Ask a Caltech Expert: Professor Pamela Bjorkman on SARS-CoV-2

QUESTION 1

Is there a means to determine whether a virus has developed naturally in the wild versus one synthesized or modified in the laboratory?

It's unfortunate that conspiracy theories are being spread (sort of like a virus) about the origins of SARS-CoV-2. When you look at the sequence of SARS-CoV-2, it's clear that it evolved from a particular bat coronavirus. There's no way, in my mind, that a scientist could design a viral sequence based on a bat coronavirus sequence or any other sequence to ensure that it would be very highly transmissible and also induce serious illness. From what we understand about COVID-19, the progress to ARDS (acute respiratory distress syndrome) is caused by our own immune system's response to the virus. I teach immunology every year, and I would have no idea how to design a coronavirus (or any other virus) to produce ARDS. Nor would any other scientist. So even if you believe that scientists would deliberately synthesize a deadly virus in the laboratory for release to the public, there's no way of someone knowing what they would have to start with and modify (e.g., a bat coronavirus) to make it easily transmissible among humans.

Additional information, June 2020:
I'd like to add a few things to my previous response that are related to the fact that the scientific community has the entire genome sequence of SARS-CoV-2. When you look at the sequence (actually sequences, because there are different isolates), you find evidence of evolution in a natural host that would not be present if humans engineered the virus. Let's assume, for the sake of argument, that someone decided to try to modify SARS-CoV (i.e., "classical" SARS, the coronavirus that is most closely related to SARS-CoV-2) to turn it into SARS-CoV-2. I guarantee that they would not have made the changes that distinguish SARS-CoV and SARS-CoV-2. For example, some of the changes in the viral spike protein are counterintuitive to anyone who wanted to design tighter binding to the host receptor (ACE2). In addition, there are random changes throughout the viral genome that do not actually result in changes to amino acids (i.e., silent mutations), which would not be added by the hypothetical engineer. More importantly, there are changes to viral proteins whose functions are not completely understood (e.g., ORFs, or open reading frame proteins, and NSPs, or non-structural proteins). Somehow, the changes resulted in a new virus, SARS-CoV-2, that is much more transmissible than SARS-CoV, for reasons that no one understands. Since we don't understand the function of all of the viral genes in a coronavirus (or any virus for that matter), how could anyone design a virus that managed to come up with the perfect (for a virus) combination of high transmissibility and a relatively low rate of killing off its host? The simple and quick answer to this question is that it is absolutely impossible that this virus was engineered by scientists—no one knows enough about viruses, virus-host interactions, and the immune response to viruses to have engineered SARS-CoV-2.

Read more: The proximal origin of SARS-CoV-2 from Nature Medicine (Andersen, K.G., Rambaut, A., Lipkin, W.I. et al)

QUESTION 2

A friend recently sent me a link to a short talk about the role of 5G in the coronavirus pandemic. Can you comment on this?

There is NO scientific evidence that 5G or any form of "electrification" of the earth plays any role in viral infections. Yes, COVID-19 hotspots can overlap with areas where 5G networks have been tested, but 5G networks are also near major metropolitan areas that have high population densities. The 5G COVID-19 conspiracy theory is a classic case of confusing correlation with causation. There is a lot of misinformation floating around in the news and online. We recommend getting information from scientific websites or articles, from organizations like the World Health Organization (WHO) and the Centers for Disease Control (CDC), or from your own doctor. It is important to make sure that conclusions related as "facts" are actually backed up by scientific and/or medical evidence.

QUESTION 3

Why do we see a lot of recent epidemics/pandemics related to coronaviruses (SARS, MERS, and now COVID-19)? What is special about coronaviruses that makes us extremely vulnerable and unprepared for these viruses? How do we prepare for the next coronavirus?

Many coronaviruses arise in bats, which are great incubators for exchanging viruses with each other and creating new strains that can potentially cross over into humans. Given time, each new coronavirus would either die out in the human population (as has almost happened with SARS and MERS) or attenuate to the point that they cause only mild symptoms, such as common cold coronaviruses. But we can't wait long enough for SARS-CoV-2 to die out or attenuate. In the long term, I think we need a vaccine. In the short term, we can hopefully slow down transmission and help people survive infections with antiviral drugs.

QUESTION 4

Can you speak to the pros and cons of different vaccine platforms and which ones are more likely to succeed?  At a time of crisis like this one, are we better off rushing to test all possible types of vaccines or should we focus our resources on fewer but better understood/better developed kinds of vaccines?

This is a hard question to answer. There are probably multiple platforms that could work to make an effective SARS-CoV-2 vaccine (because it has a relatively low mutation rate, so resistance to antibodies induced by a vaccine would probably not be an issue), but the important issue for the world today is how quickly a vaccine can be demonstrated to be safe and effective, and then produced in large enough quantities to give to everyone who needs it (billions of people). Probably the quickest platform for a vaccine candidate is an mRNA vaccine (a form of messenger RNA encoding the viral S protein), so I hope this works.

Read more: NIH clinical trial of investigational vaccine for COVID-19 begins (March 16, 2020)

QUESTION 5

Even if we develop a vaccine against COVID-19 quickly, it is not going to be a cure. Do we know how quickly COVID-19 evolves, and how do we deal with such moving targets? Any lessons we can borrow from the experience of developing flu and HIV vaccines (or failure to do so)?

The formulation of the annual flu vaccine is chosen by the WHO, which predicts which three or four influenza strains are likely to circulate during the next flu season. So, flu vaccines work best when the prediction is correct. Yes, there is information about how quickly SARS-CoV-2 evolves, and the good news is that it evolves more slowly than flu and a lot more slowly than HIV-1. Even though SARS-CoV-2 may not mutate to develop resistance, we might need an annual coronavirus vaccine if a vaccine and a natural infection produce only short-lived immunological memory.

Read more: What Immunity to COVID-19 Really Means from Scientific American

QUESTION 6

Is summer/heat really going to slow down COVID-19? Do we expect to eventually live with COVID-19 on a seasonal basis, just like flu? Or will COVID-19 be more like SARS?

I think no one knows the answers to these questions. When I see world maps showing COVID-19 in Southern Hemisphere countries where it is (or was) summer, I worry that summer/heat will not slow down the SARS-CoV-2 virus.