Impact of host genetic polymorphisms on vaccine induced antibody response

Linnik, Janina; Egli, Adrian

doi:10.1080/21645515.2015.1119345

Cited by 51 publications

(41 citation statements)

References 103 publications

(104 reference statements)

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“…Patients with infectious diseases often show heterogeneous clinical courses with a range of associated morbidities and variable mortality. This is dependent on a series of factors covering the complex aspects of host-pathogen interactions (1)(2)(3)(4)(5). IFNs play a crucial role in these interactions-defining the outcome of many viral, bacterial, fungal, and parasitic infections (6-16) (see Figure 1).…”

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confidence: 99%

Interferon Lambda: Modulating Immunity in Infectious Diseases

2017

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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.

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Interferon Lambda: Modulating Immunity in Infectious Diseases

2017

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“…Our pilot study is the first study in children with haemophilia to confirm adequate immunogenic responses to SQ diphtheria and tetanus vaccination. Factors that affect the immune response to vaccine antigens are complex and include host factors like obesity, smoking, genetic polymorphisms as well as vaccine related factors, including site of injection, and whether antigens are given as separate injections or combined with other antigens . In our study, all children received combined vaccines.…”

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Subcutaneous diphtheria and tetanus vaccines in children with haemophilia: A pilot study and review of the literature

et al. 2017

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“…Factors such as previous exposure to IAV infections or vaccines, age, and the closeness of the match between the vaccine and circulating strains are important to explain differences in vaccine effectiveness between seasons and group populations [44,46,[150][151][152]. However, multiple reports have demonstrated that the host genetic background and polymorphisms on key immune response genes modulate the immune response to infection or vaccination [153][154][155][156][157][158][159][160]. Therefore, new insights into IAV-host interaction and immune response modulating factors could allow us to design better vaccination strategies.…”

Section: Snps In Genes That Influence the Iav Vaccine Responsementioning

confidence: 99%

“…SNPs may modify the humoral immune response after IAV vaccination. Therefore, their impact on the immune responses induced after IAV vaccination are being analyzed [153][154][155][156]. The major histocompatibility complex (MHC) is localized in chromosome 6 of the human genome, it includes multiple genes and exhibits considerable diversity between populations.…”

Section: Snps In Genes That Influence the Iav Vaccine Responsementioning

confidence: 99%

Host Single Nucleotide Polymorphisms Modulating Influenza A Virus Disease in Humans

Nogales¹,

DeDiego

2019

Pathogens

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A large number of human genes associated with viral infections contain single nucleotide polymorphisms (SNPs), which represent a genetic variation caused by the change of a single nucleotide in the DNA sequence. SNPs are located in coding or non-coding genomic regions and can affect gene expression or protein function by different mechanisms. Furthermore, they have been linked to multiple human diseases, highlighting their medical relevance. Therefore, the identification and analysis of this kind of polymorphisms in the human genome has gained high importance in the research community, and an increasing number of studies have been published during the last years. As a consequence of this exhaustive exploration, an association between the presence of some specific SNPs and the susceptibility or severity of many infectious diseases in some risk population groups has been found. In this review, we discuss the relevance of SNPs that are important to understand the pathology derived from influenza A virus (IAV) infections in humans and the susceptibility of some individuals to suffer more severe symptoms. We also discuss the importance of SNPs for IAV vaccine effectiveness. multiple mechanisms, although there are some differences between strains. For that genome plasticity, IAV take advantage of multiple strategies, such as alternative splicing, frameshift mechanisms, and overlapping open reading frames (ORFs) [7][8][9]. In addition, the coding capability of the viral genome is extended by encoding multifunctional proteins that act at different steps during virus infection. of synthetized vRNP, ensuring that the vRNPs are available for packaging [24]. Moreover, NEP has also other functions during IAV infection, contributing to viral budding and to regulate viral RNA synthesis. NS1 is a multifunctional protein and a key viral factor that counteracts the host antiviral responses. NS1 has been shown to inhibit the production of interferon (IFN), the activity and expression of multiple interferon-induced genes (ISG) and the processing and nuclear transport of host mRNAs causing cellular shut-off [25,26]. Segment 3 of IAV also encodes two proteins, the polymerase component PA and PA-X. PA is translated directly from the PA mRNA, whereas PA-X is translated using a +1 frameshift mechanism from the same open reading frame (ORF) [9]. Synergistically with NS1, PA-X is also able to block the cellular antiviral responses by inhibiting host protein expression. Moreover, the PA-X protein has been shown to modulate host inflammation, immune responses, apoptosis, and virus pathogenesis [25][26][27][28][29][30].

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Impact of host genetic polymorphisms on vaccine induced antibody response

Cited by 51 publications

References 103 publications

Interferon Lambda: Modulating Immunity in Infectious Diseases

Interferon Lambda: Modulating Immunity in Infectious Diseases

Subcutaneous diphtheria and tetanus vaccines in children with haemophilia: A pilot study and review of the literature

Host Single Nucleotide Polymorphisms Modulating Influenza A Virus Disease in Humans

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