Herd immunity

Last updated

The top box shows an outbreak in a community in which a few people are infected (shown in red) and the rest are healthy but unimmunized (shown in blue); the illness spreads freely through the population. The middle box shows a population where a small number have been immunized (shown in yellow); those not immunized become infected while those immunized do not. In the bottom box, a large proportion of the population have been immunized; this prevents the illness from spreading significantly, including to unimmunized people. In the first two examples, most healthy unimmunized people become infected, whereas in the bottom example only one fourth of the healthy unimmunized people become infected. Herd immunity.svg
The top box shows an outbreak in a community in which a few people are infected (shown in red) and the rest are healthy but unimmunized (shown in blue); the illness spreads freely through the population. The middle box shows a population where a small number have been immunized (shown in yellow); those not immunized become infected while those immunized do not. In the bottom box, a large proportion of the population have been immunized; this prevents the illness from spreading significantly, including to unimmunized people. In the first two examples, most healthy unimmunized people become infected, whereas in the bottom example only one fourth of the healthy unimmunized people become infected.

Herd immunity (also called herd effect, community immunity, population immunity, or social immunity) is a form of indirect protection from infectious disease that occurs when a sufficient percentage of a population has become immune to an infection, whether through vaccination or previous infections, thereby reducing the likelihood of infection for individuals who lack immunity. [1] [2] Immune individuals are unlikely to contribute to disease transmission, disrupting chains of infection, which stops or slows the spread of disease. [3] The greater the proportion of immune individuals in a community, the smaller the probability that non-immune individuals will come into contact with an infectious individual. [1]


Individuals can become immune by recovering from an earlier infection or through vaccination. [3] Some individuals cannot become immune because of medical conditions, such as an immunodeficiency or immunosuppression, and for this group herd immunity is a crucial method of protection. [4] [5] Once the herd immunity threshold has been reached, disease gradually disappears from a population. [5] This elimination, if achieved worldwide, may result in the permanent reduction in the number of infections to zero, called eradication. [6] Herd immunity created via vaccination contributed to the eventual eradication of smallpox in 1977 and has contributed to the reduction of other diseases. [7] Herd immunity applies only to contagious disease, meaning that it is transmitted from one individual to another. [5] Tetanus, for example, is infectious but not contagious, so herd immunity does not apply. [4]

Herd immunity was recognized as a naturally occurring phenomenon in the 1930s when it was observed that after a significant number of children had become immune to measles, the number of new infections temporarily decreased, including among the unvaccinated. [8] Mass vaccination to induce herd immunity has since become common and proved successful in preventing the spread of many infectious diseases. [9] Opposition to vaccination has posed a challenge to herd immunity, allowing preventable diseases to persist in or return to populations with inadequate vaccination rates. [10] [11] [12]


Protection of those without immunity

Some individuals either cannot develop immunity after vaccination or for medical reasons cannot be vaccinated. [13] [14] [4] [13] Newborn infants are too young to receive many vaccines, either for safety reasons or because passive immunity renders the vaccine ineffective. [15] Individuals who are immunodeficient due to HIV/AIDS, lymphoma, leukemia, bone marrow cancer, an impaired spleen, chemotherapy, or radiotherapy may have lost any immunity that they previously had and vaccines may not be of any use for them because of their immunodeficiency. [4] [13] [15] [16]

A portion of those vaccinated may not develop long-term immunity. [1] [17] [18] Vaccine contraindications may prevent certain individuals from being vaccinated. [13] In addition to not being immune, individuals in one of these groups may be at a greater risk of developing complications from infection because of their medical status, but they may still be protected if a large enough percentage of the population is immune. [4] [13] [18] [19]

High levels of immunity in one age group can create herd immunity for other age groups. [7] Vaccinating adults against pertussis reduces pertussis incidence in infants too young to be vaccinated, who are at the greatest risk of complications from the disease. [20] [21] This is especially important for close family members, who account for most of the transmissions to young infants. [7] [18] In the same manner, children receiving vaccines against pneumococcus reduces pneumococcal disease incidence among younger, unvaccinated siblings. [22] Vaccinating children against pneumococcus and rotavirus has had the effect of reducing pneumococcus- and rotavirus-attributable hospitalizations for older children and adults, who do not normally receive these vaccines. [22] [23] [24] Influenza (flu) is more severe in the elderly than in younger age groups, but influenza vaccines lack effectiveness in this demographic due to a waning of the immune system with age. [7] [25] The prioritization of school-age children for seasonal flu immunization, which is more effective than vaccinating the elderly, however, has been shown to create a certain degree of protection for the elderly. [7] [25]

For sexually transmitted infections (STIs), high levels of immunity in one sex induces herd immunity for both sexes. [9] [26] [27] Vaccines against STIs that are targeted at one sex result in significant declines in STIs in both sexes if vaccine uptake in the target sex is high. [26] [27] [28] Herd immunity from female vaccination does not, however, extend to homosexual males. [27] If vaccine uptake among the target sex is low, then the other sex may need to be immunized so that the target sex can be sufficiently protected. [26] [27] High-risk behaviors make eliminating STIs difficult since even though most infections occur among individuals with moderate risk, the majority of transmissions occur because of individuals who engage in high-risk behaviors. [9] For these reasons, in certain populations it may be necessary to immunize high-risk persons or individuals of both sexes to establish herd immunity. [9] [27]

Evolutionary pressure

Herd immunity itself acts as an evolutionary pressure on certain viruses, influencing viral evolution by encouraging the production of novel strains, in this case referred to as escape mutants, that are able to "escape" from herd immunity and spread more easily. [29] [30] At the molecular level, viruses escape from herd immunity through antigenic drift, which is when mutations accumulate in the portion of the viral genome that encodes for the virus's surface antigen, typically a protein of the virus capsid, producing a change in the viral epitope. [31] [32] Alternatively, the reassortment of separate viral genome segments, or antigenic shift, which is more common when there are more strains in circulation, can also produce new serotypes. [29] [33] When either of these occur, memory T cells no longer recognize the virus, so people are not immune to the dominant circulating strain. [32] [33] For both influenza and norovirus, epidemics temporarily induce herd immunity until a new dominant strain emerges, causing successive waves of epidemics. [31] [33] As this evolution poses a challenge to herd immunity, broadly neutralizing antibodies and "universal" vaccines that can provide protection beyond a specific serotype are in development. [30] [34] [35]

