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Assessing vaccine efficacy for infectious diseases with variable immunity using a mathematical model.

ABSTRACT: This study introduces an SIRS compartmental mathematical model encompassing vaccination and variable immunity periods for infectious diseases. I derive a basic reproduction number formula and assess the local and global stability of disease-free and the local stability of the endemic equilibria. I demonstrate that the basic reproduction number in the presence of a vaccine is highly sensitive to the rate of immunity loss, and even a slight reduction in this rate can significantly contribute to disease control. Additionally, I have derived a formula to calculate the critical efficacy period required for a vaccine to effectively manage and control the disease.The analysis conducted for the model suggests that increasing the vaccine's immunity duration (efficacy) decelerates disease dynamics, leading to reduced rates of reinfection and less severe disease outcomes. Furthermore, this delay contributes to a decrease in the basic reproduction number ( R0 ), thus facilitating more rapid disease control efforts.

SUBMITTER: Al-Arydah M

PROVIDER: S-EPMC11316787 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature

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Assessing vaccine efficacy for infectious diseases with variable immunity using a mathematical model.

Al-Arydah Mo'tassem M

Scientific reports 20240810 1

This study introduces an SIRS compartmental mathematical model encompassing vaccination and variable immunity periods for infectious diseases. I derive a basic reproduction number formula and assess the local and global stability of disease-free and the local stability of the endemic equilibria. I demonstrate that the basic reproduction number in the presence of a vaccine is highly sensitive to the rate of immunity loss, and even a slight reduction in this rate can significantly contribute to di ...[more]

PMID: 39127773

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Project description:Interferon lambdas (IFN-λs; IFNL1-4) modulate immunity in the context of infections and autoimmune diseases, through a network of induced genes. IFN-λs act by binding to the heterodimeric IFN-λ receptor (IFNLR), activating a STAT phosphorylation-dependent signaling cascade. Thereby hundreds of IFN-stimulated genes are induced, which modulate various immune functions via complex forward and feedback loops. When compared to the well-characterized IFN-α signaling cascade, three important differences have been discovered. First, the IFNLR is not ubiquitously expressed: in particular, immune cells show significant variation in the expression levels of and susceptibilities to IFN-λs. Second, the binding affinities of individual IFN-λs to the IFNLR varies greatly and are generally lower compared to the binding affinities of IFN-α to its receptor. Finally, genetic variation in the form of a series of single-nucleotide polymorphisms (SNPs) linked to genes involved in the IFN-λ signaling cascade has been described and associated with the clinical course and treatment outcomes of hepatitis B and C virus infection. The clinical impact of IFN-λ signaling and the SNP variations may, however, reach far beyond viral hepatitis. Recent publications show important roles for IFN-λs in a broad range of viral infections such as human T-cell leukemia type-1 virus, rotaviruses, and influenza virus. IFN-λ also potentially modulates the course of bacterial colonization and infections as shown for Staphylococcus aureus and Mycobacterium tuberculosis. Although the immunological processes involved in controlling viral and bacterial infections are distinct, IFN-λs may interfere at various levels: as an innate immune cytokine with direct antiviral effects; or as a modulator of IFN-α-induced signaling via the suppressor of cytokine signaling 1 and the ubiquitin-specific peptidase 18 inhibitory feedback loops. In addition, the modulation of adaptive immune functions via macrophage and dendritic cell polarization, and subsequent priming, activation, and proliferation of pathogen-specific T- and B-cells may also be important elements associated with infectious disease outcomes. This review summarizes the emerging details of the IFN-λ immunobiology in the context of the host immune response and viral and bacterial infections.

Dataset Information

Assessing vaccine efficacy for infectious diseases with variable immunity using a mathematical model.

Publications

Assessing vaccine efficacy for infectious diseases with variable immunity using a mathematical model.

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