#115 - David Watkins, Ph.D.: A masterclass in immunology, monoclonal antibodies, and vaccine strategies for COVID-19

Jun 15, 2020 Episode Page ↗
Overview

David Watkins, Professor of Pathology at George Washington University, discusses immunology 101, the innate and adaptive immune systems, and how HIV and Zika research informs SARS-CoV-2 strategies. He highlights the potential of monoclonal antibodies for COVID-19 prevention and treatment.

At a Glance
9 Insights
1h 37m Duration
13 Topics
9 Concepts

Deep Dive Analysis

Introduction to David Watkins and his Research Background

The Evolution of the Immune System

Immunology 101: Innate vs. Adaptive Immune Systems

B Cells, Antibodies, and Neutralizing Antibodies

Variability in Neutralizing Antibody Response to Coronavirus

Lessons from Yellow Fever Vaccine Efficacy

T Cells: The Cellular Arm of the Adaptive Immune System

Challenges of HIV and Hepatitis C: Vaccine Development vs. Treatment

Comparing SARS-CoV-2 to Other Pandemics and Viruses

Monoclonal Antibodies: A Promising Strategy for COVID-19

Different Approaches to COVID-19 Vaccine Development

Insights from Zika Virus Research Applied to SARS-CoV-2

Why a COVID-19 Vaccine Doesn't Need to Be Perfect

Innate Immune Response

This is the initial, non-specific immune response triggered when a virus enters a cell and begins replicating. It involves cellular sensors that activate interferons, which in turn initiate the broader immune system, including the adaptive response.

Adaptive Immune Response

This advanced immune system arm, consisting of T cells and B cells, provides greater memory and specificity to pathogens. It is the fundamental basis for vaccination, allowing the body to remember and respond more effectively to future infections.

Antigen

An antigen is simply a piece of a virus or other foreign substance that the immune system recognizes as 'not self.' This recognition stimulates B cells to begin replicating and developing specific antibodies against it.

Neutralizing Antibodies

These are specific antibodies that bind to a critical part of a virus, such as the spike protein, and directly prevent it from infecting human cells. Unlike other antibodies that may bind but not block infection, neutralizing antibodies are key for protection.

Affinity Maturation

This is a beautiful evolutionary process occurring in lymph nodes where B cells, after initial weak binding to an antigen, undergo rapid replication and mutation of their surface receptors. This iterative process selects for B cells that produce antibodies with progressively higher binding affinity to the antigen.

Plasma Cells

These are large, specialized B cells that reside primarily in the bone marrow after affinity maturation. They act as 'antibody factories,' continuously producing and secreting large quantities of highly specific antibodies, including neutralizing ones, to provide long-term protection.

Cytotoxic T Cell (CD8 T cell)

Often called 'killer T cells,' these powerful immune cells recognize and destroy virus-infected cells. They identify fragments of viral proteins presented on the surface of infected cells, effectively shutting down 'virus factories' before they can release more progeny virus.

Attenuated Virus (Vaccine)

This type of vaccine uses a weakened version of a live virus that can still replicate in the body but causes mild or no disease. It elicits a robust immune response, including T and B cells, but carries a small risk for some individuals, as seen with the yellow fever vaccine.

Broadly Neutralizing Antibodies

These are rare and highly effective antibodies that can neutralize not only the specific viral strain they were generated against but also many other different strains of the same virus. They achieve this by binding to conserved regions of the virus that are essential for its function and less prone to mutation.

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What was the most significant evolutionary development in the immune system?

The advent of the adaptive immune response, involving T and B cells, was the biggest change because it allowed for greater memory and specific responses to pathogens, forming the basis for vaccination.

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What is the difference between IgM and IgG antibodies, and what do they indicate about an infection?

IgM antibodies are typically the first to appear during a new infection, indicating a very recent exposure, and they tend to tail off over time. IgG antibodies appear later and are generally responsible for long-term immunity, containing the neutralizing antibodies.

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Do all antibodies detected by common serology tests provide immunity?

No, common serology tests for IgG or IgM only measure the quantity of antibody bound to a piece of the virus, not whether those antibodies can actually neutralize the virus and prevent infection. A significant percentage of people may have antibodies but lack neutralizing ones.

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How do Cytotoxic T cells (CD8 T cells) fight viral infections?

CD8 T cells recognize and kill cells that have already been infected by a virus. They identify fragments of viral proteins presented on the surface of infected cells, then bind to and destroy these 'virus factories' before they can release more virus particles.

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Why has it been so difficult to develop a vaccine for HIV?

HIV presents unique challenges due to its enormous variability, chronic nature, and the difficulty in generating neutralizing antibodies against its sugar-shielded envelope. The virus constantly mutates and escapes immune responses, making a universal vaccine elusive.