Serotype replacement

Serotype replacement, or serotype shifting, may occur if the prevalence of a specific serotype declines due to high levels of immunity, allowing other serotypes to replace it. [36] [37] Initial vaccines against Streptococcus pneumoniae significantly reduced nasopharyngeal carriage of vaccine serotypes (VTs), including antibiotic-resistant types, [22] [38] only to be entirely offset by increased carriage of non-vaccine serotypes (NVTs). [22] [36] [37] This did not result in a proportionate increase in disease incidence though, since NVTs were less invasive than VTs. [36] Since then, pneumococcal vaccines that provide protection from the emerging serotypes have been introduced and have successfully countered their emergence. [22] The possibility of future shifting remains, so further strategies to deal with this include expansion of VT coverage and the development of vaccines that use either killed whole-cells, which have more surface antigens, or proteins present in multiple serotypes. [22] [39]

Eradication of diseases

A cow with rinderpest in the "milk fever" position, 1982. The last confirmed case of rinderpest occurred in Kenya in 2001, and the disease was officially declared eradicated in 2011. Rinderpest milk fever.jpg
A cow with rinderpest in the "milk fever" position, 1982. The last confirmed case of rinderpest occurred in Kenya in 2001, and the disease was officially declared eradicated in 2011.

If herd immunity has been established and maintained in a population for a sufficient time, the disease is inevitably eliminated—no more endemic transmissions occur. [5] If elimination is achieved worldwide and the number of cases is permanently reduced to zero, then a disease can be declared eradicated. [6] Eradication can thus be considered the final effect or end-result of public health initiatives to control the spread of infectious disease. [6] [7]

The benefits of eradication include ending all morbidity and mortality caused by the disease, financial savings for individuals, health care providers, and governments, and enabling resources used to control the disease to be used elsewhere. [6] To date, two diseases have been eradicated using herd immunity and vaccination: rinderpest and smallpox. [1] [7] [40] Eradication efforts that rely on herd immunity are currently underway for poliomyelitis, though civil unrest and distrust of modern medicine have made this difficult. [1] [41] Mandatory vaccination may be beneficial to eradication efforts if not enough people choose to get vaccinated. [42] [43] [44] [45]

Free riding

Herd immunity is vulnerable to the free rider problem. [46] Individuals who lack immunity, particularly those who choose not to vaccinate, free ride off the herd immunity created by those who are immune. [46] As the number of free riders in a population increases, outbreaks of preventable diseases become more common and more severe due to loss of herd immunity. [10] [11] [12] [43] [45] Individuals may choose to free ride for a variety of reasons, including the belief that vaccines are ineffective, [47] or that the risks associated with vaccines are greater than those associated with infection, [1] [11] [12] [47] mistrust of vaccines or public health officials, [48] bandwagoning or groupthinking, [43] [49] social norms or peer pressure, [47] and religious beliefs. [11] Certain individuals are more likely to choose not to receive vaccines if vaccination rates are high enough to convince a person that he or she may not need to be vaccinated, since a sufficient percentage of others are already immune. [1] [45]


Estimated R0 and HITs (herd immunity threshold) of well-known infectious diseases [50]
Measles Airborne12–1892–95%
Pertussis Airborne droplet12–17 [51] 92–94%
Diphtheria Saliva6–783–86%
Rubella Airborne droplet
Smallpox 5–780–86%
Polio Fecal-oral route
Mumps Airborne droplet4–775–86%
(COVID-19 pandemic)
2.5–4 [52] [53] 60–75%
(2002–2004 SARS outbreak)
2–5 [54] 50–80%
(Ebola virus epidemic in West Africa)
Bodily fluids1.5–2.5 [55] 33–60%
(influenza pandemics)
Airborne droplet1.5–1.8 [51] 33–44%

Individuals who are immune to a disease act as a barrier in the spread of disease, slowing or preventing the transmission of disease to others. [3] An individual's immunity can be acquired via a natural infection or through artificial means, such as vaccination. [3] When a critical proportion of the population becomes immune, called the herd immunity threshold (HIT) or herd immunity level (HIL), the disease may no longer persist in the population, ceasing to be endemic. [5] [29]

The critical value, or threshold, in a given population, is the point where the disease reaches an endemic steady state, which means that the infection level is neither growing nor declining exponentially. This threshold can be calculated from the effective reproduction number Re, which is obtained by taking the product of the basic reproduction number R0, the average number of new infections caused by each case in an entirely susceptible population that is homogeneous, or well-mixed, meaning each individual can come into contact with every other susceptible individual in the population, [9] [29] [42] and S, the proportion of the population who are susceptible to infection, and setting this product to be equal to 1:

S can be rewritten as (1 − p), where p is the proportion of the population that is immune so that p + S equals one. Then, the equation can be rearranged to place p by itself as follows:

so so

With p being by itself on the left side of the equation, it can be renamed as pc, representing the critical proportion of the population needed to be immune to stop the transmission of disease, which is the same as the "herd immunity threshold" HIT. [9] R0 functions as a measure of contagiousness, so low R0 values are associated with lower HITs, whereas higher R0s result in higher HITs. [29] [42] For example, the HIT for a disease with an R0 of 2 is theoretically only 50%, whereas a disease with an R0 of 10 the theoretical HIT is 90%. [29]

When the effective reproduction number Re of a contagious disease is reduced to and sustained below 1 new individual per infection, the number of cases occurring in the population gradually decreases until the disease has been eliminated. [9] [29] [56] If a population is immune to a disease in excess of that disease's HIT, the number of cases reduces at a faster rate, outbreaks are even less likely to happen, and outbreaks that occur are smaller than they would be otherwise. [1] [9] If the effective reproduction number increases to above 1, then the disease is neither in a steady state nor decreasing in incidence, but is actively spreading through the population and infecting a larger number of people than usual. [43] [56]

An assumption in these calculations is that populations are homogeneous, or well-mixed, meaning that every individual comes into contact with every other individual, when in reality populations are better described as social networks as individuals tend to cluster together, remaining in relatively close contact with a limited number of other individuals. In these networks, transmission only occurs between those who are geographically or physically close to one another. [1] [42] [43] The shape and size of a network is likely to alter a disease's HIT, making incidence either more or less common. [29] [42]

In heterogeneous populations, R0 is considered to be a measure of the number of cases generated by a "typical" infectious person, which depends on how individuals within a network interact with each other. [1] Interactions within networks are more common than between networks, in which case the most highly connected networks transmit disease more easily, resulting in a higher R0 and a higher HIT than would be required in a less connected network. [1] [43] In networks that either opt not to become immune or are not immunized sufficiently, diseases may persist despite not existing in better-immunized networks. [43]


