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The potential for vaccination-induced herd immunity against the SARS-CoV-2 B.1.1.7 variant.

ABSTRACT: We assess the feasibility of reaching the herd immunity threshold against SARS-CoV-2 through vaccination, considering vaccine effectiveness (VE), transmissibility of the virus and the level of pre-existing immunity in populations, as well as their age structure. If highly transmissible variants of concern become dominant in areas with low levels of naturally-acquired immunity and/or in populations with large proportions of < 15 year-olds, control of infection without non-pharmaceutical interventions may only be possible with a VE ≥ 80%, and coverage extended to children.

SUBMITTER: Hodgson D

PROVIDER: S-EPMC8138959 | biostudies-literature | 2021 May

REPOSITORIES: biostudies-literature

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The potential for vaccination-induced herd immunity against the SARS-CoV-2 B.1.1.7 variant.

Hodgson David D Flasche Stefan S Jit Mark M Kucharski Adam J AJ

Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin 20210501 20

We assess the feasibility of reaching the herd immunity threshold against SARS-CoV-2 through vaccination, considering vaccine effectiveness (VE), transmissibility of the virus and the level of pre-existing immunity in populations, as well as their age structure. If highly transmissible variants of concern become dominant in areas with low levels of naturally-acquired immunity and/or in populations with large proportions of < 15 year-olds, control of infection without non-pharmaceutical intervent ...[more]

PMID: 34018481

Similar Datasets

Percentages of Vaccination Coverage Required to Establish Herd Immunity against SARS-CoV-2.

Project description:The pandemic associated with SARS-CoV-2 is a worldwide public health challenge. The WHO has proposed to achieve 70% COVID-19 vaccination coverage in all countries by mid-2022. Nevertheless, the prevention strategy based on COVID-19 vaccination and other applied prevention measures has not been sufficient to prevent SARS-CoV-2 epidemic waves. This study assessed the vaccination coverage that would be required to establish herd immunity against SARS-CoV-2, taking into account virus transmissibility (Ro values from 1.1 to 10) and COVID-19 vaccination effectiveness. The study found that high percentages of vaccination coverage and high levels of vaccination effectiveness are necessary to block the transmission of Omicron and other SARS-CoV-2 variants with greater infectious capacity. COVID-19 vaccination programs could establish herd immunity against SARS-CoV-2, with Ro values ranging from 3 to 10 and levels of COVID-19 vaccination effectiveness of 70-100%. Factors reducing COVID-19 vaccination effectiveness (emergent variants, infections among vaccinated individuals, high risk individuals) and factors increasing SARS-CoV-2 transmissibility (close settings) increased the percentages of vaccination coverage that would be required to establish herd immunity. Two measures should be implemented to establish herd immunity against SARS-CoV-2: (1) achieve ≥ 90% COVID-19 vaccination coverage in all countries worldwide, and (2) increase the effectiveness of COVID-19 vaccines in preventing Omicron infection to at least 88%.

| S-EPMC9144560 | biostudies-literature

Herd immunity induced by COVID-19 vaccination programs and suppression of epidemics caused by the SARS-CoV-2 Delta variant in China.

Project description:BackgroundTo allow a return to a pre-COVID-19 lifestyle, virtually every country has initiated a vaccination program to mitigate severe disease burden and control transmission. However, it remains to be seen whether herd immunity will be within reach of these programs.MethodsWe developed a data-driven model of SARS-CoV-2 transmission for China, a population with low prior immunity from natural infection. The model is calibrated considering COVID-19 natural history and the estimated transmissibility of the Delta variant. Three vaccination programs are tested, including the one currently enacted in China and model-based estimates of the herd immunity level are provided.ResultsWe found that it is unlike to reach herd immunity for the Delta variant given the relatively low efficacy of the vaccines used in China throughout 2021, the exclusion of underage individuals from the targeted population, and the lack of prior natural immunity. We estimate that, assuming a vaccine efficacy of 90% against the infection, vaccine-induced herd immunity would require a coverage of 93% or higher of the Chinese population. However, even when vaccine-induced herd immunity is not reached, we estimated that vaccination programs can reduce SARS-CoV-2 infections by 53-58% in case of an epidemic starts to unfold in the fall of 2021.ConclusionsEfforts should be taken to increase population's confidence and willingness to be vaccinated and to guarantee highly efficacious vaccines for a wider age range.

| S-EPMC8328074 | biostudies-literature

Modelling direct and herd protection effects of vaccination against the SARS-CoV-2 Delta variant in Australia.

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| S-EPMC8662033 | biostudies-literature

Challenges in creating herd immunity to SARS-CoV-2 infection by mass vaccination.

Project description: Not available

| S-EPMC7836302 | biostudies-literature

DNA vaccination induced protective immunity against SARS CoV-2 infection in hamsterss.

Project description:The development of efficient vaccines against COVID-19 is an emergent need for global public health. The spike protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a major target for the COVID-19 vaccine. To quickly respond to the outbreak of the SARS-CoV-2 pandemic, a nucleic acid-based vaccine is a novel option, beyond the traditional inactivated virus vaccine or recombinant protein vaccine. Here, we report a DNA vaccine containing the spike gene for delivery via electroporation. The spike genes of SARS-CoV and SARS-CoV-2 were codon optimized for mammalian cell expression and then cloned into mammalian cell expression vectors, called pSARS-S and pSARS2-S, respectively. Spike protein expression was confirmed by immunoblotting after transient expression in HEK293T cells. After immunization, sera were collected for antigen-specific antibody and neutralizing antibody titer analyses. We found that both pSARS-S and pSARS2-S immunization induced similar levels of antibodies against S2 of SARS-CoV-2. In contrast, only pSARS2-S immunization induced antibodies against the receptor-binding domain of SARS-CoV-2. We further found that pSARS2-S immunization, but not pSARS-S immunization, could induce very high titers of neutralizing antibodies against SARS-CoV-2. We further analyzed SARS-CoV-2 S protein-specific T cell responses and found that the immune responses were biased toward Th1. Importantly, pSARS2-S immunization in hamsters could induce protective immunity against SARS-CoV-2 challenge in vivo. These data suggest that DNA vaccination could be a promising approach for protecting against COVID-19.

| S-EPMC8158926 | biostudies-literature

Host-directed therapies against early-lineage SARS-CoV-2 retain efficacy against B.1.1.7 variant.

