Herd Immunity and this Pandemic

by Gertrud U. Rey

Photo courtesy of Andrea Lightfoot photography

Herd immunity occurs when a large enough percentage of the population has acquired either natural or vaccine-induced immunity against an infectious disease, thereby indirectly protecting a minority of non-immune individuals who are dispersed throughout the population. During this pandemic, many prominent scientists have stated that it is impossible to achieve herd immunity in the context of COVID-19, leading some to conclude that a mass SARS-CoV-2 vaccination campaign would be pointless. However, this thinking is flawed, and I want to explain why.

Traditionally, herd immunity is thought to create a barrier for the transmission of infectious agents, resulting not only in prevention of disease, but also prevention of infection. This understanding was based on previous observations that vaccination against poliovirus, measles virus, and other pathogens led to drastic reductions in the incidence of disease burden. It is reasonable to assume that if there is no disease, there is probably also no virus; and hence no viral infection or transmission of virus. However, past vaccination campaigns were not followed up with regular testing programs, so we actually have no way of knowing whether vaccination prevented infection and transmission! Considering that the vast majority of poliovirus infections are asymptomatic, it is possible that some polio virus infections and transmission occurred even after vaccination, despite the fact that those infections did not lead to disease.

The widespread testing measures adopted during the present pandemic have revealed the approximate frequency of asymptomatic SARS-CoV-2 infections, giving us a clearer understanding of the difference and dynamics between disease and infection. The type of immunity that prevents both disease and infection is called sterilizing immunity, and it is mostly thought to be induced by neutralizing antibodies, which inactivate infectious agents before they have a chance to infect a cell, thereby directly neutralizing the biological effect of the agent. However, any immune activity that prevents replication of a pathogen directly or indirectly necessarily induces sterilizing immunity, including the activity of non-neutralizing antibodies, whose binding can trigger other immune functions that can also prevent infection and replication.

Do SARS-CoV-2 vaccines induce sterilizing immunity? The answer to this question is complicated. There are many studies showing that most people have high levels of antibodies in the months following vaccination, and this large proportion of circulating antibodies could likely sequester an incoming virus before it has a chance to enter cells, infect them, and replicate. In this sense, the SARS-CoV-2 vaccines do induce sterilizing immunity, but only within a certain time period after vaccination. As antibody levels contract over time (a normal process), they leave behind a baseline population of memory B cells that can quickly expand and mass-produce new antibodies upon a subsequent encounter with SARS-CoV-2. Likewise, memory T cells can quickly react to incoming virus and virus-triggered signals, and destroy infected cells. Therefore, it is likely that when circulating SARS-CoV-2-specific antibody levels decline months and years after vaccination, the collective activity of memory immune cells will protect one from disease, but probably not infection, meaning that the SARS-CoV-2 vaccines no longer induce sterilizing immunity at that time. In other words, vaccinated people could briefly replicate and transmit low levels of virus, at least until memory immune responses kick in, which then prevent illness and additional viral replication and spread.

The emergence of new variants that are not as well recognized by existing vaccine-induced antibodies may also allow for some increased viral transmission, thus slowing down the establishment of immunity in the population. However, immune responses are not binary, and even a low level immune response that doesn’t protect against infection and spread but prevents serious disease can play a critical role in slowing down the pandemic. Vaccination has historically been very effective at suppressing community outbreaks, despite the fact that most vaccines do not induce sterilizing immunity.

Vaccination or natural immunity do not have to prevent all infections, and immunity does not have to last a lifetime for a pandemic to end. Pediatrician and vaccinologist Paul Offit defines herd immunity as the point where the serious disease burden is reduced sufficiently so as to no longer overwhelm the healthcare system. It’s becoming pretty clear that the pandemic is slowing down in the US, especially in the context of severe disease, hospitalization, and death; and that this is likely due to increased SARS-CoV-2 immunity among US residents. It is therefore likely that reduced illness and a shortened period of transmission from immune individuals will also reduce the overall rate of community infection and transmission. And in the end, it doesn’t matter whether we call it herd immunity, community immunity or some other name; the pandemic will end because a majority of the population is no longer susceptible to severe COVID-19.

[Please check out my video Catch This Episode 29 for an explanation of sterilizing immunity.]

6 thoughts on “Herd Immunity and this Pandemic”

  1. Pingback: Herd Immunity and this Pandemic - darknight

  2. Mário Cunha

    Regarding the effectiveness of vaccines, what’s your opinion regarding the vaccines inoculated orally or nasally? The main question is the type of immunity induced (local immunity in the mucosae) that may impact the entry of the virus, even with the new VOCs. When available, should they be given complementary to the current ones? I do think that this types of vaccines will have a great impact in the end of this pandemic. Thank you for your insights.

  3. The interesting post leads me to a question. From my limited knowledge of immunulogy, there is a certain functional and operational difference between the mucosal and systemic immune systems. In many viral systems the first replication takes place at the mucosal (usually repiratory or interstinal) level and from there the pathogenic viruses reach the secondary replication sites giving rise to disease. If I am not mistaken, protection (blocking of first replication) at the mucosal level (sIgA) is short-lived (1-3 months?) compared to systemic protection (IgG – many months). It follows that sterilising immunity should be specifically linked to protection against mucosal infection. It seems to me that this is why vaccines are being developed to better stimulate mucosal immunity as well. Obviously these are just general concepts and in the wonderful and incredible variety of viral systems, they have implications that can be very different. This is also demonstrated by the existence of non-pathogenic viruses that mainly inhabit the mucous membranes, and that propagate and persist in the population thanks to a balanced relationship with the immune system of the individual host, but no less with that of the entire host population.
    I wonder how to place the Covid-19 sistem within this framework, assuming it fits. Thank you!

  4. I found this blog post beautifully written and extremely useful. I believe it summarises perfectly also what Vincent, Amy, and Twiv hosts have been saying for some time. Thanks a lot for putting all these important concepts together in one place!

  5. Thank you for that explanation.

    I would have thought that there is a difference between the rate of seriously ill casualties from a particular illness that a health care system can deal with in a relatively short term emergency (e.g. the peak of the pandemic) versus the rate that it is prepared to deal with if sustained over a very long term (endemic stage).

    U.K. government policy appears to have been to try to avoid the health care system being overwhelmed even in short term peaks; the acceptable long term steady state hospitalisation rate is presumably considerably lower.

    (If for no other reason: long term, there will eventually be a burst of casualties from some other, unrelated reason. If we’re running our emergency rooms at maximum capacity just dealing with covid cases for the next couple of decades, that leaves no spare capacity for anything else happening).

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