The cumulative proportion of individuals who get infected during the course of a disease outbreak can exceed the HIT. This is because the HIT does not represent the point at which the disease stops spreading, but rather the point at which each infected person infects fewer than one additional person on average. When the HIT is reached, the number of additional infections begins to taper off, but it does not immediately drop to zero. The difference between the cumulative proportion of infected individuals and the theoretical HIT is known as the overshoot. [57] [58] [59]



The primary way to boost levels of immunity in a population is through vaccination. [1] [60] Vaccination is originally based on the observation that milkmaids exposed to cowpox were immune to smallpox, so the practice of inoculating people with the cowpox virus began as a way to prevent smallpox. [41] Well-developed vaccines provide protection in a far safer way than natural infections, as vaccines generally do not cause the diseases they protect against and severe adverse effects are significantly less common than complications from natural infections. [61] [62]

The immune system does not distinguish between natural infections and vaccines, forming an active response to both, so immunity induced via vaccination is similar to what would have occurred from contracting and recovering from the disease. [63] To achieve herd immunity through vaccination, vaccine manufacturers aim to produce vaccines with low failure rates, and policy makers aim to encourage their use. [60] After the successful introduction and widespread use of a vaccine, sharp declines in the incidence of diseases it protects against can be observed, which decreases the number of hospitalizations and deaths caused by such diseases. [64] [65] [66]

Assuming a vaccine is 100% effective, then the equation used for calculating the herd immunity threshold can be used for calculating the vaccination level needed to eliminate a disease, written as Vc. [1] Vaccines are usually imperfect however, so the effectiveness, E, of a vaccine must be accounted for:

From this equation, it can be observed that if E is less than (1 − 1/R0), then it is impossible to eliminate a disease, even if the entire population is vaccinated. [1] Similarly, waning vaccine-induced immunity, as occurs with acellular pertussis vaccines, requires higher levels of booster vaccination to sustain herd immunity. [1] [20] If a disease has ceased to be endemic to a population, then natural infections no longer contribute to a reduction in the fraction of the population that is susceptible. Only vaccination contributes to this reduction. [9] The relation between vaccine coverage and effectiveness and disease incidence can be shown by subtracting the product of the effectiveness of a vaccine and the proportion of the population that is vaccinated, pv, from the herd immunity threshold equation as follows:

Measles vaccine coverage and reported measles cases in Eastern Mediterranean countries. As coverage increased, the number of cases decreased. Measles cases coverage eastern mediterranean.jpg
Measles vaccine coverage and reported measles cases in Eastern Mediterranean countries. As coverage increased, the number of cases decreased.

It can be observed from this equation that, all other things being equal (" ceteris paribus "), any increase in either vaccine coverage or vaccine effectiveness, including any increase in excess of a disease's HIT, further reduces the number of cases of a disease. [9] The rate of decline in cases depends on a disease's R0, with diseases with lower R0 values experiencing sharper declines. [9]

Vaccines usually have at least one contraindication for a specific population for medical reasons, but if both effectiveness and coverage are high enough herd immunity can protect these individuals. [14] [16] [19] Vaccine effectiveness is often, but not always, adversely affected by passive immunity, [67] [68] so additional doses are recommended for some vaccines while others are not administered until after an individual has lost his or her passive immunity. [15] [19]

Passive immunity

Individual immunity can also be gained passively, when antibodies to a pathogen are transferred from one individual to another. This can occur naturally, whereby maternal antibodies, primarily immunoglobulin G antibodies, are transferred across the placenta and in colostrum to fetuses and newborns. [69] [70] Passive immunity can also be gained artificially, when a susceptible person is injected with antibodies from the serum or plasma of an immune person. [63] [71]

Protection generated from passive immunity is immediate, but wanes over the course of weeks to months, so any contribution to herd immunity is temporary. [5] [63] [72] For diseases that are especially severe among fetuses and newborns, such as influenza and tetanus, pregnant women may be immunized in order to transfer antibodies to the child. [14] [73] [74] In the same way, high-risk groups that are either more likely to experience infection, or are more likely to develop complications from infection, may receive antibody preparations to prevent these infections or to reduce the severity of symptoms. [71]

Cost–benefit analysis

Herd immunity is often accounted for when conducting cost–benefit analyses of vaccination programs. It is regarded as a positive externality of high levels of immunity, producing an additional benefit of disease reduction that would not occur had no herd immunity been generated in the population. [75] [76] Therefore, herd immunity's inclusion in cost–benefit analyses results both in more favorable cost-effectiveness or cost–benefit ratios, and an increase in the number of disease cases averted by vaccination. [76] Study designs done to estimate herd immunity's benefit include recording disease incidence in households with a vaccinated member, randomizing a population in a single geographic area to be vaccinated or not, and observing the incidence of disease before and after beginning a vaccination program. [77] From these, it can be observed that disease incidence may decrease to a level beyond what can be predicted from direct protection alone, indicating that herd immunity contributed to the reduction. [77] When serotype replacement is accounted for, it reduces the predicted benefits of vaccination. [76]


Measles cases in the United States before and after mass vaccination against measles began. Measles US 1938-2019.png
Measles cases in the United States before and after mass vaccination against measles began.

The term "herd immunity" was coined in 1923. [78] Herd immunity was first recognized as a naturally occurring phenomenon in the 1930s when A. W. Hedrich published research on the epidemiology of measles in Baltimore, and took notice that after many children had become immune to measles, the number of new infections temporarily decreased, including among susceptible children. [79] [8] In spite of this knowledge, efforts to control and eliminate measles were unsuccessful until mass vaccination using the measles vaccine began in the 1960s. [8] Mass vaccination, discussions of disease eradication, and cost–benefit analyses of vaccination subsequently prompted more widespread use of the term herd immunity. [1] In the 1970s, the theorem used to calculate a disease's herd immunity threshold was developed. [1] During the smallpox eradication campaign in the 1960s and 1970s, the practice of ring vaccination , to which herd immunity is integral, began as a way to immunize every person in a "ring" around an infected individual to prevent outbreaks from spreading. [80]

Since the adoption of mass and ring vaccination, complexities and challenges to herd immunity have arisen. [1] [60] Modeling of the spread of infectious disease originally made a number of assumptions, namely that entire populations are susceptible and well-mixed, which is not the case in reality, so more precise equations have been developed. [1] In recent decades, it has been recognized that the dominant strain of a microorganism in circulation may change due to herd immunity, either because of herd immunity acting as an evolutionary pressure or because herd immunity against one strain allowed another already-existing strain to spread. [31] [37] Emerging or ongoing fears and controversies about vaccination have reduced or eliminated herd immunity in certain communities, allowing preventable diseases to persist in or return to these communities. [10] [11] [12]

See also

Related Research Articles

Vaccination Administration of a vaccine to protect against disease

Vaccination is the administration of a vaccine to help the immune system develop protection from a disease. Vaccines contain a microorganism or virus in a weakened, live or killed state, or proteins or toxins from the organism. In stimulating the body's adaptive immunity, they help prevent sickness from an infectious disease. When a sufficiently large percentage of a population has been vaccinated, herd immunity results. The effectiveness of vaccination has been widely studied and verified. Vaccination is the most effective method of preventing infectious diseases; widespread immunity due to vaccination is largely responsible for the worldwide eradication of smallpox and the elimination of diseases such as polio and tetanus from much of the world.

