In 1954, Harvard researcher Dr. Thomas Peebles showed up at the Fay School in Massachusetts during a measles outbreak to take spit and blood samples from David Edmonston, a 10 year old who caught measles in his first year there (1).  Although the disease had been known since 1911 to be caused by a virus, no one had yet grown and described it.  All they knew was that whatever caused it was extremely small and could pass through tiny filters(2).  Influenzae, mumps, Ebola and chickenpox are all diseases caused by viruses that can pass through those filters too, but growing and characterizing them would show that they belong to very different virus families.  Measles belongs to the morbillivirus family, but that fact wouldn’t be discovered until after Peebles brought David’s spit back to the lab. Eventually, we would know that two other morbilliviruses –  rinderpest virus (formerly of cows, now eliminated from the planet) and canine distemper virus (of dogs and other animals) – have an interesting relationship with measles.  Measles appears to be the eventual result of a 6th Century human being infected with rinderpest (3) and evidence points to canine distemper virus being the result of dogs becoming infected with measles in South America – likely the result of Europeans bringing the virus with them (4).   That cow to human to dog pinball thing fascinates me.

But back to David Edmonston, after 9 years of work in the lab, scientists had successfully weakened David’s virus strain (now known as “Edmonston-B”) by growing it for multiple generations in human kidney cells (specifically 24 generations), then multiple generations (specifically, 28) in human amniotic cells (a form of a stem cell extracted from the inner layer of the placenta) then multiple generations in embryonated chicken eggs (5).  Growing a virus in cells in a petri dish – where there is no immune system – relaxes evolutionary pressures on that virus and it accumulates mutations it wouldn’t otherwise accumulate in the wild.  Growing a virus in isolated cells in a petri dish generally makes the virus weaker and less able to grow in an organism with an immune system.  Viral genes needed to combat an immune system become mutated and nonfunctional in isolated cells because there is no selection pressure against these mutations.  This process is called “attenuation” and it makes the virus less able to cause disease yet still able to infect enough to trigger an immune response.

From the product sheet insert put in every box of MMRII vaccine. https://www.fda.gov/vaccines-blood-biologics/vaccines/vaccines-licensed-use-united-states

In other words, the measles virus  that infected David Edmonston in 1954 was grown and regrown to the point where it accumulated virus-weakening mutations is now grown in chick embryo cells (eggs) to this day to supply the first M in MMR: measles. Well, two of the three MMR vaccines licensed in the US (link) – the other one uses something called the Schwarz strain of measles (link).  Never heard of that one, looks like another rabbit hole 🙂

References

1 – Sullivan EA. Fay School News Detail Magazine. MAKING HISTORY: DAVID EDMONSTON ’57 AND THE MEASLES VACCINE. (link). https://www.fayschool.org/news-detail—magazine?pk=1249137

2 –  Blake & Trask. 1921 J. Exp Med. STUDIES ON MEASLES : I. SUSCEPTIBILITY OF MONKEYS TO THE VIRUS OF MEASLES (link) https://pubmed.ncbi.nlm.nih.gov/19868504/

3 – Dux et al. 2020 Science. Measles virus and rinderpest virus divergence dated to the sixth century BCE. (link) https://pubmed.ncbi.nlm.nih.gov/32554594/

4 – Quintero-Gil et al 2019. Front Microbiol. Origin of Canine Distemper Virus: Consolidating Evidence to Understand Potential Zoonoses. (link) https://pubmed.ncbi.nlm.nih.gov/31555226/

5 – Enders et al 1960. New England J. Med. Studies on an attenuated measles-virus vaccine. I. Development and preparations of the vaccine: technics for assay of effects of vaccination. (link) https://pubmed.ncbi.nlm.nih.gov/13820246/