, Wang L, Li J, et al. Hydroxychloroquine application is associated with a decreased mortality in critically ill patients with COVID-19. [cited 2020 May 3]; Available from:

19.        Magagnoli J, Narendran S, Pereira F, Cummings T, Hardin JW, Sutton SS, et al. Outcomes of hydroxychloroquine usage in United States veterans hospitalized with Covid-19. [cited 2020 May 3]; Available from:

20.        Chandwani A, Shuter J. Lopinavir/ritonavir in the treatment of HIV-1 infection: A review. Vol. 4, Therapeutics and Clinical Risk Management. Dove Press; 2008. p. 1023–33.

21.        De Wilde AH, Jochmans D, Posthuma CC, Zevenhoven-Dobbe JC, Van Nieuwkoop S, Bestebroer TM, et al. Screening of an FDA-approved compound library identifies four small-molecule inhibitors of Middle East respiratory syndrome coronavirus replication in cell culture. Antimicrob Agents Chemother. 2014;58(8):4875–84.

22.        Choy KT, Wong AYL, Kaewpreedee P, Sia SF, Chen D, Hui KPY, et al. Remdesivir, lopinavir, emetine, and homoharringtonine inhibit SARS-CoV-2 replication in vitro. Antiviral Res. 2020 Jun 1;178:104786.

23.        Fuk-Woo Chan J, Yao Y, Yeung M-L, Deng W, Bao L, Jia L, et al. Treatment With Lopinavir/Ritonavir or Interferon-β1b Improves Outcome of MERS-CoV Infection in a Nonhuman Primate Model of Common Marmoset. 2015;

24.        Neil M. Ampel M. Lopinavir-Ritonavir Was Not Effective for COVID-19. NEJM J Watch. 2020 Mar 24;2020.

25.        Li Y, Xie Z, Lin W, Cai W, Wen C, Guan Y, et al. An exploratory randomized, controlled study on the efficacy and safety of lopinavir/ritonavir or arbidol treating adult patients hospitalized with mild/moderate COVID-19 (ELACOI). medRxiv [Internet]. 2020 Apr 15 [cited 2020 May 5];2020.03.19.20038984. Available from:

26.        Cao B, Wang Y, Wen D, Liu W, Wang J, Fan G, et al. A Trial of Lopinavir–Ritonavir in Adults Hospitalized with Severe Covid-19. N Engl J Med [Internet]. 2020 Mar 18 [cited 2020 May 5];NEJMoa2001282. Available from:

27.        Sallard E, Lescure FX, Yazdanpanah Y, Mentre F, Peiffer-Smadja N. Type 1 interferons as a potential treatment against COVID-19. Antiviral Res. 2020 Jun 1;178:104791.

28.        Sheahan TP, Sims AC, Leist SR, Schäfer A, Won J, Brown AJ, et al. Comparative therapeutic efficacy of remdesivir and combination lopinavir, ritonavir, and interferon beta against MERS-CoV. [cited 2020 May 3]; Available from:

29.        Dong L, Hu S, Gao J. Discovering drugs to treat coronavirus disease 2019 (COVID-19). Drug Discov Ther [Internet]. 2020 [cited 2020 May 3];14(1). Available from:

30.        Zhou Q, Chen V, Shannon CP, Wei X-S, Xiang X, Wang X, et al. Interferon-α2b treatment for COVID-19. [cited 2020 May 3]; Available from:

31.        Mcguire LW, Redden WR. The use of convalescent human serum in in-fluenza pneumonia – a preliminary report. Am J Public Health. 1918;8(10):741–4.

32.        Marano G, Vaglio S, Pupella S, Facco G, Catalano L, Liumbruno GM, et al. Convalescent plasma: new evidence for an old therapeutic tool?

33.        Cheng Y, Wong · R, Soo YOY, Wong · W S, Lee · C K, Ng · M H L, et al. Use of convalescent plasma therapy in SARS patients in Hong Kong. Eur J Clin Microbiol Infect Dis. 2005;24:44–6.