Vaccine Pathogen-derived preparation that provides acquired immunity to an infectious disease

A vaccine is a biological preparation that provides active acquired immunity to a particular infectious disease. A vaccine typically contains an agent that resembles a disease-causing microorganism and is often made from weakened or killed forms of the microbe, its toxins, or one of its surface proteins. The agent stimulates the body's immune system to recognize the agent as a threat, destroy it, and to further recognize and destroy any of the microorganisms associated with that agent that it may encounter in the future. Vaccines can be prophylactic, or therapeutic.

Antiviral drugs are a class of medication used for treating viral infections. Most antivirals target specific viruses, while a broad-spectrum antiviral is effective against a wide range of viruses. Unlike most antibiotics, antiviral drugs do not destroy their target pathogen; instead they inhibit its development.

Measles Viral disease affecting humans

Measles is a highly contagious infectious disease caused by measles virus. Symptoms usually develop 10–12 days after exposure to an infected person and last 7–10 days. Initial symptoms typically include fever, often greater than 40 °C (104 °F), cough, runny nose, and inflamed eyes. Small white spots known as Koplik's spots may form inside the mouth two or three days after the start of symptoms. A red, flat rash which usually starts on the face and then spreads to the rest of the body typically begins three to five days after the start of symptoms. Common complications include diarrhea, middle ear infection (7%), and pneumonia (6%). These occur in part due to measles-induced immunosuppression. Less commonly seizures, blindness, or inflammation of the brain may occur. Other names include morbilli, rubeola, red measles, and English measles. Both rubella, also known as German measles, and roseola are different diseases caused by unrelated viruses.

Rubella Human viral disease

Rubella, also known as German measles or three-day measles, is an infection caused by the rubella virus. This disease is often mild with half of people not realizing that they are infected. A rash may start around two weeks after exposure and last for three days. It usually starts on the face and spreads to the rest of the body. The rash is sometimes itchy and is not as bright as that of measles. Swollen lymph nodes are common and may last a few weeks. A fever, sore throat, and fatigue may also occur. In adults joint pain is common. Complications may include bleeding problems, testicular swelling, encephalitis, and inflammation of nerves. Infection during early pregnancy may result in a miscarriage or a child born with congenital rubella syndrome (CRS). Symptoms of CRS manifest as problems with the eyes such as cataracts, deafness, as well as affecting the heart and brain. Problems are rare after the 20th week of pregnancy.

Immunization Process by which an individuals immune system becomes fortified against an agent

Immunization, or immunisation, is the process by which an individual's immune system becomes fortified against an agent.

Mathematical models can project how infectious diseases progress to show the likely outcome of an epidemic and help inform public health interventions. Models use basic assumptions or collected statistics along with mathematics to find parameters for various infectious diseases and use those parameters to calculate the effects of different interventions, like mass vaccination programmes. The modelling can help decide which intervention/s to avoid and which to trial, or can predict future growth patterns, etc.

Vaccine hesitancy, also known as anti-vaccination or anti-vax, is a reluctance or refusal to be vaccinated or to have one's children vaccinated against contagious diseases despite the availability of vaccination services. It was identified by the World Health Organization as one of the top ten global health threats of 2019. The term encompasses outright refusal to vaccinate, delaying vaccines, accepting vaccines but remaining uncertain about their use, or using certain vaccines but not others. Arguments against vaccination are contradicted by overwhelming scientific consensus about the safety and efficacy of vaccines.

Original antigenic sin

Original antigenic sin, also known as the Hoskins effect, refers to the propensity of the body's immune system to preferentially utilize immunological memory based on a previous infection when a second slightly different version of that foreign entity is encountered. This leaves the immune system "trapped" by the first response it has made to each antigen, and unable to mount potentially more effective responses during subsequent infections. The phenomenon of original antigenic sin has been described in relation to influenza virus, dengue fever, human immunodeficiency virus (HIV), and to several other viruses.

A breakthrough infection is a case of illness in which a vaccinated individual becomes sick from the same illness that the vaccine is meant to prevent. Simply, they occur when vaccines fail to provide immunity against the pathogen they are designed to target. Breakthrough infections have been identified in individuals immunized against a variety of different diseases including Mumps, Varicella, and Influenza. The character of breakthrough infections is dependent on the virus itself. Often, the infection in the vaccinated individual results in milder symptoms and is of a shorter duration than if the infection was contracted naturally.

Pneumococcal vaccine

Pneumococcal vaccines are vaccines against the bacterium Streptococcus pneumoniae. Their use can prevent some cases of pneumonia, meningitis, and sepsis. There are two types of pneumococcal vaccines: conjugate vaccines and polysaccharide vaccines. They are given by injection either into a muscle or just under the skin.

Polio eradication Effort to permanently eliminate all cases of poliomyelitis infection

Polio eradication, the permanent global cessation of circulation by the poliovirus and hence elimination of the poliomyelitis (polio) it causes, is the aim of a multinational public health effort begun in 1988, led by the World Health Organization (WHO), the United Nations Children's Fund (UNICEF) and the Rotary Foundation. These organizations, along with the U.S. Centers for Disease Control and Prevention (CDC) and The Gates Foundation, have spearheaded the campaign through the Global Polio Eradication Initiative (GPEI). Successful eradication of infectious diseases has been achieved twice before, with smallpox and bovine rinderpest.

Vaccination policy is the health policy a government adopts in relation to vaccination. Vaccination policies have been developed over the approximately two centuries since the invention of vaccination with the purpose of eradicating disease from, or creating a herd immunity for, the population the government aims to protect. Vaccination advisory committees within each country are usually responsible for providing information to governments that is used to make evidence-based decisions regarding vaccine and immunization policy.

