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COVID-19: the anti-viral immune response

Published on July 25, 2022   24 min

Other Talks in the Series: The Immune System - Key Concepts and Questions

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0:00
Hello and welcome to this talk on COVID-19: the Anti-viral Immune Response. I'm Danny Altmann. I'm a professor of immunology at Imperial College, London.
0:13
To start at the beginning. For this talk, I'll start quite basic and build up to where we've come to on the specifics of the immune response in the time of COVID. If I date the dawn of modern T cell and B cell cellular immunology to around 50 years ago, since then immunologists have learned an enormous amount about the nature of protective immunity to some of the key viruses that infect humans. I guess we've accumulated very large datasets from studies looking at some of the major pathogens that have concerned us, things like HIV, EBV, CMV, flu, Hepatitis, Dengue and even Zika. But the coronavirus family that we've all become so obsessed with in the last few years, even including the common cold coronaviruses as well as SARS and MERS, hadn't really been amongst the most extensively studied or understood. But if you look at a little graphic I've put here of numbers of papers of content published through 2019 to 2021, you'll see that the immunology of SARS-CoV-2, the virus that causes COVID-19, has become one of the most massively studied topics ever in human immunology.
1:32
Let's start at the very beginning and move on from there. Obviously, when one learns about protective immunity, one tends to stratify it into innate immunity and adaptive immunity. What do I mean by that? Innate immunity refers to intrinsic defence mechanisms for recognising microbial attack, that something has got into the body from the environment that shouldn't be there and could be dangerous. This includes everything from the mucosal secretions in the nasal pharynx, but also white blood cells such as neutrophils and macrophages, and the basic cellular responses such as type 1 interferons. These responses are very rapid but can be insufficient on their own to prevent infection. The key point is they have no memory. What do I mean by the analogy of the word memory? I mean that the response will comprise precisely the same features and kinetics on the first, second, or third encounter. It doesn't get any different or any better. Also, the response isn't particularly specific to one virus compared to another.

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