Blog COVID-19 Virology

Viral Disease Emergence: Separating the Fact from the Fiction

Viral diseases have shaped human history. A sudden emergence has the power to cause huge social changes, like ones we’re currently experiencing. But how do they do this? What causes a virus to jump, or ‘spill over’ into a new species?

What is an emerging virus and how do they emerge?

An emerging virus is a virus which has entered a new population where it previously didn’t exist or is expanding its geographical range. Global disease emergence is increasing for many reasons and we’ll discuss why this is occurring and why most emerging viruses that normally infect animals are now infecting humans.

What’s important to remember is there are no singular reasons for viral disease emergence, and we might never know what occurred to cause a disease to break into new populations. But there’s many ways this can happen, ranging from the virus’s genetics all the way through to human-environment interactions. Here we’re going to focus on RNA viruses as these are the viruses which most commonly cross species barriers1. Let’s start with the genetics first.


Enzyme Errors

RNA viruses contain an enzyme called RdRp. This enzyme replicates RNA. RNA is a form of genetic code like DNA, so it encodes genes. However, RdRp is prone to making mistakes, it might miss a base, it might use the wrong one and its common for this to happen. This means a virus can be produced with different properties, this can range from being able to target a new cell type to replicating faster. One case where this occurred was during the 1918 Spanish Flu, where a mutation allowed the virus to replicate in tissues outside the respiratory tract2.

A picture containing clock

Description automatically generated
Figure 1: Replication of RNA with mutation highlighted in yellow.

Reassortment of segmented genomes

Reassortment is the process where genetic material might get ‘mixed up’. When a cell is infected with two different but closely related viruses there’s a chance this might occur. Think of it like mixing your favourite drinks. It could work, and you might have a new flavour, or it might not! It’s easier for segmented genomes, so the genetic code is in multiple segments and is common in viruses like influenza. H1N1 is an influenza virus which is made up of bird, pig and human influenza strains3.  

A close up of a logo

Description automatically generated
Figure 2: Viral co-infection of two viruses (A and B). Inside cell shows 2 different genomes, with reassorted virus containing genomes of both virus A and B having egressed.

Recombination of RNA genomes

Recombination is a random event which occurs when RdRp, the enzyme which makes new RNA, falls off the genome its copying onto a different one. It ultimately will produce an RNA genome which is a combination of two different viruses. This is another common event and many virus families have evidence of this occurring, including Herpesviruses, HIV and even Coronaviruses4,5

A close up of a map

Description automatically generated
Figure 3: Recombination of RNA genome in 5′ to 3′ directionality.


Changes in weather

Climate change isn’t only impacting our weather, it’s also changing disease distributions through temperature but also causing changes in host territory. Ultimately this changes how we interact with hosts of viruses as well as their biology. For example, Japanese Encephalitis Virus (JEV). This virus is carried by mosquitoes, so a higher temperature alters host territory as well as allowing for mosquito development to occur where it didn’t previously. This is because mosquitos have a minimum temperature where development will occur, and for the mosquito which carries JEV its 22-23 °C. However, viral diseases can have a minimum transmission temperature, and JEV has one of 25-26 °C. If more countries have temperatures above this range, then the virus can be transmitted in new populations. What this all means is as global temperatures rise it’s very likely countries will experience diseases they haven’t previously6

Bush meat and live animal markets

Consumption of bush meat and live animal markets remove natural barriers in place, meaning that close contact between animals and humans now occurs. Outbreaks may occur due to consumption of an animal which died of a disease, and not of more natural causes. This is how Ebola outbreaks have started before. However, it is important to consider the socio-economic conditions found within regions where consumption of bush meat occurs. Protein sources in these regions can be expensive and the local population may not have the choices we do7. Reducing disease emergence from live animal markets can be done safely by reducing inter-species interactions, essentially handling the animals less and making the markets less crowded. However, it could also be done through limiting the days of operation8.  

Korea, Wet, Market, Meat, Seafoods, Vendor, People
Figure 4: Wet market in South Korea. Source: Stocksnap, Pixabay.