Health in the United States is the overall health of the population of the United States.

Number needed to vaccinate (NNV) is a metric used in the evaluation of vaccines, and in the determination of vaccination policy. It is a specific application of the number needed to treat metric (NNT) that incorporates the implications of herd immunity.

Cocooning (immunization)

Cocooning, also known as the Cocoon Strategy, is a vaccination strategy to protect infants and other vulnerable individuals from infectious diseases by vaccinating those in close contact with them. If the people most likely to transmit an infection are immune, their immunity creates a "cocoon" of protection around the newborn.

Vaccine-naive Resistance of vaccination

Vaccine-naive is a lack of immunity, or immunologic memory, to a disease because the person has not been vaccinated. There are a variety of reasons why a person may not have received a vaccination, including contraindications due to preexisting medical conditions, lack of resources, previous vaccination failure, religious beliefs, personal beliefs, fear of side-effects, phobias to needles, lack of information, vaccine shortages, physician knowledge and beliefs, social pressure, and natural resistance.

Targeted immunization strategies

Targeted immunization strategies are approaches designed to increase the immunization level of populations and decrease the chances of epidemic outbreaks. Though often in regards to use in healthcare practices and the administration of vaccines to prevent biological epidemic outbreaks, these strategies refer in general to immunization schemes in complex networks, biological, social or artificial in nature. Identification of at-risk groups and individuals with higher odds of spreading the disease often plays an important role in these strategies.

Non-specific effect of vaccines Unintended side effects of vaccines which may be beneficial or bad

Non-specific effects of vaccines are effects which go beyond the specific protective effects against the targeted diseases. Non-specific effects can be strongly beneficial by increasing protection against non-targeted infections. This has been shown with two live attenuated vaccines, BCG vaccine and measles vaccine, through multiple randomized controlled trials. Theoretically, non-specific effects of vaccines may be detrimental, increasing overall mortality despite providing protection against the target diseases. Although observational studies suggest that diphtheria-tetanus-pertussis vaccine (DTP) may be detrimental, these studies are at high risk of bias and have failed to replicate when conducted by independent groups.

Ring vaccination vaccination strategy

Ring vaccination is a strategy to inhibit the spread of a disease by vaccinating only those who are most likely to be infected.


