Bacillus Seropositivity
Introduction
Background
Bacillus seropositivity refers to the presence of detectable antibodies against Bacillus species in an individual's blood serum. These antibodies are produced by the immune system in response to exposure to bacillary pathogens, indicating a past infection or immune activation. Serological tests, often employing methods like fluorescent bead-based multiplex serology, are used to measure total antibody levels, typically quantified as median fluorescence intensity (MFI). A specific seropositivity threshold is established to distinguish between seropositive and seronegative individuals. [1] This measurement provides valuable insight into an individual's immunological history regarding Bacillus exposure.
Biological Basis
The human immune system mounts an antibody-mediated response to infectious agents, including Bacillus species. Individual variations in this immune response, including the likelihood of developing seropositivity and the magnitude of antibody levels, are influenced by genetic factors. Genome-Wide Association Studies (GWAS) are employed to identify single nucleotide polymorphisms (SNPs) associated with both the presence (seropositivity) and the quantitative levels of antibodies. [1] A significant number of these genetic associations are often found within the Major Histocompatibility Complex (MHC) region on chromosome 6, which encodes Human Leukocyte Antigen (HLA) genes such as HLA-A, HLA-B, HLA-C, HLA-DRB1, HLA-DRB3, HLA-DRB4, HLA-DRB5, HLA-DPA1, HLA-DPB1, HLA-DQA1, and HLA-DQB1. [1] Studies also demonstrate that antibody levels to various pathogens exhibit heritability, further underscoring the genetic contribution to immune responses. [2]
Clinical Relevance
Understanding bacillus seropositivity and its genetic underpinnings holds significant clinical relevance. The presence of antibodies can indicate prior exposure or infection, which may confer a degree of immunity or, conversely, highlight a history of infection that could impact an individual's health. Identifying genetic variants associated with seropositivity or antibody levels can help predict an individual's susceptibility to bacillary infections or their ability to mount an effective immune response. Such insights may inform personalized risk assessments, guide prophylactic strategies like vaccination, and aid in the development of targeted therapies. [1]
Social Importance
From a public health perspective, studying bacillus seropositivity in large cohorts, such as the UK Biobank, contributes to a broader understanding of population-level immune landscapes. [1] This knowledge can be crucial for monitoring the prevalence of bacillary infections, understanding disease transmission dynamics, and evaluating the effectiveness of public health interventions. Genetically informed approaches can help identify subgroups within a population that may be more vulnerable or more resilient to specific pathogens, enabling tailored public health strategies and potentially guiding resource allocation for disease prevention and control.
Methodological and Statistical Constraints
Research into bacillus seropositivity, like many genetic studies of infectious diseases, faces several methodological and statistical challenges that can influence the interpretation of findings. Specifically, the analysis for bacillus seropositivity was conducted with one of the smallest sample sizes among the studied infectious agents, involving only 1371 individuals. This limited sample size raises concerns about statistical power, increasing the risk of unstable statistics, genomic inflation, and an elevated rate of false-positive associations, making it difficult to confidently identify true genetic determinants. [1] Furthermore, the broader field of human infectious disease GWAS often struggles with small sample sizes or relies on self-reported diagnoses, which can further decrease statistical power and complicate clinical interpretation . [3], [4], [5] The diverse methodologies employed across the few published GWAS on infectious diseases also impede direct comparisons and replication efforts, highlighting a need for more standardized approaches.
The reliance on serological tests for phenotype definition introduces additional complexities, as these tests are inherently susceptible to low-level cross-binding with non-specific antibodies that may not accurately reflect a true infection. [1] Although quantitative analyses were restricted to samples above a predefined seropositivity threshold to mitigate some of these issues, the absence of clear exposure history for individuals remains a significant limitation. Ideally, future serological studies would include participants with confirmed exposure status to enhance the specificity of serological tests and improve the likelihood of identifying clinically meaningful genetic associations. [1] The large number of statistical tests performed in genome-wide and HLA association studies also necessitates stringent significance thresholds and careful interpretation to avoid spurious findings.
Generalizability and Ancestry Limitations
The findings regarding bacillus seropositivity are primarily derived from analyses restricted to individuals of White British ancestry within the UK Biobank cohort. This specific focus was implemented to minimize bias from population stratification, a common confounder in genetic studies. [1] However, this methodological choice inherently limits the generalizability of the results to other ancestral populations, as genetic architectures and allele frequencies can vary significantly across diverse ethnic groups. Consequently, the identified genetic variants associated with bacillus seropositivity may not hold the same effect sizes or even be present in populations with different genetic backgrounds, underscoring the need for multi-ancestry studies to validate and extend these findings.