Changing land use and farming practices

Deforestation of land for farming and urban development is forcing disease hosts to come into closer contact with humans, one example where this is occurring is Australia. Here, horse farms are traditionally where fruit bats reside however urbanisation has resulted in loss of the natural habitat, forcing greater interactions with the human population9.  

So, there we have it. Several mechanisms on how viruses can emerge into human populations. But what about SARS-CoV-2? Well, the jury’s still out. Though early cases were linked to a seafood market many weren’t, indicating the source of the virus likely wasn’t here. In the meantime, scientists will be hard at work hoping to solve many puzzles, including this!  If you have any questions about what was discussed drop us a message below or on Facebook, Twitter or Instagram and we’ll get back to you.

For more information on the origins of SARS-CoV-2 read our blogpost breaking down a Nature paper by Dr Jordan Clark here

For more information on viral disease emergence check out ‘Spillover’ by David Quammen. 


1.J Woolhouse, M. E., Adair, K. & Brierley, L. RNA Viruses: A Case Study of the Biology of Emerging Infectious Diseases. Microbiol. Spectr. 1, 10.1128/microbiolspec.OH-0001–2012 (2013). 

2.Taubenberger, J. K. The origin and virulence of the 1918 ‘Spanish’ influenza virus. Proc. Am. Philos. Soc. 150, 86–112 (2006). 

3.Vijaykrishna, D. et al. Reassortment of pandemic H1N1/2009 influenza A virus in swine. Science 328, 1529 (2010). 

4.Fleischmann, W. J. Medical Microbiology. (University of Texas Medical Branch, 1996). 

5.Su, S. et al. Epidemiology , Genetic Recombination , and Pathogenesis of Coronaviruses. Trends Microbiol. 24, 490–502 (2016). 

6.Wu, X., Lu, Y., Zhou, S., Chen, L. & Xu, B. Impact of climate change on human infectious diseases : Empirical evidence and human adaptation. Environ. Int. 86, 14–23 (2016). 

7.Kurpiers, L. A., Schulte-Herbrüggen, B., Ejotre, I. & Reeder, D. M. Bushmeat and Emerging Infectious Diseases: Lessons from Africa BT  – Problematic Wildlife: A Cross-Disciplinary Approach. in (ed. Angelici, F. M.) 507–551 (Springer International Publishing, 2016). doi:10.1007/978-3-319-22246-2_24 

8.Karesh, W. B., Cook, R. A., Bennett, E. L. & Newcomb, J. Wildlife trade and global disease emergence. Emerg. Infect. Dis. 11, 1000–1002 (2005). 

9.Plowright, R. K. et al. Urban habituation, ecological connectivity and epidemic dampening: the emergence of Hendra virus from flying foxes (Pteropus spp.). Proceedings. Biol. Sci. 278, 3703–3712 (2011). 

Image may contain: 1 person, text
Written by Charlotte Rigby.

Blog Virology

Bats and Viruses

The 17th of April marks International Bat Appreciation Day. This is because bats begin to emerge from hibernation at this time of year. Despite all the bad press bats get, especially in light of the coronavirus outbreak, they actually play an important roll in nature.

Bats are insectivorous creatures, and reduce the number of many annoying insects. Did you know a bat can eat up to 1000 mosquitoes in an hour?!

Bats are fascinating mammals. Unique in several ways, including their ability to fly, they also have a harmonious relationship with many viruses that can be devastating to humans.

Viruses such as Ebola virus, Coronaviruses (e.g. SARS), and Hendra virus are examples of Zoonotic viruses that are found in bats. Zoonotic is the term for viruses that jump species barriers or “spill over”, i.e. from bats to humans. These viruses often cause no physical symptoms in bats, and due to their lifestyle of roosting in large colonies, can spread easily through large populations. 

Wynee and Wang (2013) from CSIRO Australian Animal Health Laboratory, Geelong, Australia, released an open-access article in PNAS asking whether bats are friends or foe. They remind us that bats are just as diverse as the viruses that infect them. The picture below, also found in their article shows different species of bats, and electron microscope images of the viruses that can infect them (1).

“Bats are diverse, as are the viruses that infect them.

