Welcome to Naturally Speaking’s blog series on COVID-19. This post is about the virus and the severity of infection. If we don’t answer all your most pressing questions, please feel free to ask them in the Comments section below – we’ll do our best to respond. We’ll also aim to provide any updates as advice and knowledge evolves. For extra details and links, click here to read more about the virus and about severity of infection.

The Virus

Q. What kind of virus is causing COVID-19?

A. The virus causing COVID-19 belongs to a large family of viruses, known as coronaviruses, which infect a range of mammals and birds. In humans, there are four seasonal coronaviruses that circulate widely, generally causing mild illness; these account for around 15% of common colds. In recent years, coronaviruses that normally infect animals have caused a few more serious disease outbreaks in people. The virus associated with an outbreak of severe acute respiratory syndrome in 2002-2004 was identified as a coronavirus and named the SARS coronavirus (SARS-CoV). Another novel coronavirus, known as Middle East Respiratory Syndrome-related coronavirus (MERS-CoV), has caused intermittent outbreaks of serious disease since 2012. The COVID-19 virus has been identified as the seventh coronavirus to infect humans. Genetically, it is related to the virus that caused the earlier SARS outbreak (sharing around 80% of their genetic material) and so has been named SARS coronavirus 2 or SARS-CoV-2.

Q. What does this virus look like?

A. The COVID-19 virus is roughly spherical in shape and is coated with spikes of protein. Coronaviruses are named for their distinctive appearance whereby the spikes cause the virus to resemble a solar corona (corona is Latin for crown) when viewed under a powerful microscope. Laid out side by side, 10,000 of these viruses would only span around a single millimetre. The spike proteins allow the virus to bind to and infect host cells. However, these same spike proteins are also the part of the virus ‘seen’ by the immune system and so may be important for vaccine development. Below the spikes is a layer of fatty (lipid) membrane; this membrane can be disrupted by soap and alcohol gels which is why handwashing is an important part of disease control. Within this spherical membrane is the virus’ genetic material, or genome. While humans have a DNA genome consisting of over 3 billion base pairs, the SARS-CoV-2 virus has an RNA genome with just under 30 thousand nucleotides – small compared to ours, but actually pretty big for an RNA virus genome.

Q. Where did the COVID-19 virus come from?

A. We can be very confident that the COVID-19 virus originally comes from an animal source, although it is now spreading from person to person. Bats and pangolins (scaly ant-eaters) have both been suggested as possible sources. However, so far no virus found in animals is similar enough to be the direct ancestor of the virus in humans and the exact origins of this outbreak remain unknown.

It has been suggested in the news that the virus originally escaped from a lab or was genetically engineered and intentionally released, but there is no evidence for this based on the genetic material of the COVID-19 virus. Genetic, serological and epidemiological data are all consistently pointing to a start of the outbreak in November/December 2019 in China.

Q. Can humans transmit the COVID-19 virus to animals?

A. Various animal species appear to have been infected with SARS-CoV-2 as a result of human-to-animal transmission, while the susceptibility of others has been assessed experimentally. It remains to be determined exactly how susceptible different species are, whether infected species will suffer illness, and whether there is a risk that onward transmission within these species will become established. 

Q. Has the COVID-19 virus mutated, and if so, has this affected disease severity or the transmissibility of the virus?

A. Mutations are changes to the genetic code that arise naturally as viruses replicate – they are perfectly normal and most do not change the characteristics of the virus. Occasionally mutations may change virus traits such as pathogenicity or transmissibility; however, there is no clear evidence that genetic changes to the COVID-19 virus have altered characteristics of the virus during the outbreak.

Severity of Infection

Q. Why do some people respond better or worse to the virus than others? 

A. We don’t know yet. Clear risk factors include age, diabetes, high blood pressure, obesity, respiratory problems/ asthma, immunocompromised/HIV and other comorbidities, which are present more in the elderly. Men also seem to have more serious disease outcomes than women, with twice as many COVID-19-related deaths, although the reasons for this are not fully understood. It has been suggested that these differences might be due in part to overall health differences between men and women, and/or sex-related differences in immune response.

An excellent review paper (still in pre-print) recently summarized the characteristics of nearly 17,000 patients that presented with severe COVID-19 in the UK. The median age of those who presented to hospital with serious cases was 72, with the middle 50% of cases (interquartile range) aged between 57 and 82. The main comorbidities were cardiac disease (29%), diabetes (19%), non-asthmatic chronic pulmonary disease (19%), and asthma (14%). Just under half of the overall hospitalized cases included in the study (47%) had no known comorbidity. A higher proportion of cases were in men (60%), who also had higher levels of mortality.

Q. What is the risk of COVID-19 for children and young adults? How important are they in spreading the virus?

A. Younger people are much less likely to become seriously ill or to die from COVID-19. However, children seem to be as likely to become infected as the rest of the population, with similar viral loads. Children could therefore be playing an important role in the transmission of the disease, although this requires further study. Given the current uncertainty around the role of children in COVID-19 virus transmission, it is difficult to evaluate what kind of impact school closures (and re-openings) might have on reducing virus spread, although it is currently believed that this is less important than other social distancing measures.

Q. There seem to be conflicting messages about asthma being a risk factor for COVID-19. What is the current evidence? 

A. Given that COVID-19 has been primarily thought of as a respiratory disease, it is perhaps surprising that asthma and other chronic respiratory diseases have so far not been among the most common comorbidities in reported cases. It seems that those with mild or moderate asthma are unlikely to be more at risk of becoming infected, or of having more severe disease. Consequently, simply having asthma does not necessarily mean that people should be ‘shielding’ (severely restricting their contact with other people to reduce their chances of becoming infected). The British Thoracic Society provides guidance on making this decision. Those with severe asthma, and particularly those on certain types of medication, are considered in the group at very high risk of severe illness from coronavirus. UK medical guidance encourages those with asthma to continue taking their medication, with the goal of keeping their asthma in check. 

Q. Is COVID-19 more or less severe than the SARS coronavirus? How does it compare with the flu virus?

A. COVID-19 seems to be more contagious, but with less severe symptoms than the 2003 SARS virus. The case fatality rate for SARS was estimated at around 15%. It is difficult to estimate the overall case fatality rate of COVID-19 because most of the less severe infections go unreported, and strategies for testing vary widely across the world. As testing increases, so too will the number of confirmed cases – including those that are less severe – which will lead to a decrease in the case fatality rate. The best available current estimate of the fatality rate for overall infected cases is about 1.4%.

Feature image is original artwork by PhD candidate Chiara Crestani, ©2020.