Environmental Confounding and Etiological Gaps
The complex interplay between host genetics and environmental factors is a critical aspect of infectious disease susceptibility and immune response, yet it remains challenging to fully capture in genetic studies. For bacillus seropositivity, it is plausible that unmeasured environmental or socioeconomic confounders could have influenced the observed associations. [1] The environment is recognized as a major non-heritable determinant of infectious diseases, implying that genetic studies that do not adequately account for these external factors may present an incomplete picture of disease etiology. Future research efforts would benefit from integrating detailed environmental data to better elucidate gene-environment interactions and their impact on seropositivity.
Furthermore, despite identifying genetic associations, the underlying pathophysiology linking infectious agents to host immune responses and, in some cases, non-communicable diseases, often remains poorly understood. Establishing the true causal effects of specific genetic variants on bacillus seropositivity or its downstream consequences is challenging without a comprehensive understanding of these biological mechanisms. [1] Addressing these knowledge gaps requires integrating genetic findings with functional studies and longitudinal cohort data that can capture dynamic interactions over time.
Variants
Genetic variations play a crucial role in shaping the human immune response to infectious agents, influencing both susceptibility to infection and the nature of the antibody response. Genome-wide association studies (GWAS) are instrumental in identifying these genetic determinants by analyzing large populations, comparing seropositive and seronegative individuals, or examining quantitative antibody levels. [1] Such studies aim to uncover how specific single nucleotide polymorphisms (SNPs) might alter gene function and, consequently, impact the body's ability to combat pathogens, including bacillus species. [2]
The variant rs4745643 is located within the GNA14 gene, which encodes a guanine nucleotide-binding protein alpha-14 subunit. GNA14 is a vital component of G protein-coupled receptor signaling pathways, participating in a wide array of cellular processes, including cell proliferation, differentiation, and immune cell activation. As an intronic SNP, rs4745643 may influence GNA14 gene expression or mRNA splicing, potentially altering the quantity or functionality of the GNA14 protein. Such alterations could impact immune cell signaling cascades, thereby affecting the host's innate and adaptive immune responses to bacterial infections, including those caused by bacillus species, and influencing the development of bacillus seropositivity. [1] Identifying genetic variants that affect immune responses is essential for understanding host defense mechanisms against various pathogens. [6]
Another significant variant, rs7913103, is found within the C10orf90 gene. C10orf90, also known as APOOL, is a gene whose precise function in immunity is still being elucidated, but it has been implicated in processes such as apoptosis and lipid metabolism. Variations like rs7913103, an intronic SNP, can affect the transcription or processing of C10orf90 mRNA, potentially leading to altered levels or modified forms of its gene product. If C10orf90 plays a role in immune cell regulation or pathogen response pathways, changes induced by rs7913103 could modulate the immune system's handling of bacillus infections, affecting the efficacy of antigen presentation or the longevity of immune memory cells, which are crucial for maintaining seropositivity. [1] Understanding these genetic influences helps to explain varying antibody-mediated immune responses within populations. [1]
The variant rs71646793 is located in the ITPKB gene, which encodes inositol 1,4,5-trisphosphate 3-kinase B. ITPKB is a critical enzyme involved in the inositol phosphate signaling pathway, primarily by phosphorylating inositol 1,4,5-trisphosphate (IP3) to inositol 1,3,4,5-tetrakisphosphate (IP4), which is essential for regulating intracellular calcium levels and T-cell activation. As an intronic variant, rs71646793 could impact the expression or splicing of ITPKB, consequently influencing T-cell development, proliferation, and cytokine production. Altered ITPKB function due to this variant may affect the strength and duration of the adaptive immune response against bacillus pathogens, potentially influencing an individual's ability to clear infections or establish stable seropositivity. [1] Such genetic determinants are important for understanding host susceptibility and the variability in antibody levels observed following exposure to infectious agents. [2]
Key Variants
| RS ID | Gene | Related Traits |
|---|---|---|
| rs4745643 | GNA14 | bacillus seropositivity |
| rs7913103 | C10orf90 | bacillus seropositivity |
| rs71646793 | STUM - ITPKB | bacillus seropositivity |
Definition and Measurement of Seropositivity
Seropositivity, in the context of infectious agents, is precisely defined by the presence of specific antibodies in an individual's serum, indicating a past or current infection. [1] This trait conceptually reflects the host's humoral immune response to an encountered pathogen. Operational definitions involve quantitative measurements of total antibody levels, most commonly IgG, against various antigens associated with the infectious agent. [2] These measurements are typically performed using high-throughput methods such as fluorescent bead-based multiplex serology, utilizing platforms like Luminex 100, which yield a median fluorescence intensity (MFI) as a standardized quantification of antibody amount. [1] Alternatively, enzyme-linked immunosorbent assay (ELISA) is frequently employed, providing optical density (OD) values that correlate with antibody levels. [2] The validity of these measurement approaches, including the chosen seropositivity thresholds, is often established through rigorous validation processes involving reference gold standards. [1]