The Chinese horseshoe bat (ARhinolophus sinicus) is one of many Rhinolophus sp. that are a natural host of SARS-like coronaviruses (B; scale bar 100 nm). The spectacled flying fox (CPteropus conspicillatus) along with other Pteropus sp. are reservoirs for the Australian Bat lyssavirus (D; scale bar 100 nm). A number of African fruit bats including Hypsignathus monstrosus (E) have been found to host Ebola virus (F; Ebola Reston, scale bar 200 nm). The Malayan flying fox (GPteropus vampyrus) is the natural host of Nipah virus (H; scale bar 200 nm). All four pteropid Australian bat species including Pteropus alecto (I) have been found to carry Hendra virus (J; scale bar 200 nm).”

The reasons for why bats can tolerate these viruses are not fully understood, but there are some characterised differences in their immune system response that are thought to account for this (2)

One relatively well supported hypothesis for the underlying reason is due to their flight, which puts a large amount of stress on the body. Evidence suggests that they have managed to deal with this stress by the evolution of an altered immune response, which then allows the bats to control viral replication whilst minimising any counter-productive over response (3)

All of this is great for bats, but becomes a problem for us when these viruses jump into the human population. Our immune systems respond differently to bats, and this results in the diseases we see. So, what can we do?  

To some, the obvious response may be to exterminate wild bat populations. Even without considering the obvious moral objections to this, it would also be counter-productive for many reasons. Bats are incredibly important to ecosystems, playing crucial roles in pollination, insect control, and seed dispersal (4)

In order to reduce the chances of spill over events, it is important to look at the ways that human activity brings us into more frequent contact with bats, such as deforestation and the possibility of bats passing diseases to us via animals in our food supply chains. We can then find ways to minimise these.  

In the meantime, researchers can learn a lot from the differences between the immune system response of humans and bats, in order to identify ways in which ours is not effective in tackling viruses. (2)

We should appreciate these wonderful mammals, understand the ways they can be dangerous, and learn to live alongside them whilst minimising contact. It will suit both us and them!


1: Bats and Viruses: Friend or Foe? – Wynne & Wang, 2013

2: Innate Immune Responses of Bat and Human Cells to Filoviruses: Commonalities and Distinctions – Kuzmin et al, 2017 

3: Novel Insights Into Immune Systems of Bats – Banerjee et al, 2020 

4: Education to Action: Improving Public Perception of Bats – Hoffmaster et al, 2016 

Written by Ben Jones
Blog COVID-19 Mental Health

Staying Sane and Safe During the Lockdown


Humans are naturally social animals so it’s no surprise that Isolation is linked to lower mood and poor mental health. It can be hard to maintain relationships during a lockdown but they’re very important for our wellbeing.

Take time out of your day to talk to the people in your household, try using video call software to reach out to friends and colleagues or even just send a good old fashioned e-mail or text. Now could be a good time to join an online community too, if you have a hobby, chances are there are lots of other people who do too, why not join a forum or discussion group and make some new friends?

Get Active

Exercise has been shown to increase mood and feelings of wellbeing in both the short and long-term. Getting the blood flowing releases feel-good chemicals called endorphins for a natural boost. Think how great you’ll look and feel when this is all over.

You are allowed one outside exercise session per day, it can be a great chance to get out of the house and see some nature (which also boosts mental wellbeing!). If you’re self-isolating and can’t leave the house, there are plenty of workouts you can do from your bedroom, your home gym or even your armchair!


Learning a new skill is a great way to boost your self-esteem and can give a sense of direction and purpose. Learning new skills also helps to keep your brain healthy and your mind active, fighting off those lockdown blues.

There are lots of free and accessible online courses for nearly anything you could be interested in. Learn a language, an instrument, a new recipe or a DIY job. It doesn’t matter what it is you learn, that’s up to you, just that you’re interested enough to keep it up and that it’s challenging enough to keep you engaged without being so difficult you give up. Don’t worry about earning certificates unless you want to, it should be fun, not a chore!

Check out Coursera, future learn and edx, for example.