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What is the potential role of monoclonal antibodies in combating COVID-19?

Monoclonal antibodies offer a promising strategy for both preventing and treating COVID-19 by providing immediate, pre-made neutralizing antibodies. These can be engineered to last for several months and could protect high-risk populations or treat already infected individuals.

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Why doesn't a COVID-19 vaccine need to be 'perfect' to be effective?

A COVID-19 vaccine doesn't necessarily need to provide sterilizing immunity (complete prevention of infection). Its effectiveness would be measured by its ability to significantly reduce viral load, prevent severe symptoms, decrease hospitalizations, and lower transmission rates.

1. Adopt Multi-faceted Viral Defense

When confronting a viral epidemic, implement a comprehensive strategy that integrates multiple interventions, including social distancing, drug treatments, and vaccines, as this combined approach is essential for effective control.

2. Explore Monoclonal Antibody Therapy

Consider monoclonal antibodies as a highly promising strategy for both preventing and treating viral infections, especially for high-risk individuals or those with suboptimal vaccine responses, as they can provide direct, temporary immunity for 3-6 months.

3. Set Realistic Vaccine Expectations

Understand that a successful vaccine for viruses like coronavirus may not achieve “sterilizing immunity” but can still be highly effective by significantly reducing viral load, preventing severe illness, and shortening the duration of infectiousness.

4. Interpret Antibody Tests Cautiously

Be aware that standard antibody tests (IgG/IgM) do not differentiate between neutralizing and non-neutralizing antibodies, meaning a positive result does not guarantee protective immunity against infection.

5. Boost Elderly Vaccine Response

Recognize that elderly individuals may not generate robust immune responses from traditional vaccines; therefore, consider monoclonal antibodies as a supplementary or alternative strategy to enhance their protection against viruses.

6. Practice Humility with New Viruses

Approach the understanding and prediction of new viruses with humility, acknowledging that initial assumptions can be incorrect and that many unknown factors influence a pathogen’s behavior and impact.

7. Learn From Past Epidemics

Apply lessons and strategies from previous viral epidemics, such as HIV, to inform and improve current responses to new threats like coronavirus, as historical challenges offer valuable guidance.

8. Prepare for Future Pandemics

Proactively anticipate and prepare for future viral pandemics, drawing insights from current experiences and past outbreaks, rather than solely reacting to crises as they emerge.

9. Value Human Clinical Data

When evaluating the efficacy and safety of health interventions, especially vaccines, prioritize human clinical trial data above animal model data, as human responses are the ultimate and most reliable determinant.

I used to think that the most important cell in the body was the cytotoxic T cell. And worse than that, I used to think that the heart had one function and that is to pump T cells around.

David Watkins

I'll admit something kind of embarrassing. I did not know that until I met you and Stanley Perlman.

Peter Attia

Science is truly wonderful.

Peter Attia

This is not the first SARS virus we've seen in the last 20 years. So need to try to anticipate the next one. And I think that monoclonal antibodies, for me, are the way forward to treat almost all infectious disease, to prevent and treat.

David Watkins

Human data trumps everything.

Vaccinologist (quoted by David Watkins)
Over 100,000
Research samples destroyed in truck fire David Watkins' accumulated research samples from 30 years of work.
1 in 300,000
Risk of getting sick from 17D yellow fever vaccine Higher risk for older individuals; some may die from the attenuated virus.
Almost 20%
Proportion of seropositive individuals without neutralizing antibodies for coronavirus Observed in a study of 70 individuals by a Rockefeller lab.
1 to 5,000
High titer of neutralizing antibodies (dilution) Seen in some individuals vaccinated against yellow fever or making strong coronavirus responses.
1 to 100
Common titer of neutralizing antibodies (dilution) More typical level for neutralizing antibodies.
7 to 14 days
Time for B cells to exit lymph nodes after affinity maturation After which they become memory B cells or plasma cells.
24 hours
Time for a virus to replicate and burst an infected cell Example given for HIV, leading to thousands of copies.
10 to 100 million copies per ml
Initial virus replication levels in HIV/SIV infection Massive population size and variability in the first 2-3 weeks.
Up to 30%
Structural difference between various HIV envelopes Illustrates the high variability of the virus.
75 million
People infected by HIV globally Historical cumulative figure.
32 million
People died from HIV globally Historical cumulative figure.
50 to 100 million people
Estimated deaths from 1918 flu pandemic Global estimate.
3 to 6 months
Duration monoclonal antibodies can last If genetically engineered for extended presence.
From 50% to about 15%
Reduction in Ebola death rate with monoclonal antibody treatment Observed in a trial.
30 to 60 days
Duration of medication course to cure Hepatitis C Using modern drug therapies.