Diagnostic and Research Criteria for Classification
The classification of an individual as seropositive or seronegative relies on specific diagnostic criteria, primarily involving predefined thresholds or cut-off values for measured antibody levels. [1] For instance, a sample may be deemed seropositive if its MFI or optical density exceeds a predetermined threshold, which can be assay-specific and sometimes referenced against a positive control value. [7] In some cases, particularly for complex infectious agents like Chlamydia trachomatis or Helicobacter pylori, seropositivity may be based on a combination of reactions to multiple antigens, such as being positive for a specific antigen or for a minimum number of different antigens. [1] For research purposes, especially in genome-wide association studies (GWAS), seropositivity is often treated as a binary outcome (case-control status). [1] Quantitative antibody levels, when used for research, may undergo statistical transformations like inverse-normalization by rank or logarithmic transformation to meet the assumptions of genetic analyses and manage skewed data distributions. [2]
Terminology and Classification Systems
Key terminology in serological assessment includes "seropositivity" and "seronegativity" to denote the presence or absence of detected antibodies, respectively. [1] "Antibody levels" or "antibody titer" refers to the concentration or amount of specific antibodies in a sample, often quantified as MFI or optical density. [1] The term "seroprevalence" describes the proportion of individuals in a population who are seropositive for a particular infectious agent. [1] Classification systems for serological traits typically involve a categorical approach, dividing individuals into binary seropositive or seronegative groups, which is fundamental for case-control studies. [1] However, a dimensional approach is also widely utilized, employing the continuous quantitative antibody levels to assess variations in immune response within the seropositive population. [1] Further gradations of serological status can be established by categorizing quantitative values into several groups based on defined absorbance ranges, allowing for a more nuanced assessment of antibody strength. [7]
There is no information about the signs and symptoms of bacillus seropositivity in the provided context.
Causes of Bacillus Seropositivity
Bacillus seropositivity, indicating the presence of antibodies against Bacillus species, arises from a complex interplay of genetic predispositions, environmental exposures, and host-specific factors. Understanding these causal elements is crucial for elucidating the mechanisms of immune response and susceptibility to infection. Research, including genome-wide association studies (GWAS), has begun to unravel the intricate determinants influencing antibody-mediated immunity to various infectious agents. [1]
Genetic Architecture of Seropositivity
Genetic factors play a substantial role in determining an individual's seropositivity status and the magnitude of their antibody-mediated immune response. Studies have identified significant heritability for serological measures of common infections, indicating a strong inherited component. [2] Genome-wide association studies have frequently pinpointed loci within the Major Histocompatibility Complex (MHC) on chromosome 6 as critical genetic determinants, influencing both the presence of antibodies and the variability in their levels. [1]
Environmental and Lifestyle Influences
Exposure to infectious agents is a primary environmental determinant of seropositivity. The frequency and timing of exposure, particularly early in life, can significantly impact the immune response; for instance, early-age primary infection with certain viruses can lead to poorly controlled viral loads. [8]
Gene-Environment Interactions
The susceptibility to infection and the subsequent immune response are not solely dictated by either genes or environment but by their intricate interactions. Genetic variants that influence an individual's immune response can determine whether exposure to an infectious agent results in a higher or lower risk of developing seropositivity. [9]
Host-Specific and Other Modifiers
Beyond direct genetic and environmental factors, several host-specific attributes and comorbidities can modify an individual's likelihood of achieving seropositivity or influencing antibody levels. Age and sex are consistently included as covariates in genetic association studies, suggesting their role in modulating immune responses. [1]
Immune Recognition and Antibody Production
The body's defense against infectious agents relies on a complex adaptive immune response, primarily involving B cells that produce antibodies. The diversity of B-cell receptors, which are crucial for recognizing a vast array of antigens, is generated through somatic rearrangements of gene segments, along with the insertion and deletion of nucleotides, and further refined by somatic hypermutation. [10] This intricate process allows the immune system to recognize specific epitopes, which are distinct molecular parts of antigens. [10]