  1. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 Fine, P.; Eames, K.; Heymann, D. L. (1 April 2011). "'Herd immunity': A rough guide". Clinical Infectious Diseases . 52 (7): 911–16. doi: 10.1093/cid/cir007 . PMID   21427399.
  2. Gordis, L. (2013). Epidemiology. Elsevier Health Sciences. pp. 26–27. ISBN   978-1455742516 . Retrieved 29 March 2015.
  3. 1 2 3 4 Merrill, R. M. (2013). Introduction to Epidemiology. Jones & Bartlett Publishers. pp. 68–71. ISBN   978-1449645175 . Retrieved 29 March 2015.
  4. 1 2 3 4 5 "Herd Immunity". Oxford Vaccine Group, University of Oxford. Retrieved 12 December 2017.
  5. 1 2 3 4 5 6 Somerville, M.; Kumaran, K.; Anderson, R. (2012). Public Health and Epidemiology at a Glance. John Wiley & Sons. pp. 58–59. ISBN   978-1118308646 . Retrieved 29 March 2015.
  6. 1 2 3 4 Cliff, A.; Smallman-Raynor, M. (11 April 2013). Oxford Textbook of Infectious Disease Control: A Geographical Analysis from Medieval Quarantine to Global Eradication. Oxford University Press. pp. 125–36. ISBN   978-0199596614 . Retrieved 29 March 2015.
  7. 1 2 3 4 5 6 7 Kim, T. H.; Jonhstone, J.; Loeb, M. (September 2011). "Vaccine herd effect". Scandinavian Journal of Infectious Diseases. 43 (9): 683–89. doi:10.3109/00365548.2011.582247. PMC   3171704 . PMID   21604922.
  8. 1 2 3
  9. 1 2 3 4 5 6 7 8 9 10 11 Garnett, G. P. (1 February 2005). "Role of Herd Immunity in Determining the Effect of Vaccines against Sexually Transmitted Disease". The Journal of Infectious Diseases. 191 (Suppl 1): S97–106. doi: 10.1086/425271 . PMID   15627236.
  10. 1 2 3 Quadri-Sheriff, M.; Hendrix, K. S.; Downs, S. M.; Sturm, L. A.; Zimet, G. D.; Finnell, S. M. (September 2012). "The role of herd immunity in parents' decision to vaccinate children: a systematic review". Pediatrics. 130 (3): 522–30. doi: 10.1542/peds.2012-0140 . PMID   22926181.
  11. 1 2 3 4 5 Dubé, E.; Laberge, C.; Guay, M.; Bramadat, P.; Roy, R.; Bettinger, J. (August 2013). "Vaccine hesitancy: an overview". Human Vaccines & Immunotherapeutics. 9 (8): 1763–73. doi:10.4161/hv.24657. PMC   3906279 . PMID   23584253.
  12. 1 2 3 4 Ropeik, D. (August 2013). "How society should respond to the risk of vaccine rejection". Human Vaccines & Immunotherapeutics. 9 (8): 1815–18. doi:10.4161/hv.25250. PMC   3906287 . PMID   23807359.
  13. 1 2 3 4 5 Cesaro, S.; Giacchino, M.; Fioredda, F.; et al. (2014). "Guidelines on vaccinations in paediatric haematology and oncology patients". Biomed Res. Int. 2014: 707691. doi:10.1155/2014/707691. PMC   4020520 . PMID   24868544.
  14. 1 2 3 Munoz, F. M. (2013). "Maternal immunization: An update for pediatricians". Pediatric Annals. 42 (8): 153–58. doi:10.3928/00904481-20130723-09. PMID   23910028.
  15. 1 2 3 National Center for Immunization and Respiratory Diseases (2011). "General recommendations on immunization – recommendations of the Advisory Committee on Immunization Practices (ACIP)". MMWR. Recommendations and Reports / Centers for Disease Control. 60 (2): 1–64. PMID   21293327.
  16. 1 2 Wolfe, R. M. (2012). "Update on adult immunizations". The Journal of the American Board of Family Medicine. 25 (4): 496–510. doi: 10.3122/jabfm.2012.04.100274 . PMID   22773718.
  17. Esposito, S; Bosis, S; Morlacchi, L; Baggi, E; Sabatini, C; Principi, N (2012). "Can infants be protected by means of maternal vaccination?". Clinical Microbiology and Infection. 18 (Suppl 5): 85–92. doi: 10.1111/j.1469-0691.2012.03936.x . PMID   22862749.
  18. 1 2 3 Rakel, D.; Rakel, R. E. (2015). Textbook of Family Medicine. Elsevier Health Sciences. pp. 99, 187. ISBN   978-0323313087 . Retrieved 30 March 2015.
  19. 1 2 3 Tulchinsky, T. H.; Varavikova, E. A. (26 March 2014). The New Public Health: An Introduction for the 21st Century. Academic Press. pp. 163–82. ISBN   978-0124157675 . Retrieved 30 March 2015.
  20. 1 2 McGirr, A; Fisman, D. N. (2015). "Duration of Pertussis Immunity After DTaP Immunization: A Meta-analysis" (PDF). Pediatrics. 135 (2): 331–43. doi:10.1542/peds.2014-1729. PMID   25560446. S2CID   8273985.
  21. Zepp, F; Heininger, U; Mertsola, J; Bernatowska, E; Guiso, N; Roord, J; Tozzi, A. E.; Van Damme, P (2011). "Rationale for pertussis booster vaccination throughout life in Europe". The Lancet Infectious Diseases. 11 (7): 557–70. doi:10.1016/S1473-3099(11)70007-X. PMID   21600850.
  22. 1 2 3 4 5 6 Pittet, L. F.; Posfay-Barbe, K. M. (2012). "Pneumococcal vaccines for children: A global public health priority". Clinical Microbiology and Infection. 18 (Suppl 5): 25–36. doi: 10.1111/j.1469-0691.2012.03938.x . PMID   22862432.
  23. Nakagomi, O; Iturriza-Gomara, M; Nakagomi, T; Cunliffe, N. A. (2013). "Incorporation of a rotavirus vaccine into the national immunisation schedule in the United Kingdom: A review". Expert Opinion on Biological Therapy. 13 (11): 1613–21. doi:10.1517/14712598.2013.840285. PMID   24088009. S2CID   5405583.
  24. Lopman, B. A.; Payne, D. C.; Tate, J. E.; Patel, M. M.; Cortese, M. M.; Parashar, U. D. (2012). "Post-licensure experience with rotavirus vaccination in high and middle income countries; 2006 to 2011". Current Opinion in Virology. 2 (4): 434–42. doi:10.1016/j.coviro.2012.05.002. PMID   22749491.
  25. 1 2 Kim, T. H. (2014). "Seasonal influenza and vaccine herd effect". Clinical and Experimental Vaccine Research. 3 (2): 128–32. doi:10.7774/cevr.2014.3.2.128. PMC   4083064 . PMID   25003085.
  26. 1 2 3 Lowy, D. R.; Schiller, J. T. (2012). "Reducing HPV-associated cancer globally". Cancer Prevention Research. 5 (1): 18–23. doi:10.1158/1940-6207.CAPR-11-0542. PMC   3285475 . PMID   22219162.
  27. 1 2 3 4 5 Lenzi, A; Mirone, V; Gentile, V; Bartoletti, R; Ficarra, V; Foresta, C; Mariani, L; Mazzoli, S; Parisi, S. G.; Perino, A; Picardo, M; Zotti, C. M. (2013). "Rome Consensus Conference – statement; human papilloma virus diseases in males". BMC Public Health. 13: 117. doi:10.1186/1471-2458-13-117. PMC   3642007 . PMID   23391351.
  28. Garland, S. M.; Skinner, S. R.; Brotherton, J. M. (2011). "Adolescent and young adult HPV vaccination in Australia: Achievements and challenges". Preventive Medicine. 53 (Suppl 1): S29–35. doi:10.1016/j.ypmed.2011.08.015. PMID   21962468.
  29. 1 2 3 4 5 6 7 8 Rodpothong, P; Auewarakul, P (2012). "Viral evolution and transmission effectiveness". World Journal of Virology. 1 (5): 131–34. doi:10.5501/wjv.v1.i5.131. PMC   3782273 . PMID   24175217.