Project description:Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in millions of deaths worldwide and massive societal and economic burden. Recently, a new variant of SARS-CoV-2, known as B.1.1.7, was first detected in the United Kingdom and is spreading in several other countries, heightening public health concern and raising questions as to the resulting effectiveness of vaccines and therapeutic interventions. We and others previously identified host-directed therapies with antiviral efficacy against SARS-CoV-2 infection. Less prone to the development of therapy resistance, host-directed drugs represent promising therapeutic options to combat emerging viral variants as host genes possess a lower propensity to mutate compared to viral genes. Here, in the first study of the full-length B.1.1.7 variant virus , we find two host-directed drugs, plitidepsin (aplidin; inhibits translation elongation factor eEF1A) and ralimetinib (inhibits p38 MAP kinase cascade), as well as remdesivir, to possess similar antiviral activity against both the early-lineage SARS-CoV-2 and the B.1.1.7 variant, evaluated in both human gastrointestinal and lung epithelial cell lines. We find that plitidepsin is over an order of magnitude more potent than remdesivir against both viruses. These results highlight the importance of continued development of host-directed therapeutics to combat current and future coronavirus variant outbreaks.

| S-EPMC7836107 | biostudies-literature

BNT162b2 Booster Vaccination Induced Immunity against SARS-CoV-2 Variants among Hemodialysis Patients.

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| S-EPMC9227334 | biostudies-literature

Contact-adjusted Immunity Levels against SARS-CoV-2 in Korea and Prospects for Achieving Herd Immunity.

Project description:The proportion of population vaccinated cannot be directly translated into the herd immunity. We have to account for the age-stratified contact patterns to calculate the population immunity level, since not every individual gathers evenly. Here, we calculated the contact-adjusted population immunity against severe acute respiratory syndrome coronavirus 2 in South Korea using age-specific incidence and vaccine uptake rate. We further explored options to achieve the theoretical herd immunity with age-varying immunity scenarios. As of June 21, 2021, when a quarter of the population received at least one dose of a coronavirus disease 2019 (COVID-19) vaccine, the contact-adjusted immunity level was 12.5% under the social distancing level 1. When 80% of individuals aged 10 years and over gained immunity, we could achieve a 58.2% contact-adjusted immunity level. The pros and cons of vaccinating children should be weighed since the risks of COVID-19 for the young are less than the elderly, and the long-term safety of vaccines is still obscure.

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Potential transmission chains of variant B.1.1.7 and co-mutations of SARS-CoV-2.

Project description:The presence of SARS-CoV-2 mutants, including the emerging variant B.1.1.7, has raised great concerns in terms of pathogenesis, transmission, and immune escape. Characterizing SARS-CoV-2 mutations, evolution, and effects on infectivity and pathogenicity is crucial to the design of antibody therapies and surveillance strategies. Here, we analyzed 454,443 SARS-CoV-2 spike genes/proteins and 14,427 whole-genome sequences. We demonstrated that the early variant B.1.1.7 may not have evolved spontaneously in the United Kingdom or within human populations. Our extensive analyses suggested that Canidae, Mustelidae or Felidae, especially the Canidae family (for example, dog) could be a possible host of the direct progenitor of variant B.1.1.7. An alternative hypothesis is that the variant was simply yet to be sampled. Notably, the SARS-CoV-2 whole-genome represents a large number of potential co-mutations. In addition, we used an experimental SARS-CoV-2 reporter replicon system to introduce the dominant co-mutations NSP12_c14408t, 5'UTR_c241t, and NSP3_c3037t into the viral genome, and to monitor the effect of the mutations on viral replication. Our experimental results demonstrated that the co-mutations significantly attenuated the viral replication. The study provides valuable clues for discovering the transmission chains of variant B.1.1.7 and understanding the evolutionary process of SARS-CoV-2.

| S-EPMC8203788 | biostudies-literature

Limited cross-variant immunity from SARS-CoV-2 Omicron without vaccination.

Project description:SARS-CoV-2 Delta and Omicron are globally relevant variants of concern. Although individuals infected with Delta are at risk of developing severe lung disease, infection with Omicron often causes milder symptoms, especially in vaccinated individuals1,2. The question arises of whether widespread Omicron infections could lead to future cross-variant protection, accelerating the end of the pandemic. Here we show that without vaccination, infection with Omicron induces a limited humoral immune response in mice and humans. Sera from mice overexpressing the human ACE2 receptor and infected with Omicron neutralize only Omicron, but not other variants of concern, whereas broader cross-variant neutralization was observed after WA1 and Delta infections. Unlike WA1 and Delta, Omicron replicates to low levels in the lungs and brains of infected animals, leading to mild disease with reduced expression of pro-inflammatory cytokines and diminished activation of lung-resident T cells. Sera from individuals who were unvaccinated and infected with Omicron show the same limited neutralization of only Omicron itself. By contrast, Omicron breakthrough infections induce overall higher neutralization titres against all variants of concern. Our results demonstrate that Omicron infection enhances pre-existing immunity elicited by vaccines but, on its own, may not confer broad protection against non-Omicron variants in unvaccinated individuals.

| S-EPMC9279157 | biostudies-literature

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