Upon encountering a pathogen, B cells are activated to differentiate into plasma cells, which secrete large quantities of antibodies into circulation. These antibodies, primarily immunoglobulin G (IgG) in the context of seropositivity for past infections, bind specifically to pathogen antigens to neutralize them or mark them for destruction. [2] While immunoglobulin E (IgE) antibodies are typically associated with allergic responses, IgG is the focus for detecting seropositivity, indicating a host's previous exposure and the resulting antibody-mediated immune response. [10]
Genetic Regulation of Antibody Responses
Genetic factors play a significant role in shaping an individual's antibody-mediated immune responses to infectious diseases. A key component is the human leukocyte antigen (HLA) system, encoded by the major histocompatibility complex (MHC) gene complex on chromosome 6. [1] The MHC region is characterized by a high density of highly polymorphic genes, and these genetic variations, including specific HLA alleles and amino acid residues, are strongly associated with the variability in immune responses and susceptibility to infectious agents. [1]
Genome-wide association studies (GWAS) have been instrumental in identifying single nucleotide polymorphisms (SNPs) and other genetic variants that influence both the likelihood of seropositivity and the quantitative levels of antibodies within seropositive populations. [1] For example, genes such as ATF1 and S100A9 have been found to be enriched in TLR-related pathways, suggesting their role in influencing bacterial colonization and the host's response to infections. [11] These genetic determinants can impact the efficiency of antigen presentation, immune cell activation, and ultimately the magnitude and duration of antibody production. [1]
Molecular and Cellular Pathways of Seropositivity Detection
Seropositivity indicates the presence of antibodies against a specific pathogen in an individual's blood, signifying past exposure or infection. This status is typically determined by detecting antibody-antigen binding above a predefined threshold, often using methods like enzyme-linked immunosorbent assays (ELISAs) or fluorescent bead-based multiplex serology. [1] The median fluorescence intensity (MFI) is a standardized measure quantifying the amount of antibody in a sample, reflecting the strength of the immune response. [1]
Advanced techniques such as phage-displayed immunoprecipitation sequencing (PhIP-Seq) allow for a comprehensive determination of antibody-antigen interactions, providing detailed insights into the human antibody epitope repertoire. [10] However, all serological tests carry a risk of low-level cross-binding with non-specific antibodies, which necessitates careful establishment of seropositivity thresholds to accurately distinguish true immune responses from background noise. [1] Understanding these molecular interactions and detection methods is crucial for accurately assessing an individual's immune history and potential protection against pathogens.
Systemic and Environmental Influences on Immune Variability
The variability in antibody-mediated immune responses is not solely determined by genetics but is also significantly influenced by systemic host factors and environmental interactions. For instance, infections with pathogens like Epstein-Barr virus (EBV) and cytomegalovirus (CMV) are associated with characteristic changes in immune cell populations, such as altered lymphocyte and neutrophil counts, which can have long-term systemic effects. [10] Furthermore, factors like age and sex can influence antibody titers and disease prevalence, with EBV antibody-bound peptides, for example, showing higher prevalence in females. [10]
While genetic factors contribute to the heritability of antibody-bound peptides, environmental and socioeconomic factors are major non-heritable determinants of infectious diseases and can confound genetic studies. [1] Antibody levels are known to fluctuate over time due to these multiple host and environmental influences, highlighting the dynamic nature of the immune system. Therefore, a holistic understanding of seropositivity requires considering the intricate interplay between an individual's genetic makeup, their physiological state, and the environmental exposures they encounter. [1]
Host Immune Signaling and Recognition of Bacterial Antigens
The host immune system employs intricate signaling pathways to recognize bacterial components, ultimately contributing to bacillus seropositivity. Key among these are cell surface receptor-linked signal transduction pathways, including G-protein coupled receptor (GPCR) signaling, which are crucial for initial pathogen sensing and subsequent immune responses [11] Upon activation, these receptors initiate intracellular signaling cascades, such as the phosphorylation of CREB through the activation of CaMKII, leading to altered gene expression and immune cell activation [3] Toll-like receptor (TLR)-related pathways also contribute to sensing bacterial patterns, with genes like ATF1 and S100A9 being enriched in these pathways, modulating the host's response to bacterial colonization and infection . The HLA region, in particular, emerges as an important genetic locus implicated in these immune responses across various pathogens. [1] This genetic predisposition, evidenced by the considerable heritability observed for antibody levels against different bacterial pathogens (e.g., C. pneumoniae at 0.32 and H. pylori at 0.36), underscores the crucial role of an individual's genetic makeup in shaping their immune profile. [2] Understanding these genetic determinants allows for the identification of individuals at potentially higher risk for certain bacterial exposures or for developing particular immune responses, thereby paving the way for personalized medicine approaches.
