As we delve into this new series – a scientists’ toolkit, we start with the microscope. From its history through to its applications. Its uses are endless and we will show you why!
There are many different types, from light to electron, some are binocular others are not. There are digital, stereo, USB and pocket microscopes. Here are just a few of them below. Depending on the purpose different microscopes may be used, it is just about picking the right one for the job! (7)
Digital light microscope: invented in Japan in 1986. Uses principles of light microscopy, but connects to a computer similar to a printer/ Allowing for ease of observation. (7)
Stereo light microscope: Also known as a dissecting microscope, is used to view images three dimensionally by having 2 optical paths. (7)
Electron microscope: more powerful than a light microscope, and allows scientists to see things at nano size, there are two types; the scanning and transmission type. (7)
Microscopes are used by scientists for lots of different reasons- primarily to observes microscopic structures, and changes that cannot be seen by the naked eye. Allowing scientists to understand structure and physiology. This can help when trying to understand normal processes in the body, as well as changes due to disease, the effect of different therapies on the body, and possible therapeutic targets.
They can be used to visualize structures, conduct cell counts, diagnose disease and conduct qualitative scoring.
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:
Measles Mump and Rubella Vaccine
If you are big on your travelling, you may have had the Yellow Fever Vaccine or the oral typhoid vaccination.
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.
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.
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.
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.
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 Medicine50, 110-120, doi:10.1080/07853890.2017.1407035 (2018).
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.
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.
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.
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.
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.
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. Science328, 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).
We’ve been sent some great questions already and wanted to start by answering those most commonly asked. If you have any questions for us to field, email us and we’ll investigate 🕵🏻 🔍 or comment below! ⬇️
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 Nature, Kristian G. Andersen, Andrew 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.
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.
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.
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 https://thesciencesocial694680041.wordpress.com/?p=104
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.
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 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. https://theconversation.com/uk/covid-19
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.
The Lancet, Emerging understandings of 2019-nCoV, The Lancet, Volume 395, Issue 10221, 2020, Page 311, ISSN 0140-6736, https://doi.org/10.1016/S0140-6736(20)30186-0. (http://www.sciencedirect.com/science/article/pii/S0140673620301860)
Bateman C. Paying the price for AIDS denialism. S Afr Med J. 2007;97(10):912
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.