COVID-19 101: Q&A with Prof Ed Rybicki

06 April 2020 | Story Nadia Krige. Photo Supplied. Read time 7 min.
We can expect more outbreaks like the coronavirus, and more frequently, as human populations increasingly infringe upon wild animal habitats, said Prof Ed Rybicki.
We can expect more outbreaks like the coronavirus, and more frequently, as human populations increasingly infringe upon wild animal habitats, said Prof Ed Rybicki.

In times of crisis, the human imagination tends to fluctuate between two extremes: being employed as a powerful tool for survival or wielded as a toxic weapon of destruction. As the COVID-19 pandemic spreads around the globe, leaving economic and social chaos in its wake, we’ve seen countless expressions of both extremes flick across our screens.

In the case of the former, there has been a surge in solidarity as people find creative ways to encourage others, create community and spread positivity. Sadly, however, the latter seems to be present too – especially in the spread of fake news, false information and fearmongering.

In an effort to get some COVID-19 facts straight, UCT News consulted with Professor Ed Rybicki, director of the Biopharming Research Unit in the University of Cape Town’s (UCT) Department of Molecular and Cell Biology. Rybicki is a plant virologist by training, and a biotechnologist and vaccinologist by funding circumstances. He has extensive experience in molecular virology and virus diversity studies with plant and human and animal viruses, which has led to his working with a number of vaccine and expression system platforms.   

This interview, the first of two, delves into frequently asked questions about COVID-19. The second interview looks specifically at the development of a possible vaccine.

Nadia Krige (NK): What is the definition of a novel virus? How do they develop? How common are novel viruses? 

Ed Rybicki (ER): A novel virus is just one we haven’t seen before – and given that we have only just scratched the surface (5 000-odd characterised viruses total) of the estimated 340 000 viruses that probably infect mammals alone, they are extremely common.

One species of fruit bat alone, in Bangladesh, was found to harbour around 60 viruses. They were all from families of viruses that we know something about, but nearly all were “novel” – exactly as this SARS-CoV-2 [Severe acute respiratory syndrome coronavirus 2] (COVID-19) is.

NK: Why is COVID-19 causing so much more havoc than previous novel viruses, such as H1N1, for example?

ER: I don’t think it is in fact causing more havoc. The original H1N1 that emerged in 1918 – the so-called “Spanish Flu” – caused a lot more havoc than this virus: it killed 50 to 100 million people worldwide and infected over one-third of the estimated 1 500 million alive at the time – and it travelled around the world by ship and by train.

The “Asian” flu that emerged in 1957 – H2N2 – killed over 2 million people, at a time when the world population was only nearly 3 billion, and air travel was not nearly so common.

The H1N1 that emerged in 2009 was related both to the original 1918 virus and to circulating viruses, which included H1N1 and had adapted to mammals by circulating in pigs, so it was less virulent. It still killed 240 000 people worldwide, though.

NK: From an academic/scientific perspective, was a pandemic of this magnitude anticipated? If so, why did it catch the world so off guard? 

ER: This kind of pandemic, if not one caused by this specific virus, has been predicted for many years. Organisations like the World Health Organization have been talking about preparedness for “Virus X” for years; I have been teaching students at UCT about “The Big One” for more than 30 years, although I had flu in mind. The film Contagion was based on exactly this kind of scenario – a virus popping out of a setting where wild animals are placed in proximity to domesticated ones in meat markets.

[COVID-19] apparently caught the world unawares because governments – although not infectious disease epidemiologists – simply haven’t put time, effort and money into establishing the infrastructure to deal with it.

China is in fact an exception: they had entire hospitals built as prefabricated units after the original SARS scare in 2003, in anticipation of a resurgence of SARS, and they were able to put them up and deploy them in record time. Everyone else, well, they could have watched what was happening in China and acted pre-emptively, but they simply didn’t.

Denialism of a sort, I suppose?

South Africa has actually acted far earlier and far more decisively in our epidemic than just about any country in Europe, and especially quicker than the United States.

NK: Can you explain how measures like social distancing and complete lockdowns help to stem the spread of the virus, ie how does “flattening the curve” work?

ER: This article from The Washington Post actually explains it very well, with an active simulator you can play with. 

What distancing and isolation does is to drastically limit the potential for spread of the virus. Instead of giving the virus to another 2.5 or so people in an uncontrolled setting, each infected person infects one or none; if the transmission rate goes below 1, the virus dies out as it is not propagated enough.

In a limited but not total lockdown scenario, the virus spread is slowed down dramatically, so that even if the same number of people get infected as would have been in an uncontrolled setting (unlikely), it happens much more slowly, and medical facilities are not overwhelmed by a huge rush of serious cases all at once, and can actually cope.

NK: I read somewhere that COVID-19 could become a seasonal occurrence (similar to the flu). Is this accurate? If so, would it become less lethal the more people have become immune/vaccinated? 

ER: This is possible: several coronaviruses currently infect humans seasonally, and all cause variations of the “common cold”, along with a variety of rhinoviruses (related to polioviruses) and even adenoviruses.

Burtram Fielding from the University of the Western Cape wrote a thought-provoking piece on The Conversation recently wherein he speculated on how a supposed influenza pandemic in 1889 could have been a bovine coronavirus, which has since become a mild seasonal infection in humans.

As long as there are people still infected – and these could be asymptomatic – the virus could maintain itself in humans indefinitely. Having had it or having been vaccinated could significantly lessen this, especially for people with comorbidities.

NK: With a burgeoning world population and unprecedented movement between continents and countries, what are the chances of outbreaks like these occurring more often? 

ER: Sadly, excellent. We have seen three outbreaks of betacoronaviruses alone in 17 years (SARS, MERS [Middle East respiratory syndrome-related coronavirus] and SARS-2); we had a flu pandemic in 2009; Ebola jumped out to cause two major outbreaks in West and Central Africa in four years. We can expect more, and more frequently, as human populations increasingly infringe upon wild animal habitats.

Read the second interview with Professor Rybicki for insight into the development of a vaccine for COVID-19. His blog post “Plant-made vaccines and reagents for SARS-CoV-2 in South Africa” also makes for excellent reading on a possible vaccine.


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