The identification of specific genetic loci linked to seropositivity and antibody levels offers substantial potential for enhanced risk stratification and targeted prevention strategies. By recognizing genetic predispositions to specific bacterial infections or their immune sequelae, clinicians could, in the future, tailor screening protocols or prophylactic interventions for high-risk populations. [2] Furthermore, these genetic insights can inform the development of novel therapeutic targets and vaccine strategies, leveraging host genetics to improve resistance or modulate immune responses to bacterial pathogens. [1] This genetics-informed prioritization of therapeutic targets has previously shown success in multiple diseases.
Clinical Applications and Prognostic Value
Seropositivity to bacterial agents serves as a fundamental diagnostic tool, indicating prior exposure and the presence of an antibody-mediated immune response. [1] Quantitative measures, such as median fluorescence intensity (MFI), provide a standardized quantification of antibody levels, which can be critical for monitoring the dynamics of an immune response over time or assessing the robustness of immunological memory. [1] Such serological data, especially when combined with genetic information, holds significant prognostic value, potentially predicting an individual's susceptibility or resistance to future infections and the likely course of disease progression.
The predictive power of seropositivity extends to informing treatment selection and evaluating long-term implications for patient care. Insights into antibody titer levels and their genetic underpinnings may enable clinicians to anticipate treatment response or identify individuals prone to more severe disease outcomes. [2] This comprehensive understanding could lead to the development of novel prevention and treatment methods, moving beyond mere diagnosis to proactive management based on an individual's unique immunological and genetic profile. [2]
Associations with Comorbidities and Long-term Health
Seropositivity to various bacterial agents contributes to the concept of "pathogen burden," a cumulative measure of an individual's exposure to multiple infectious agents. [2] Studies indicate that a higher total pathogen burden can be associated with increased risks for certain chronic conditions, such as coronary artery disease and elevated C-reactive protein levels. [12] This suggests that the collective history of bacterial infections, as reflected by seropositivity, may have long-term implications for systemic inflammation and cardiovascular health. [13]
Understanding the associations between seropositivity to bacterial pathogens and comorbidities is crucial for a holistic approach to patient care. The interplay between past infections and chronic disease development highlights the importance of considering an individual's infectious history in risk assessment and preventive strategies. [12] Further research into these overlapping phenotypes and potential syndromic presentations could uncover common biological pathways linking bacterial immune responses to other health outcomes, thereby improving comprehensive patient management.
Frequently Asked Questions About Bacillus Seropositivity
These questions address the most important and specific aspects of bacillus seropositivity based on current genetic research.
1. Why do some people fight off infections easily, but I struggle?
Your immune system's response to infections, including how well you produce antibodies, is influenced by your unique genetic makeup. Variations in genes, especially those in the Major Histocompatibility Complex (MHC) region like HLA genes, can lead to differences in how effectively your body recognizes and fights off pathogens. Studies show that the strength of your antibody response to various pathogens is significantly heritable, meaning it runs in families.
2. If my blood test shows bacillus antibodies, does that mean I was sick before?
Yes, a positive test for bacillus antibodies generally means your immune system has been activated by exposure to Bacillus species in the past. This indicates you've either had a prior infection or your immune system encountered the pathogen and mounted a response, producing these protective antibodies.
3. Will my kids inherit my body's way of fighting off certain germs?
Your children can inherit genetic factors that influence their immune response. Research indicates that the levels of antibodies your body produces against various pathogens exhibit heritability, meaning there's a genetic contribution. This can impact their likelihood of developing seropositivity and the magnitude of their antibody levels, similar to how your body responds.
4. Does my ethnic background change how my body reacts to infections?
Yes, your ancestral background can influence your body's immune responses. Genetic architectures and the frequencies of specific genetic variants, including those related to immunity, can differ significantly across diverse ethnic groups. Therefore, findings from studies on one population may not fully apply to individuals from different genetic backgrounds.
5. Can a special genetic test tell me if I'm more likely to get sick?
Identifying specific genetic variants associated with antibody levels or seropositivity can indeed help predict your susceptibility to certain infections or how well your immune system might respond. Such insights could inform personalized risk assessments and potentially guide strategies like vaccination, though current research has limitations in scope and generalizability.
