If a vaccine for coronavirus were to be developed, people could be protected from an infectious disease en masse, thanks to herd immunity.

Herd immunity results when a huge population develops immunity against a virus. Polio was virtually eradicated this way.

Of course, the ideal way to develop herd immunity is through vaccination. But, since a COVID-19 vaccine has not yet been discovered, researchers have chosen to first study antibodies.

Recently, epidemiologists at Yale School of Public Health and Harvard University studied the proposed benefit of herd immunity by analyzing a specific immune response to SARS-CoV-2 infection - the release of antibodies that fight the body's foreign invaders. SARS-CoV-2 is the virus that causes COVID-19. This measure generally can indicate how many people have had the infection and recovered. Their research projects that to date only 10% of the U.S. population has shown antibodies in their blood. Therefore, the U.S. is still a far cry away from the 60% threshold required to achieve herd immunity, scientifically speaking.

In an email interview with Medical Daily, Stuart C. Ray, MD, tells us why he believes producing natural antibodies is not the only route to herd immunity. Dr. Ray is vice chair of Medicine for Data Integrity and Analytics, and a professor in the Division of Infectious Diseases within the Department of Medicine. Additionally, he holds secondary appointments in Viral Oncology and Health Sciences Informatics at Johns Hopkins.

Excerpts:

Q. Can you explain to our readers what exactly herd immunity means? Why do you think this is not an immediate solution to stopping the spread of SARS-CoV-2 in the United States?

A . Herd immunity is reached when the infection is resolving faster than it’s spreading, due to a high proportion of immune people. A person with SARS-CoV-2 infection tends to spread it to 2-3 other people, so we estimate that about 60% of people would need to be immune to reach the herd immunity threshold. We are far from reaching that 60% threshold via immunity after natural infection, both because not that many people have been infected and also because natural infection does not seem to provide long-lasting immunity.

Q. Is vaccination the only way to achieve this?

A. Based on experience with other coronaviruses, it seems likely that natural infection with SARS-CoV-2 will generate immunity for a period of months. If immunity does wane over a period of months, and with growing evidence that reinfections can occur with SARS-CoV-2, it seems unlikely that we will reach herd immunity through natural infection - we’ll always be playing catch-up. In addition, every natural infection with SARS-CoV-2 carries a risk of death and long-term symptoms, some of which we’re only just beginning to appreciate.

In contrast to natural infection, vaccines that have been properly evaluated for efficacy and safety can generate can generate stronger immunity than natural infection because vaccines are engineered and proven to generate a protective response, whereas viruses have evolved to diminish the protective immune response during natural infection. The main difference is that vaccines are designed to leave out the part of the virus that hinders the protective response.

Q. In your opinion, what are the various steps that a country needs to take to realistically establish herd immunity? What would the appropriate time period be, since a surge in the number of cases was reported within a month when Sweden tried it?

A. We don’t know of a safe path to herd immunity, except through vaccination. Sweden recently announced that their death rate in the first half of 2020 is their highest in 150 years of record-keeping, and it appears that they still haven’t reached herd immunity.

Q. You disagree with testing antibodies, which indicate how the virus could be transmitted in the future, though this measure could help determine herd immunity. Why is that?

A. Antibodies are one part of our immune response. They are important but present a very incomplete picture. We also have T cells, NK cells and a variety of other players, part of the immune response. Antibodies are relatively easy to measure, but we don’t know whether they are sufficient to protect us against SARS-CoV-2 infection. Some types of antibodies might be contributing to an uncommon but severe form of COVID-19.

In addition, the tests for antibodies vary dramatically in their sensitivity and specificity. For instance, you get a positive test from 100 people who’ve recovered and many people out of 100 with a positive test could actually have SARS-CoV-2. Even if antibodies are a key part of protection, they may disappear over time. They are useful tests in research but have lots of complexity for routine use. It appears that reinfections occur and might sometimes be more severe than the first infection.

Q. Scientists have reported reinfections with different variants of SARS-CoV-2 strains. Also, some research says that COVID-19 could become a seasonal virus , which cannot have a uniform vaccine. So, is herd immunity against COVID-19, therefore, possible at all?

A. When scientists talk about reinfections with different strains, it is not because there is evidence that there are strain-specific differences in immunity – much to the contrary, we have no such evidence of strain-specific immunity. What scientists are saying when they show SARS-CoV-2 genome A, then later SARS-CoV-2 genome B, is that it was not just the same virus that might have been sticking around all that time. They can see differences in the viral genome that can’t be explained by evolution; therefore, it must be a separate infection or reinfection.

It is true that coronaviruses that cause about a third of common cold illnesses, with catchy names like OC43 and HKU1, are with us to stay and have seasonal peaks in winter. These natural infections don’t appear to generate lasting immunity. That does not mean that an effective vaccine for them cannot be developed. So, this also teaches us that we are unlikely to reach herd immunity to SARS-CoV-2 through natural infection, but we may be able to do so with a safe and effective vaccine.

Q. We might need to practice intermittent social distancing until a vaccine is manufactured. Does this step positively or negatively affect the development of herd immunity?

A. Every SARS-CoV-2 infection is a baby step toward herd immunity, but it carries risk of death and long-term consequences. If immunity wanes and reinfections occur, it doesn’t seem like progress at all – just health costs without known health benefits. Considering all of that, and the pace at which our clinical care of severe COVID-19 is improving, I see great benefits in slowing down the infection rate if we can mitigate the educational, emotional, economic and other costs of these restrictions.

Q. Also, can cross-immunity from being infected with other human coronaviruses in the past help in any way when it comes to herd immunity?

A. During the early parts of this pandemic, we have seen groups on ships, buses and in churches with attack rates approaching 100%, so cross-reactivity with common coronaviruses doesn’t seem to have prevented infections very well. Cross-reactivity might explain some of the variation in severity among people who are infected. More work is needed on this.

Q. Lastly, as an infectious disease specialist, could you draw parallels to other diseases?

A. Some aspects of COVID-19 have reminded me of the HIV epidemic in the 1990s, when some leaders were neglecting the problem even when AIDS was killing so many people. The impacts were felt most severely by those long affected by systemic racism amplifying health disparities; HIV disease and its many manifestations were a deep stigma for those affected. Antiretroviral treatment was ineffective, toxic and insanely expensive. The single best drug we had to improve survival was co-trimoxazole/Bactrim, while pseudoscience had a corrosive effect on the national conversation.