COVID Q & A – The Virus & Severity of Infection

COVID Q & A

Scientifically-informed, data-driven answers to your burning questions about the coronavirus pandemic

Post #3: The Virus and Severity of Infection

Welcome to Naturally Speaking’s weekly blog series on COVID-19. This third post about the virus and infection severity comes in two flavours:

  1. Short and sweet – bite size summary
  2. Hungry for more? Look no further! This version includes a bit more detail and links to further resources.

If we don’t answer all your most pressing questions, please feel free to post 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.

The Virus

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

A. It seems likely 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, but the exact origins of this outbreak remain unknown.

Diseases that are transmitted from animals to humans are known as ‘zoonoses’. Other recent coronavirus outbreaks are also thought to have zoonotic origins, with bats representing the main reservoir from which the virus has been transmitted to humans via another intermediate host. For instance, the 2003 SARS coronavirus is believed to have jumped to humans from bats via the civet cat, since some coronaviruses isolated from civet cats have been almost identical to the SARS coronavirus (sharing 99.8% of their genome). Finding nearly identical viruses in a suspected host species is taken as strong evidence of that species being the source. In order to pin-point the likely source, however, many samples need to be taken and sequenced, which can take a long time (and a certain degree of luck!).

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. Have changes in the COVID-19 virus’ genetic material affected the severity of the disease?

A. Viruses mutate all the time as they divide and replicate, which is normal. However, there is so far no evidence that the virus has changed in a way that affects the severity of the disease or the potential success of treatments or vaccines that are under development. In short, a vaccine should be effective everywhere and there is no reason to believe the virus is evolving rapidly enough to reduce the protection provided by the vaccination. 

Because mutations happen at an average speed over time, accumulated changes in the genetic material of the virus can be used to track how the virus has spread. These changes are being tracked almost in real time using whole genome sequences from the viruses, which are being made publicly available so that scientists worldwide can monitor how the virus is evolving. These data can also help to understand how many independent introductions of the virus have occurred into an area and whether introductions continue to occur after certain interventions (like travel bans) have been implemented.

Severity of infection outcomes

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, respiratory problems/asthma, immunocompromised/HIV and other co-morbidities, which are more often present among the elderly. On average, men also seem to have more serious disease outcomes than women, although the reasons for this are unknown. Only a small proportion of people who develop symptoms will become seriously ill to the point of requiring hospitalization (about 30%), and only 2.4% require critical care.  

Everything we know about risk factors for severe illness comes out of the last few months from cases in China and more recently Italy and other European countries. These populations are not necessarily transferable to the UK (or elsewhere). However, general risk factors appear consistent globally (age, respiratory problems, etc.). Gender-related differences observed in China are also being corroborated in the UK and the US. It has been suggested that differences in disease outcome between men and women might be in part due to differences in immune response. 

In younger people, severe illness (and death) sometimes manifest, although they are much less likely to become seriously ill. That being said, children seem to be as likely to become infected as the rest of the population, and could therefore be playing an important role in the transmission of the disease. It has been hypothesized that disease severity is linked to something called a cytokine storm – an excessive inflammatory response generated by the body’s immune system to try to get rid of the virus. The under-developed immune systems of children may be less likely to develop this type of immune response, consequently protecting them from some of the most harmful effects of the virus that ironically come from the body’s own ‘protective’ response.

Another factor which might contribute to differences in the severity of coronavirus-related disease across age groups is the interaction between COVID-19 virus and cold viruses, which are very closely related, and probably use the same receptors in the respiratory tract for entering the host. Since children are so often exposed to viruses that cause the common cold, this might interfere with COVID-19 transmission, resulting in a milder form of illness.

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 SARS. 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 around 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. Keeping in mind these challenges, the World Health Organisation’s (WHO) most recent estimate is that about 3.4% of reported cases have resulted in death. This is much higher than seasonal flu (which kills much fewer than 1% of those infected).

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

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