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JAMA Insights
October 19, 2020

Herd Immunity and Implications for SARS-CoV-2 Control

Author Affiliations
  • 1Yale Institute for Global Health, New Haven, Connecticut
  • 2Departments of Internal Medicine and Epidemiology of Microbial Diseases, Yale Schools of Medicine and Public Health, New Haven, Connecticut
  • 3Section of Infectious Diseases and Global Health, Department of Pediatrics, Yale School of Medicine, New Haven, Connecticut
  • 4Yale School of Public Health, New Haven, Connecticut
  • 5Yale School of Management, New Haven, Connecticut
JAMA. 2020;324(20):2095-2096. doi:10.1001/jama.2020.20892

Herd immunity, also known as indirect protection, community immunity, or community protection, refers to the protection of susceptible individuals against an infection when a sufficiently large proportion of immune individuals exist in a population. In other words, herd immunity is the inability of infected individuals to propagate an epidemic outbreak due to lack of contact with sufficient numbers of susceptible individuals. It stems from the individual immunity that may be gained through natural infection or through vaccination. The term herd immunity was initially introduced more than a century ago. In the latter half of the 20th century, the use of the term became more prevalent with the expansion of immunization programs and the need for describing targets for immunization coverage, discussions on disease eradication, and cost-effectiveness analyses of vaccination programs.1

Eradication of smallpox and sustained reductions in disease incidence in adults and those who are not vaccinated following routine childhood immunization with conjugated Haemophilus influenzae type B and pneumococcal vaccines are successful examples of the effects of vaccine-induced herd immunity.1

Herd Immunity Threshold

The herd immunity threshold is defined as the proportion of individuals in a population who, having acquired immunity, can no longer participate in the chain of transmission. If the proportion of immune individuals in a population is above this threshold, current outbreaks will extinguish and endemic transmission of the pathogen will be interrupted. In the simplest model, the herd immunity threshold depends on the basic reproduction number (R0; the average number of persons infected by an infected person in a fully susceptible population) and is calculated as 1 − 1/R0 (Figure).2,3 The effective reproduction number incorporates partially immune populations and accounts for dynamic changes in the proportion of susceptible individuals in a population, such as seen during an outbreak or following mass immunizations. A highly communicable pathogen, such as measles, will have a high R0 (12-18) and a high proportion of the population must be immune to decrease sustained transmission. Since the beginning of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, most of the studies estimated the SARS-CoV-2 R0 to be in the range of 2 to 3.2 Assuming no population immunity and that all individuals are equally susceptible and equally infectious, the herd immunity threshold for SARS-CoV-2 would be expected to range between 50% and 67% in the absence of any interventions.

Figure.  Herd Immunity Thresholds by Disease
Herd Immunity Thresholds by Disease

The locations included are the locations in which the threshold was measured.

Duration of Protection

For both naturally acquired and vaccine-induced immunity, the durability of immune memory is a critical factor in determining population-level protection and sustaining herd immunity. In the case of measles, varicella, and rubella, long-term immunity has been achieved both with infection as well as vaccination. With seasonal coronaviruses, durable immunity has not been observed or has been short lived.4 For infections that produce transient immunity, the pool of susceptible individuals soon increases in the absence of a vaccine and outbreaks reappear. With an effective vaccine and vaccine program, herd immunity can be sustained (even if periodic vaccination is required to do so) and outbreaks can be curtailed as long as the community maintains the necessary levels.

Role of Heterogeneity

Nominal herd immunity thresholds assume random mixing between individuals in a population. However, daily life is more complicated; individuals mix nonrandomly and some individuals have higher numbers of interactions than others. Empirically validated network models have shown that individuals who have higher numbers of interactions get infected earlier in outbreaks.5 This may contribute to slowing of community spread of an infection before reaching the nominal herd immunity threshold. However, there is uncertainty regarding the precise effect of heterogeneity in social mixing on herd immunity against SARS-CoV-2.

