Inconsistent trends regarding the association between ABO blood groups and susceptibility to SARS-CoV-2 infections

ABO antigens, produced from the ABO gene, are known to impact host interactions with various viruses. One characteristic is the host’s susceptibility to viral infections. Host interaction with viral particles is altered by the blood type-determined combination of ABO antigens on the cellular surface. SARS-CoV-2 is a novel strain of the coronavirus family known to have structural similarities with SARS-CoV. Considering ABO antigens’ association with SARS-CoV, studies have examined their relationship with SARS-CoV-2 as well. We reviewed current perspectives on the relationship between host susceptibility to SARS-CoV-2 infections and ABO antigens by examining cohort studies observing proportional differences between patients of varying blood types. While many studies indicated a higher risk of type A patients and a lower risk for type O patients, trends tended to vary per population. Consequently, we investigated the differences in study design between cohort studies that produced the variation in trends. Additionally, we examined genome-wide association studies that indicate a genetic association between the variables. We present the need for a standardized calculation method determining the significance of each blood group in its relationship with SARS-CoV-2 susceptibility per cohort.

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From bedside to bench: regulation of host factors in SARS-CoV-2 infection

Experimental & Molecular Medicine ◽

10.1038/s12276-021-00595-x ◽

2021 ◽

Author(s):

Samantha Y. Q. Ong ◽

Ilya M. Flyamer ◽

Wendy A. Bickmore ◽

Simon C. Biddie

Keyword(s):

Association Studies ◽

Host Factor ◽

Host Factors ◽

Genome Wide Association Studies ◽

Angiotensin Converting Enzyme 2 ◽

Host Interactions ◽

Genome Wide ◽

Therapeutic Development ◽

Transmembrane Serine Protease ◽

Chromatin Biology

AbstractThe zoonotic coronavirus SARS-CoV-2 (severe acute respiratory syndrome coronavirus-2), which causes COVID-19 (coronavirus disease-2019), has resulted in a pandemic. This has led to an urgent need to understand the molecular determinants of SARS-CoV-2 infection, factors associated with COVID-19 heterogeneity and severity, and therapeutic options for these patients. In this review, we discuss the role of host factors in SARS-CoV-2 infection and describe variations in host factor expression as mechanisms underlying the symptoms and severity of COVID-19. We focus on two host factors, angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2), implicated in SARS-CoV-2 infection. We also discuss genetic variants associated with COVID-19 severity revealed in selected patients and based on genome-wide association studies (GWASs). Furthermore, we highlight important advances in cell and chromatin biology, such as single-cell RNA and chromatin sequencing and chromosomal conformation assays, as methods that may aid in the discovery of viral–host interactions in COVID-19. Understanding how regulation of host factor genes varies in physiological and pathological states might explain the heterogeneity observed in SARS-CoV-2 infection, help identify pathways for therapeutic development, and identify patients most likely to progress to severe COVID-19.

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Inherited genetic variation in childhood acute lymphoblastic leukemia

Blood ◽

10.1182/blood-2014-12-580001 ◽

2015 ◽

Vol 125 (26) ◽

pp. 3988-3995 ◽

Cited By ~ 73

Author(s):

Takaya Moriyama ◽

Mary V. Relling ◽

Jun J. Yang

Keyword(s):

Acute Lymphoblastic Leukemia ◽

Association Studies ◽

Lymphoblastic Leukemia ◽

Genetic Variations ◽

Host Susceptibility ◽

Genome Wide Association Studies ◽

Childhood All ◽

Germline Variants ◽

Complex Interactions ◽

Genome Wide

Abstract Although somatically acquired genomic alterations have long been recognized as the hallmarks of acute lymphoblastic leukemia (ALL), the last decade has shown that inherited genetic variations (germline) are important determinants of interpatient variability in ALL susceptibility, drug response, and toxicities of ALL therapy. In particular, unbiased genome-wide association studies have identified germline variants strongly associated with the predisposition to ALL in children, providing novel insight into the mechanisms of leukemogenesis and evidence for complex interactions between inherited and acquired genetic variations in ALL. Similar genome-wide approaches have also discovered novel germline genetic risk factors that independently influence ALL prognosis and those that strongly modify host susceptibility to adverse effects of antileukemic agents (eg, vincristine, asparaginase, glucocorticoids). There are examples of germline genomic associations that warrant routine clinical use in the treatment of childhood ALL (eg, TPMT and mercaptopurine dosing), but most have not reached this level of actionability. Future studies are needed to integrate both somatic and germline variants to predict risk of relapse and host toxicities, with the eventual goal of implementing genetics-driven precision-medicine approaches in ALL treatment.

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Glycosaminoglycan biosynthesis pathway in host genome is associated with Helicobacter pylori infection

Scientific Reports ◽

10.1038/s41598-021-97790-7 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Dingxue Hu ◽

Yueqi Lu ◽

Daoming Wang ◽

Chao Nie ◽

Yan Li

Keyword(s):

Helicobacter Pylori ◽

Chinese Population ◽

Association Studies ◽

Host Susceptibility ◽

Genome Wide Association ◽

Genome Wide Association Studies ◽

Gastric Diseases ◽

Association Analyses ◽

Genome Wide ◽

H Pylori

AbstractHelicobacter pylori is a causative pathogen of many gastric and extra-gastric diseases. It has infected about half of the global population. There were no genome-wide association studies (GWAS) for H. pylori infection conducted in Chinese population, who carried different and relatively homogenous strain of H. pylori. In this work, we performed SNP (single nucleotide polymorphism)-based, gene-based and pathway-based genome-wide association analyses to investigate the genetic basis of host susceptibility to H. pylori infection in 480 Chinese individuals. We also profiled the composition and function of the gut microbiota between H. pylori infection cases and controls. We found several genes and pathways associated with H. pylori infection (P < 0.05), replicated one previously reported SNP rs10004195 in TLR1 gene region (P = 0.02). We also found that glycosaminoglycan biosynthesis related pathway was associated with both onset and progression of H. pylori infection. In the gut microbiome association study, we identified 2 species, 3 genera and several pathways had differential abundance between H. pylori infected cases and controls. This paper is the first GWAS for H. pylori infection in Chinese population, and we combined the genetic and microbial data to comprehensively discuss the basis of host susceptibility to H. pylori infection.

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