6. Could my antibody test result for a past infection be misleading?
It's possible for serological tests to sometimes show low-level cross-binding with non-specific antibodies, which might not always reflect a true past infection with the specific pathogen. While quantitative analyses often try to mitigate this by setting thresholds, a clear history of exposure helps confirm the specificity of the test results.
7. If I have antibodies, does that protect me from getting sick again?
The presence of antibodies generally indicates prior exposure or infection, which can often confer a degree of immunity, meaning your body is better prepared to fight off that specific pathogen in the future. This is the biological basis for how vaccines work, by stimulating antibody production to protect against future illness.
8. Why might my body react differently to a vaccine than my friend's?
Individual variations in immune responses, including how strongly you respond to a vaccine by producing antibodies, are influenced by genetic factors. Your unique genetic makeup, particularly in genes like the HLA genes in the MHC region, can determine the likelihood and magnitude of your antibody levels, explaining why responses can differ between people.
9. If my test is positive for bacillus, does that mean I'm currently sick?
Not necessarily. A positive bacillus seropositivity test indicates the presence of antibodies, which are produced by your immune system in response to past exposure or infection. It tells you about your immunological history and immune activation, but doesn't typically confirm an active, ongoing infection.
10. Can I change my lifestyle to overcome my genetic risk for infections?
The interplay between your genetics and environmental factors is crucial for infectious disease susceptibility and immune response. While genetic predispositions play a role, lifestyle and environmental factors are also important, though their precise influence on bacillus seropositivity is complex and still being fully understood.
This FAQ was automatically generated based on current genetic research and may be updated as new information becomes available.
Disclaimer: This information is for educational purposes only and should not be used as a substitute for professional medical advice. Always consult with a healthcare provider for personalized medical guidance.
References
[1] Butler-Laporte G et al. "Genetic Determinants of Antibody-Mediated Immune Responses to Infectious Diseases Agents: A Genome-Wide and HLA Association Study." Open Forum Infect Dis, 2020.
[2] Rubicz R et al. "Genome-wide genetic investigation of serological measures of common infections." Eur J Hum Genet, 2015.
[3] Roberts, C. H. et al. "Pathway-Wide Genetic Risks in Chlamydial Infections Overlap between Tissue Tropisms: A Genome-Wide Association Scan." Mediators Inflamm, 2018.
[4] Sham, P. C., and S. M. Purcell. “Statistical power and significance testing in large-scale genetic studies.” Nature Reviews Genetics, vol. 15, no. 5, 2014, pp. 335–346.
[5] Chen, Q.-R., R. Braun, Y. Hu et al. “Multi-SNP analysis of GWAS data identifies pathways associated with nonalcoholic fatty liver disease.” PLoS One, vol. 8, no. 7, 2013, article e65982.
[6] Muckian MD et al. "Mendelian randomisation identifies priority groups for prophylactic EBV vaccination." BMC Infect Dis, 2023.
[7] Smatti, M. K., et al. "Genome-wide association study identifies several loci for HEV seropositivity." iScience, 2023. PMID: 37664632.
[8] Piriou, E. et al. "Early age at time of primary Epstein-Barr virus infection results in poorly controlled viral infection in infants from Western Kenya: clues to the etiology of endemic Burkitt lymphoma." The Journal of Infectious Diseases, 2012.
[9] Avramopoulos, D. et al. "Infection and inflammation in schizophrenia and bipolar disorder: a genome wide study for interactions with genetic variation." PLoS One, 2015.
[10] Andreu-Sanchez, S et al. "Phage display sequencing reveals that genetic, environmental, and intrinsic factors influence variation of human antibody epitope repertoire." Immunity, vol. 58, no. 6, 2023, pp. 1152-1166.e7.
[11] Fan, W. et al. "Association between Human Genetic Variants and the Vaginal Bacteriome of Pregnant Women." mSystems, 2021.
[12] Zhu, J, Quyyumi, AA, Norman, JE, et al. "Effects of total pathogen burden on coronary artery disease risk and C-reactive protein levels." Am J Cardiol, vol. 85, 2000, pp. 140–146.
[13] Epstein, SE, Zhu, J, Burnett, MS, Zhou, YF, Vercellotti, G, and Hajjar, D. "Infection and atherosclerosis: potential roles of pathogen burden and molecular mimicry." Arterioscler Thromb Vasc Biol, vol. 20, 2000, pp. 1417–1420.