T-Cell Cross-reactivity

T-cells are important mediators of immunity. Recent reports have suggested that cross-reactivity with other coronaviruses may confer relative protection of the population from coronavirus disease 2019 (COVID-19).6 It is less clear that T-cell cross-reactivity could provide sterilizing immunity (ie, that the host could not carry nor transmit infection) as opposed to reducing the severity of illness.

Infection-Based Herd Immunity as Policy

An infection-based herd immunity approach (ie, letting the low-risk groups become infected while “sequestering” the susceptible groups) has been proposed to slow the spread of SARS-CoV-2. However, such a strategy is fraught with risks. For example, even with modest infection fatality ratios, a new pathogen will result in substantial mortality because most, if not all, of the population would not have immunity to the pathogen. Sequestering the high-risk populations is impractical because infections that initially transmit in low-mortality populations can spread to high-mortality populations. Moreover, so far, there is no example of a large-scale successful intentional infection-based herd immunity strategy.

There are only rare instances of seemingly sustained herd immunity being achieved through infection. The most recent and well-documented example relates to Zika in Salvador, Brazil. Early in the COVID-19 pandemic, as other countries in Europe were locking down in late February and early March of 2020, Sweden made a decision against lockdown. Initially, some local authorities and journalists described this as the herd immunity strategy: Sweden would do its best to protect the most vulnerable, but otherwise aim to see sufficient numbers of citizens become infected with the goal of achieving true infection-based herd immunity. By late March 2020, Sweden abandoned this strategy in favor of active interventions; most universities and high schools were closed to students, travel restrictions were put in place, work from home was encouraged, and bans on groups of more than 50 individuals were enacted. Far from achieving herd immunity, the seroprevalence in Stockholm, Sweden, was reported to be less than 8% in April 2020,7 which is comparable to several other cities (ie, Geneva, Switzerland,8 and Barcelona, Spain9).

The population of the United States is about 330 million. Based on World Health Organization estimates of an infection fatality rate of 0.5%, about 198 million individuals in the United States are needed to be immune to reach a herd immunity threshold of approximately 60%, which would lead to several hundred thousand additional deaths. Assuming that less than 10% of the population has been infected so far,10 with an infection-induced immunity lasting 2 to 3 years (duration unknown), infection-induced herd immunity is not realistic at this point to control the pandemic. SARS-CoV-2 vaccines will help to reach the herd immunity threshold, but the effectiveness of the vaccine(s) and the vaccine coverage are to be seen.

Conclusions

Herd immunity is an important defense against outbreaks and has shown success in regions with satisfactory vaccination rates. Importantly, even small deviations from protective levels can allow for significant outbreaks due to local clusters of susceptible individuals, as has been seen with measles over the past few years. Therefore, vaccines must not only be effective, but vaccination programs must be efficient and broadly adopted to ensure that those who cannot be directly protected will nonetheless derive relative protections.

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Article Information

Corresponding Author: Saad B. Omer, MBBS, MPH, PhD, Yale University, 1 Church St, New Haven, CT 06510 (saad.omer@yale.edu).

Published Online: October 19, 2020. doi:10.1001/jama.2020.20892

Conflict of Interest Disclosures: Dr Yildirim reported being a member of the mRNA-1273 Study Group. No other disclosures were reported.