Acts of giving and simple kindness can increase your mood and give you a sense of purpose and self-worth. Plus, it makes someone else feel good too as an added bonus!

You can start small and reach out to help colleagues or friends who might just want someone to talk to. There are also plenty of volunteer schemes to get involved with if you’re symptom free and want to help with the crisis.

GoodSAM can help you find volunteering opportunities during the coronavirus outbreak.

Pay Attention

Mindfulness is paying attention in the present moment: to your body, your thoughts, the world around you and how you’re feeling. It can boost mood and make you appreciate life more.

The lockdown will affect us all differently, pay attention to how you feel and take time each day to check in with yourself.

Some mindfulness apps to get you going: Headspace, Calm, Aura, Stop, Breath and Think, Insight Timer. Or why not try out some Yoga – be active and mindful all at once. We like Adriene and Kassandra.

Connect, Get Active, Learn, Give and Pay Attention

If you do notice your mental health suffering, don’t feel like there’s nothing you can do. There are still plenty of services that are remaining open during this lockdown because mental health is just as important as physical health. If you don’t feel right, don’t feel like you have to suffer alone.

A final note: self-care is incredibly personal, and you should take these only as suggestions alongside things you know work well for you. None of us are obligated to come out of the end of this with new skills, a summer body, or anything else. If you keep yourself feeling well and functioning, you are doing well in this stressful time.

If you need support here are some resources:

Written by Mark Platt

Blog COVID-19 Research Summaries

Coronavirus: A natural phenomenon or a man-made weapon?

Often during virus outbreaks, conspiracy theories arise which purportedly explain the emergence of the virus. These range from deliberate government release as an agent of population control to Illuminati concocted plagues designed to disrupt our way of life in order to usher in the New World Order. The Covid-19 pandemic is no exception and there has been a wave of conspiracy theories relating to SARS-COV-19, the virus behind Covid-19. Writing in NatureKristian G. AndersenAndrew Rambaut , Ian Lipkin, Edward C. Holmes  and Robert F. Garry sought to investigate the origins of SARS-COV-2, not only in order to dispel some of these theories, but also because during a pandemic it’s important to know where the virus came from as this may inform future preventative strategies. 

Read the article yourself here:

The authors first start by analysing the receptor binding domain (RBD) of the SARS-COV-2 spike protein. This protein is present on the outside of the SARS-COV-2 virus particle and is responsible for the binding of the virus to the receptor ACE2, which is found on the surface of cells. It’s this protein which the virus exploits to enter our cells, and it’s been shown to be very important for coronavirus host range and pathogenicity. 

Spike proteins are present on the outside of the virus particle which bind with to ACE2 receptors on the outside of our cells.

While it’s clear the SARS-COV-2 RBD is able to successfully bind the ACE2 receptor found in human, ferret and other similar species, this interaction is not exactly perfect. In fact, SARS-COV-2 binds with less efficiency than SARS. If a super plague was generated in a lab, computational studies could have been carried out to formulate better binding of ACE2, therefore improving the infectivity of the pathogen. Pretty sloppy work, Illuminati. It’s much more likely that the RBD of SARS-COV-2 evolved to bind a human-like ACE2 and has been acted upon by natural selection. What do I mean by a human-like ACE2? Remember that we share about 98.5% of our DNA with chimps and around 85% with mice, so its highly likely that SARS-COV-2 evolved to infect a similar, but different species, which provided it with some limited ability to infect humans. Once this human transmission was set up natural selection can allow the virus to adjust to humans in order to infect us more efficiently – more on that later. 

There’s also good evidence that SARS-COV-2 wasn’t generated in a lab due to the fact it doesn’t appear to have been designed according to other viral “reverse genetics” systems. Reverse genetics systems are what scientists use to produce genetically manipulated viruses in the lab. These techniques employ the use of the virus genetic material which has been probed and packaged through a variety of molecular techniques which allows infectious virus to be generated. The authors make it quite clear that SARS-COV-2 shows no evidence of being generated by the use of these existing virus reverse genetics systems. So, if SARS-COV-2 is naturally occurring, how did it infect humans in the first place and start the whole pandemic off? 