  30. 1 2 Corti, D; Lanzavecchia, A (2013). "Broadly neutralizing antiviral antibodies". Annual Review of Immunology. 31: 705–42. doi:10.1146/annurev-immunol-032712-095916. PMID   23330954.
  31. 1 2 3 Bull, R. A.; White, P. A. (2011). "Mechanisms of GII.4 norovirus evolution". Trends in Microbiology. 19 (5): 233–40. doi:10.1016/j.tim.2011.01.002. PMID   21310617.
  32. 1 2 Ramani, S; Atmar, R. L.; Estes, M. K. (2014). "Epidemiology of human noroviruses and updates on vaccine development". Current Opinion in Gastroenterology. 30 (1): 25–33. doi:10.1097/MOG.0000000000000022. PMC   3955997 . PMID   24232370.
  33. 1 2 3 Pleschka, S (2013). "Overview of Influenza Viruses". Swine Influenza. Current Topics in Microbiology and Immunology. 370. pp. 1–20. doi:10.1007/82_2012_272. ISBN   978-3642368707. PMID   23124938.
  34. Han, T; Marasco, W. A. (2011). "Structural basis of influenza virus neutralization". Annals of the New York Academy of Sciences. 1217 (1): 178–90. Bibcode:2011NYASA1217..178H. doi:10.1111/j.1749-6632.2010.05829.x. PMC   3062959 . PMID   21251008.
  35. Reperant, L. A.; Rimmelzwaan, G. F.; Osterhaus, A. D. (2014). "Advances in influenza vaccination". F1000Prime Reports. 6: 47. doi:10.12703/p6-47. PMC   4047948 . PMID   24991424.
  36. 1 2 3 Weinberger, D. M.; Malley, R; Lipsitch, M (2011). "Serotype replacement in disease after pneumococcal vaccination". The Lancet. 378 (9807): 1962–73. doi:10.1016/S0140-6736(10)62225-8. PMC   3256741 . PMID   21492929.
  37. 1 2 3 McEllistrem, M. C.; Nahm, M. H. (2012). "Novel pneumococcal serotypes 6C and 6D: Anomaly or harbinger". Clinical Infectious Diseases. 55 (10): 1379–86. doi:10.1093/cid/cis691. PMC   3478140 . PMID   22903767.
  38. Dagan, R (2009). "Impact of pneumococcal conjugate vaccine on infections caused by antibiotic-resistant Streptococcus pneumoniae". Clinical Microbiology and Infection. 15 (Suppl 3): 16–20. doi:10.1111/j.1469-0691.2009.02726.x. PMID   19366365.
  39. Lynch Jp, 3rd; Zhanel, G. G. (2010). "Streptococcus pneumoniae: Epidemiology and risk factors, evolution of antimicrobial resistance, and impact of vaccines". Current Opinion in Pulmonary Medicine. 16 (3): 217–25. doi:10.1097/MCP.0b013e3283385653. PMID   20375783. S2CID   205784538.
  40. Njeumi, F; Taylor, W; Diallo, A; Miyagishima, K; Pastoret, P. P.; Vallat, B; Traore, M (2012). "The long journey: A brief review of the eradication of rinderpest". Revue Scientifique et Technique (International Office of Epizootics). 31 (3): 729–46. PMID   23520729.
  41. 1 2 Smith, K. A. (2013). "Smallpox: Can we still learn from the journey to eradication?". The Indian Journal of Medical Research. 137 (5): 895–99. PMC   3734679 . PMID   23760373.
  42. 1 2 3 4 5 Perisic, A; Bauch, C. T. (2009). "Social contact networks and disease eradicability under voluntary vaccination". PLOS Computational Biology. 5 (2): e1000280. Bibcode:2009PLSCB...5E0280P. doi:10.1371/journal.pcbi.1000280. PMC   2625434 . PMID   19197342.
  43. 1 2 3 4 5 6 7 Fu, F; Rosenbloom, D. I.; Wang, L; Nowak, M. A. (2011). "Imitation dynamics of vaccination behaviour on social networks" (PDF). Proceedings of the Royal Society B: Biological Sciences. 278 (1702): 42–49. doi:10.1098/rspb.2010.1107. PMC   2992723 . PMID   20667876.
  44. Wicker, S; Maltezou, H. C. (2014). "Vaccine-preventable diseases in Europe: Where do we stand?". Expert Review of Vaccines. 13 (8): 979–87. doi:10.1586/14760584.2014.933077. PMID   24958075. S2CID   23471069.
  45. 1 2 3 Fukuda, E.; Tanimoto, J. (2014). Impact of Stubborn Individuals on a Spread of Infectious Disease under Voluntary Vaccination Policy. Springer. pp. 1–10. ISBN   978-3319133591 . Retrieved 30 March 2015.
  46. 1 2 Barrett, Scott (2014). "Global Public Goods and International Development". In J. Warren Evans; Robin Davies (eds.). Too Global To Fail: The World Bank at the Intersection of National and Global Public Policy in 2025. World Bank Publications. pp. 13–18. ISBN   978-1464803109.
  47. 1 2 3 Gowda, C; Dempsey, A. F. (2013). "The rise (and fall?) of parental vaccine hesitancy". Human Vaccines & Immunotherapeutics. 9 (8): 1755–62. doi:10.4161/hv.25085. PMC   3906278 . PMID   23744504.
  48. Ozawa, S; Stack, M. L. (2013). "Public trust and vaccine acceptance – international perspectives". Human Vaccines & Immunotherapeutics. 9 (8): 1774–78. doi:10.4161/hv.24961. PMC   3906280 . PMID   23733039.
  49. Parker, A. M.; Vardavas, R; Marcum, C. S.; Gidengil, C. A. (2013). "Conscious consideration of herd immunity in influenza vaccination decisions". American Journal of Preventive Medicine. 45 (1): 118–21. doi:10.1016/j.amepre.2013.02.016. PMC   3694502 . PMID   23790997.
  50. Unless noted, R0 values are from: History and Epidemiology of Global Smallpox Eradication Archived 17 March 2017 at the Wayback Machine From the training course titled "Smallpox: Disease, Prevention, and Intervention". The Centers for Disease Control and Prevention and the World Health Organization. Slide 17. Retrieved 13 March 2015.
  51. 1 2 Biggerstaff, M; Cauchemez, S; Reed, C; Gambhir, M; Finelli, L (2014). "Estimates of the reproduction number for seasonal, pandemic, and zoonotic influenza: A systematic review of the literature". BMC Infectious Diseases. 14: 480. doi:10.1186/1471-2334-14-480. PMC   4169819 . PMID   25186370.
  52. Fontanet A, Cauchemez S (9 September 2020). "COVID-19 herd immunity: where are we?". Nat Rev Immunol. 20 (10): 583–584. doi: 10.1038/s41577-020-00451-5 . PMC   7480627 . PMID   32908300.
  53. Randolph HE, Barreiro LB (19 May 2020). "Herd Immunity: Understanding COVID-19". Immunity. 52 (5): 737–741. doi: 10.1016/j.immuni.2020.04.012 . PMC   7236739 . PMID   32433946.
  54. Wallinga, J; Teunis, P (2004). "Different epidemic curves for severe acute respiratory syndrome reveal similar impacts of control measures". American Journal of Epidemiology. 160 (6): 509–16. doi: 10.1093/aje/kwh255 . PMC   7110200 . PMID   15353409.
  55. Althaus, C. L. (2014). "Estimating the Reproduction Number of Ebola Virus (EBOV) During the 2014 Outbreak in West Africa". PLOS Currents. 6. arXiv: 1408.3505 . Bibcode:2014arXiv1408.3505A. doi:10.1371/currents.outbreaks.91afb5e0f279e7f29e7056095255b288. PMC   4169395 . PMID   25642364.