References
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Reproduction number (R) and growth rate (r) of the COVID-19 epidemic in the UK: methods of estimation, data sources, causes of heterogeneity, and use as a guide in policy formulation. The Royal Society. Preprint posted August 24, 2020. Accessed October 16, 2020. https://royalsociety.org/-/media/policy/projects/set-c/set-covid-19-R-estimates.pdf
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van den Driessche  P.  Reproduction numbers of infectious disease models.   Infect Dis Model. 2017;2(3):288-303.PubMedGoogle Scholar
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    3 Comments for this article
    EXPAND ALL
    Estimated Infections in US
    Tom Kocsis, BS ME, MS Telecom | Private Citizen
    The statement "assuming that less than 10% of the population has been infected so far" is open to question. That statement is made based on a study of "Prevalence of SARS-CoV-2 antibodies in a large nationwide sample of patients on dialysis in the USA" (the paper's reference 10).  That seems a very limited and narrow group of individuals from which to base the 10% assumption. Further, the existence of antibodies is not the sole confirmation of whether an individual had a SARS-CoV-2 infection previously. I continue to meet people who believe they had SARS-CoV-2 in the Jan-Apr 2020 timeframe before testing was widely available. Some of those folks went for an antibody test later in the Aug-Sep timeframe and their tests came back negative. I think there's still much to be learned on what is a good test for prior infection. Further, there's the entire subject of "asymptomatic" individuals.  How many of these individuals never even go in for a test later on since they won't know or suspect they've been infected? I do appreciate this article and its insights despite the criticism stated above and hope that the research community discovers more about this virus and how it is resisted by the human immune system in asymptomatic individuals and that it would lead to a much more effective and revealing test to possibly arrive at a more accurate picture of infection across the US. Also, I'd really like to see new research on how this virus is mutating over time and whether its "deadliness" is declining based on the death rates that we see in the US as having declined and flattened since early Aug while the number of infections has continued to increase at a high rate. Is this due to the virus becoming less "deadly" as it spreads thru the population or is it because of the treatments that are being administered now? Appreciate all the research and work to battle this new virus.
    CONFLICT OF INTEREST: None Reported
    READ MORE
    The Myth of SARS-CoV-2 Control
    Paul von Ebers, MBA Health Administration | Health care consultant, insurance executive
    Omir, Yildrim, and Forman argue that herd immunity in the absence of an effective vaccine is not a realistic strategy for SARS-CoV-2 control. They leave open the question of what a realistic strategy would be. Common wisdom is that masking, handwashing, social distancing, and avoiding large gatherings is the strategy that will bring an end to the pandemic. This argument has merit, given reductions in infection rates following the implementation of these strategies in various places around the world. However, a key, unanswered question is whether this strategy is sustainable.

    The authors,
    for example, state what appears to be true: "Importantly, even small deviations from protective levels can allow for significant outbreaks due to local clusters of susceptible individuals." Human behavior has probably changed more dramatically in response to Covid than any other health issue in recent history and yet it has not been enough to stop the virus. Renewed outbreaks are happening even in locations where significant restrictions on person to person contact were put in place for considerable periods of time. Indeed, now the White House coronavirus task force is warning about small family gatherings for holidays as a major risk factor.

    Assuming we are as far from herd immunity as the authors state, it appears that the authors are arguing for protracted periods of social isolation and reduced normal human behavior unless an effective vaccine is developed. And the authors have some doubt about how soon and how effective a vaccine will be.

    The authors argue that protecting the vulnerable while allowing the virus to burn out in the less vulnerable population is not possible. Even if they are right, they fail to consider social determinants of health impacted by the common wisdom strategy. We know that unnecessary non-Covid deaths are occurring due to reductions in needed care. Preventive care and chronic disease management has been reduced. Low income children are losing valuable school experience and food support due to school closings. Low income parents are losing their incomes due to business closures. Income and health disparities are growing as a direct result of the social isolation strategy. Elderly patients at the end of life without Covid are dying without the comfort of their families. Covid restrictions are not only "an inconvenience" as many public health experts have claimed. They are affecting the morbidity, mortality and lifetime economic prospects (which is correlated to health) of millions of people worldwide.
    CONFLICT OF INTEREST: None Reported
    READ MORE
    Is herd immunity even possible
    Garreth Debiegun, MD | Maine Medical Center
    This article states that infection-based herd immunity has never actually been achieved. I was aware of this before and hypothesize that it can never be achieved because, as the proportion of susceptible individuals decreases, so will the prevalence of the virus. This will continue until a balance is left that enables the virus to persist in the community at lower levels. Otherwise many viruses and other illnesses we see regularly would cease to exist. I’m not an epidemiologist or virologist, is this true? Is infection-achieved herd immunity actually possible?
    CONFLICT OF INTEREST: None Reported
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