The authors provide two hypotheses:

1) The virus arose in animals and, through natural selection, acquired the necessary genetic changes needed to infect humans, whereupon it jumped the species barrier and infected people. 

 2) The virus jumped from an animal species into humans, whereupon it spread through the human population and, through natural selection, acquired the genetic changes needed to successfully cause a pandemic. 

By comparing the genetic material of SARS-COV-2 and other coronaviruses which have been sampled from different species, it has been shown that SARS-COV-2 shares high sequence similarity with those coronaviruses found in bats. The Huanan market in Wuhan is considered to be ground zero for this pandemic and it is known that bats were stored and sold here, in addition to a myriad of other species. It is therefore highly probable that one of these species was host to the progenitor of SARS-COV-2, which then found its way into the human population. 

Interestingly, the RBD of SARS-COV-2 is unlike those found in bats but shares high homology with those found in pangolins. Pangolins are an endangered, and very cute, little species of mammal which are the most illegally trafficked animals in the world. Coronaviruses isolated from these creatures exhibit RBDs with high similarity to those found in SARS-COV-2. Pangolins are also thought to have been present at the Huanan market in Wuhan. 

A very cute, pangolin.×360/p066n3f4.jpg

Coronaviruses are also known to undergo genetic recombination, in which they swap genetic material. This happens when two different coronaviruses find themselves infecting the same host. It’s therefore highly likely that SARS-COV-2 arose from a recombination event between two coronaviruses, possibly from bats and pangolins, which was then able to jump into humans. 

There’s one more feature of SARS-COV-2 that the authors draw attention to: the addition of a polybasic cleavage site which sits between the two subunits of the spike protein. This site is unique to SARS-COV-2 and may result in efficient cleavage by cellular proteases such as furin. This sounds quite complicated. Simply, the virus has evolved a site in the portion of the virus which is responsible for invading our cells which improves its ability to function, therefore making it more infectious. 

We see such adaptations in avian influenza all the time – they arise through natural selection when flu spreads through chicken populations. Such adaptations result in the generation of highly pathogenic bird flu strains and are a major public health concern. Mutations of this type which affect the spike protein subunit junction have also been found in nature many times before. These inserted residues also change the structure of the spike protein slightly in a way that the authors hypothesise may help the virus evade the host immune response. 

“OK, so where did this genetic change come from? Is it possible for this to happen in the lab? Can it happen in nature?” 

Simply, both are possible, but one is less likely. Looking at our two theories it’s entirely possible that this mutation, which likely allows for increased pathogenicity, arose during repeated human to human transmission, similar to what we see in birds with flu. This would mean that, after making the jump from bats/pangolins/unknown species to human, SARS-COV-2 spread through the human populace, acquiring this mutation, and then setting off the chain of events which led to the pandemic. We see this in SARS often, in which the virus jumps from camels to humans and then spreads from human to human for a short period. Crucially SARS has not yet been able to sustain its human-human transmission, whereas SARS-COV-2 has. It’s also possible that this mutation arose in the progenitor to SARS-COV-2 in an animal host. To have arisen this would require sustained transmission between hosts that are in high density and have human-like ACE2 receptors. 

Both theories are plausible…

What isn’t as likely is that the virus gained this adaptation in a laboratory setting. In labs around the world viruses are routinely grown in cell culture. Viruses are introduced to cells in culture, allowed to grow, and eventually harvested. This is known as “passage”. For this mutation to arise in cell culture the virus must have been serially passaged through cells which contain a human-like ACE2 receptor. While these passages take place, the virus is continually evolving, so much so that serial passage in cells eventually leads to viruses getting so good at infecting cells in culture they become worse at infecting whole animals. It’s theoretically possible that the virus could have been serially passaged through an animal, one which contains sufficiently human-like ACE2, however this has never been documented. 