  56. 1 2 Dabbaghian, V.; Mago, V. K. (2013). Theories and Simulations of Complex Social Systems. Springer. pp. 134–35. ISBN   978-3642391491 . Retrieved 29 March 2015.
  57. Handel, Andreas; Longini, Ira M; Antia, Rustom (22 March 2007). "What is the best control strategy for multiple infectious disease outbreaks?". Proceedings of the Royal Society B: Biological Sciences. 274 (1611): 833–837. doi:10.1098/rspb.2006.0015. ISSN   0962-8452. PMC   2093965 . PMID   17251095. In general, the number of infecteds grows until the number of susceptibles has fallen to Sth. At this point, the average number of secondary infections created by an infected person drops below 1 and therefore the number of infecteds starts to decrease. However, right at this inflection point, the maximum number of infecteds is present. These infecteds will create on average less than 1, but still more than zero further infections, leading to additional depletion of susceptibles and therefore causing an overshoot.
  58. Fung, Isaac Chun-Hai; Antia, Rustom; Handel, Andreas (11 June 2012). "How to Minimize the Attack Rate during Multiple Influenza Outbreaks in a Heterogeneous Population". PLOS ONE. 7 (6): e36573. doi:10.1371/journal.pone.0036573. ISSN   1932-6203. PMC   3372524 . PMID   22701558.
  59. Bergstrom, Carl T.; Dean, Natalie (1 May 2020). "Opinion: What the Proponents of 'Natural' Herd Immunity Don't Say". The New York Times. Retrieved 30 May 2020.
  60. 1 2 3 Rashid, H; Khandaker, G; Booy, R (2012). "Vaccination and herd immunity: What more do we know?". Current Opinion in Infectious Diseases. 25 (3): 243–249. doi:10.1097/QCO.0b013e328352f727. PMID   22561998. S2CID   19197608.
  61. Maglione, M. A.; Das, L; Raaen, L; Smith, A; Chari, R; Newberry, S; Shanman, R; Perry, T; Goetz, M. B.; Gidengil, C (2014). "Safety of vaccines used for routine immunization of U.S. Children: A systematic review". Pediatrics. 134 (2): 325–37. doi: 10.1542/peds.2014-1079 . PMID   25086160.
  62. Di Pietrantonj, Carlo; Rivetti, Alessandro; Marchione, Pasquale; Debalini, Maria Grazia; Demicheli, Vittorio (20 April 2020). "Vaccines for measles, mumps, rubella, and varicella in children". The Cochrane Database of Systematic Reviews. 4: CD004407. doi:10.1002/14651858.CD004407.pub4. ISSN   1469-493X. PMC   7169657 . PMID   32309885.
  63. 1 2 3 Pommerville, J. C. (2014). Fundamentals of Microbiology: Body Systems Edition. Jones & Bartlett Publishers. pp. 559–63. ISBN   978-1284057102 . Retrieved 30 March 2015.
  64. Papaloukas, O; Giannouli, G; Papaevangelou, V (2014). "Successes and challenges in varicella vaccine". Therapeutic Advances in Vaccines. 2 (2): 39–55. doi:10.1177/2051013613515621. PMC   3991154 . PMID   24757524.
  65. Shann, F (2013). "Nonspecific effects of vaccines and the reduction of mortality in children". Clinical Therapeutics. 35 (2): 109–14. doi:10.1016/j.clinthera.2013.01.007. PMID   23375475.
  66. Visser, A; Hoosen, A (2012). "Haemophilus influenzae type b conjugate vaccines – a South African perspective". Vaccine. 30 (Suppl 3): C52–57. doi:10.1016/j.vaccine.2012.06.022. hdl: 2263/20792 . PMID   22939022.
  67. Leuridan, E; Sabbe, M; Van Damme, P (2012). "Measles outbreak in Europe: Susceptibility of infants too young to be immunized". Vaccine. 30 (41): 5905–13. doi:10.1016/j.vaccine.2012.07.035. PMID   22841972.
  68. Hodgins, D. C.; Shewen, P. E. (2012). "Vaccination of neonates: Problem and issues". Vaccine. 30 (9): 1541–59. doi:10.1016/j.vaccine.2011.12.047. PMID   22189699.
  69. Chucri, T. M.; Monteiro, J. M.; Lima, A. R.; Salvadori, M. L.; Kfoury Jr, J. R.; Miglino, M. A. (2010). "A review of immune transfer by the placenta". Journal of Reproductive Immunology. 87 (1–2): 14–20. doi:10.1016/j.jri.2010.08.062. PMID   20956021.
  70. Palmeira, P; Quinello, C; Silveira-Lessa, A. L.; Zago, C. A.; Carneiro-Sampaio, M (2012). "IgG placental transfer in healthy and pathological pregnancies". Clinical and Developmental Immunology. 2012: 1–13. doi:10.1155/2012/985646. PMC   3251916 . PMID   22235228.
  71. 1 2 Parija, S. C. (2014). Textbook of Microbiology & Immunology. Elsevier Health Sciences. pp. 88–89. ISBN   978-8131236246 . Retrieved 30 March 2015.
  72. Detels, R.; Gulliford, M.; Karim, Q. A.; Tan, C. C. (2015). Oxford Textbook of Global Public Health. Oxford University Press. p. 1490. ISBN   978-0199661756 . Retrieved 30 March 2015.
  73. Demicheli, Vittorio; Barale, Antonella; Rivetti, Alessandro (6 July 2015). "Vaccines for women for preventing neonatal tetanus". The Cochrane Database of Systematic Reviews (7): CD002959. doi:10.1002/14651858.CD002959.pub4. ISSN   1469-493X. PMC   7138051 . PMID   26144877.
  74. Swamy, G. K.; Garcia-Putnam, R (2013). "Vaccine-preventable diseases in pregnancy". American Journal of Perinatology. 30 (2): 89–97. doi:10.1055/s-0032-1331032. PMID   23271378.
  75. Bärnighausen, T.; Bloom, D. E.; Cafiero-Fonseca, E. T.; O'Brien, J. C. (26 August 2014). "Valuing vaccination". Proc Natl Acad Sci U S A. 111 (34): 12313–19. Bibcode:2014PNAS..11112313B. doi:10.1073/pnas.1400475111. PMC   4151736 . PMID   25136129.
  76. 1 2 3 Deogaonkar, R.; Hutubessy, R.; van der Putten I.; Evers S.; Jit M. (16 October 2012). "Systematic review of studies evaluating the broader economic impact of vaccination in low and middle income countries". BMC Public Health. 12: 878. doi:10.1186/1471-2458-12-878. PMC   3532196 . PMID   23072714.
  77. 1 2 Jit, M.; Newall, A. T.; Beutels, P. (April 2013). "Key issues for estimating the impact and cost-effectiveness of seasonal influenza vaccination strategies". Hum Vaccin Immunother. 9 (4): 834–40. doi:10.4161/hv.23637. PMC   3903903 . PMID   23357859.
  78. Topley, W. W. C.; Wilson, G. S. (May 1923). "The Spread of Bacterial Infection. The Problem of Herd-Immunity". The Journal of Hygiene . 21 (3): 243–49. doi:10.1017/s0022172400031478. PMC   2167341 . PMID   20474777.
  79. Hedrich, A. W. (1933). Monthly Estimates of the Child Population Susceptible to Measles, 1900–1931, Baltimore, Md. American Journal of Epidemiology, 17(3), 613–636.
  80. Strassburg, M. A. (1982). "The global eradication of smallpox". American Journal of Infection Control. 10 (2): 53–59. doi:10.1016/0196-6553(82)90003-7. PMID   7044193.