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Robert J. Gifford edited this page Nov 7, 2024 · 12 revisions

Overview

Initially developed with a focus on managing and analyzing virus sequence data, GLUE was designed to address the high variability and rapid evolution characteristic of viral genomes. However, its flexible design and robust approach to comparative genomics also make it well-suited for studying host genes, particularly those that exhibit substantial genetic diversity. Host genes with high variability can benefit from GLUE's capacity to capture and analyze genetic variation at scale.

GLUE organizes alignments in a linked hierarchical structure, facilitating a streamlined, comparative approach to analyzing sequences with significant variability. This structure supports precise comparisons across genome segments and accommodates the complexities of genetic variation within populations. By tracking homology relationships in detail, GLUE enables researchers to efficiently explore gene evolution and variation across species.

Additionally, GLUE's extensible database schema makes it an effective off-the-shelf platform for constructing customized databases tailored to specific gene families. With its ability to link sequences to rich metadata, GLUE supports context-driven queries and in-depth analyses, enabling the examination of gene variation in structural, functional, and evolutionary contexts.



IFNL-GLUE

Background

Interferon lambda (IFNL) is a group of type III interferons that play a key role in antiviral defense, particularly at mucosal surfaces like those found in the respiratory and gastrointestinal tracts. This family includes IFNL1, IFNL22, IFNL3, and IFNL4, all of which activate antiviral responses by inducing the expression of interferon-stimulated genes (ISGs). IFNL functions similarly to type I interferons (IFN-α and IFN-β) by activating the JAK-STAT signaling pathway, but it has a much narrower target range, focusing primarily on epithelial cells. This selectivity is due to the restricted expression of the IFNL receptor (IFNLR1), making IFNL highly effective at controlling infections in localized tissues without triggering widespread immune activation.

The limited inflammatory response induced by IFNL distinguishes it from other interferons, as it can suppress viral replication while minimizing collateral tissue damage. This makes IFNL an attractive candidate for therapeutic applications, especially for infections affecting mucosal surfaces. Research has shown that IFNL's targeted antiviral effects, combined with its capacity to produce fewer systemic side effects, offer a promising alternative for managing infections without excessive inflammation. Furthermore, genetic variations in IFNL4, such as frameshift mutations, have shown links to differences in infection outcomes, underlining the importance of this interferon family in host immunity and disease susceptibility.

Scope & History

Features

Core Project Overview

Property Description
Scope Interferon Lambda Genes
Development Period 2020-present
Lead Developers Robert J. Gifford
Main Objectives Comparative genomics
Data Sources NCBI
Associated Tools BLAST+, MAFFT, RAXML
Offline Project GitHub
Online Access Not planned
Status Alpha Version
User Guide None Yet

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