It is very unlikely that SARS-COV-2 originated in a laboratory setting

…and it doesn’t exhibit the genetic fingerprints we’d expect a genetically modified super plague to exhibit. Unfortunately, at the moment all we can do is theorise about its origins until the exact host, or progenitor virus, is found. There are a staggering number of viruses present in nature which we simply haven’t discovered yet (think of a tip of the iceberg kind of thing) which are currently quietly circulating in animals, and possibly humans, throughout the world. The conditions which we saw at the Huanan market in Wuhan in which various different exotic animals are stacked, live and dead, in cages in close proximity to each other, and humans, makes the perfect melting pot for these pandemics to arise. Furthermore, as humans clear more habitat, and as global temperature rise allowing vector species such as mosquitos and midges to extend into higher latitudes, it’s a matter of time until this happens again. While this pandemic is ongoing, the next one in line is lurking out there and it’s vitally important that we learn what we can from SARS-COV-2 so that we are prepared when it finally emerges. 



Coronavirus: A natural phenomenon or a man-made weapon? Read a lay summary of @NatureMedicine article: The proximal origin of SARS-CoV-2 by @K_G_Andersen, @arambaut and @edwardcholmes and co. Written by @jordandoesflu with @thescisocial #covid19 #sarscov2 #mythbusters

Written by Dr Jordan Clark


Misinformation: Believe, Share, Avoid?

Misinformation and fake news are a modern day problem driven by the powers of social media. However, as we live in a world experiencing a pandemic, misinformation could put people at risk. Scientists have come together to discuss the public health implications of misinformation 1, 2. These scientists highlighted that reputable information provided by the World Health Organisation (WHO) and the US Centers of Disease Control Prevention (CDC) had engagement values in the hundreds of thousands. Compare that to clicks on conspiracy sites and hoax information which had a whopping 52 million engagements. Clearly, there is a problem with the uptake of unverified information.

During the Human Immunodeficiency Virus (HIV) epidemic which emerged in the 1980s, the information available to the public was plagued with conspiracy theories, rumours and misinformation. Occasionally you will still hear that “HIV does not exist”, despite much evidence confirming the contrary. Mian & Khan remind us how these false arguments influenced government policy during the South African HIV epidemic in early 2000. Governmental denial of the HIV and the effectiveness of its treatment, resulted in the refusal of medication for pregnant women. This ultimately led to unnecessary mother-to-child virus transmission, costing over 300,000 lives 3, 4.

This is not the only time misinformation has swayed our views during an outbreak, throughout the ebola virus outbreak in 2014, social media influenced the social views of healthcare workers and created additional challenges in the effort to control the epidemic 5,6.

American scientists designed a study to determine how twitter bots and “trolls” contributed to online health content. They found that misinformation disseminated by twitter bots masquerading as legitimate users created false equivalency, which in turn eroded public consensus on vaccination 7. As a consequence, the vaccination programme was stunted. Thus demonstrating how misinformation can have detrimental effects on population health. A concern… I think so.

So, have we learnt from the past?

It appears not. Did you know that the “coronavirus was artificially created in a lab by a rogue government with an agenda” originated from social media accounts and websites, where no evidence for the statement was supplied. Please read our breakdown on the Nature article supporting why the coronavirus was not created in a lab, or… read the article yourself!

We want to give you the skills to call information out, and keep that finger far, far away from the share button, except for ours of course. It is our social responsibility to make sure erroneous and dangerous information is not propagated. Especially when we live in a world where the wrong information is shared more than that which will benefit us. Will you join us in ending this misinformation crisis?

How to avoid it?

In short – you can’t. Unfortunately, misinformation will continue to be an entity that exists for as long a social media does. What you can do is learn how to identify misinformation, question it, and challenge it. This all starts by understanding what good quality information really is.

1. If you’re not sure – don’t share

The unknown drives fear and stress which can impact our decision making. In this unprecedented time, it is easy to click, read and share without considering how accurate the information really is. Fake news is often interesting to read and framed to look credible with a name drop from a ‘reliable’ source or institution. It is likely that by the time you come across the post, it has been shared tens or hundreds of times, lending credence to its faux authenticity. Always consider the source of this material. If there’s a reputable name drop, fact check and search the original website or article for yourself. If you can’t find the source material or you’re not sure, don’t share. 

2. Consider the source

Before you believe the words you read, question them. In academia, it is gold standard to reference where you got your information from, this must always be from a credible or peer-reviewed source. To write a sentence without referencing it would imply that; it is common knowledge, you are the first person to say this, or it is your idea. Referencing is a way to acknowledge the work of others in your work, argument or ponderings. It provides integrity to your discussion and crucial evidence to support your point. It is commonplace to reference papers or articles that have been published by a scientific journal. In order for a paper to be published, it must be peer-reviewed by other experts in the field. This process ensures the work is necessary and relevant, robust in design and most importantly, offers reliable data.

The next time you read something, think about who wrote it and ask; what are the author’s credentials and what is the evidence?

3. For the geeks… be cautious of preprint

The way research is published is forever changing. Researchers now have a platform where they can publish their findings without peer review. If you’re into science, you may have come across research yourself on platforms such as BioRxiv and MedRxiv. This is great for researchers, scientists and hobbyists to browse the most recent work, but preprint is a double edged sword. It is important to bear in mind that the article has not yet been assessed for its publication suitability. Remember, the peer review process ensures reliability and prevents poorly conducted research from being published. This is not to say that research available in a preprint journal is not reliable, but the reader should remain cautious when drawing conclusions from the evidence.

4. We are forever learning

We are learning new things every single day. The pursuit of science and research works to prove and disprove our current understanding and so guide our thinking. Whilst this dynamic is exciting for the field, the result may be a surge of ever-changing information. This is especially obvious in a pandemic situation, as governance and policy are rapidly adapting to keep up. Although the growing wealth of knowledge may be vital to how we move forward as a nation, it can be extremely frustrating and stressful for individuals. We understand that it is difficult to filter through what is and isn’t useful, what to read and what to do next.

The internet is a minefield of information, it is important that we provide the people around us with the skills to read information, digest it and make an informed decision on whether it is reliable or not. Like the virus itself, we must stop the spread of misinformation.

The Science Social would like to help you remain aware of what’s current, challenge your sources and give you the opportunity to engage in the conversation.


To guide you in your quest for trustworthy information:

The Conversation

The Conversation provides news and views sourced from the academic and research community. If you want to keep up with what’s going on, this is a great place to be.

World Health Organisation

The World Health Organisation is perhaps the most trustworthy and up-to-date site. As an organisation responsible for international public health, there are links and features covering all manner of public health issues. The link below will take you directly to a COVID-19 dashboard covering issues and questions as they arise.

NHS (or equivalent healthcare service)

The NHS website provides guidance on symptoms and action to take if you are concerned you may have COVID-19. Always check with your national healthcare provider and follow the recommended advice.


The government website has a comprehensive repository of information relevant to the UK. It details current guidelines and government actions which are, at present, updated daily.


  1. Mian, A., Khan, S. Coronavirus: the spread of misinformation. BMC Med 18, 89 (2020).
  2. The Lancet, Emerging understandings of 2019-nCoV, The Lancet, Volume 395, Issue 10221, 2020, Page 311, ISSN 0140-6736, (
  3. Bateman C. Paying the price for AIDS denialism. S Afr Med J. 2007;97(10):912
  4. Nlooto M, Naidoo P. Traditional, complementary and alternative medicine use by HIV patients a decade after public sector antiretroviral therapy roll out in South Africa: a cross sectional study. BMC Complement Altern Med. 2016;16:128.
  6. Chou WS, Oh A, Klein WMP. Addressing Health-Related Misinformation on Social Media. JAMA. 2018;320(23):2417–2418. doi:10.1001/jama.2018.16865
  7. David A. Broniatowski, Amelia M. Jamison, SiHua Qi, Lulwah AlKulaib, Tao Chen, Adrian Benton, Sandra C. Quinn, and Mark Dredze, 2018: Weaponized Health Communication: Twitter Bots and Russian Trolls Amplify the Vaccine Debate American Journal of Public Health 108, 1378_1384,

Misinformation: Believe, Share, Avoid? Written by @reebola95 with @thescisocial #nofakenews #notsuredontshare

Written by Rebee Penrice-Randal