Which virus is driving this disease? Paste your GWAS or disease risk genes and discover documented viral protein interactions across 48 human viruses.
Open the Atlas →ViralGene Atlas cross-references your gene list against a curated database of documented viral protein interactions. Every interaction is backed by peer-reviewed publications and protein-level evidence. Four independent layers of analysis give you the full picture.
Viral proteins that directly bind, cleave, ubiquitinate, phosphorylate, or transcriptionally regulate your genes. Each hit linked to its PubMed source.
Two-step chains: viral protein activates gene X, gene X regulates your gene Y. 224+ curated directed edges in the regulatory network.
Detects tissue-level imbalances between viral damage patterns and gene maintenance functions across 12 categories, from ECM degradation to protein aggregation.
Identifies host gene variants where loss or gain of function creates a cellular environment permissive to viral activity. These are not viral targets, but host-side vulnerabilities that let viruses operate more effectively.
A viral protein directly binds, cleaves, ubiquitinates, phosphorylates, or transcriptionally regulates one of your genes. Each interaction is backed by at least one peer-reviewed publication with protein-level evidence. Example: EBV LMP1 activates TRAF1, TRAF2, and TRAF3, driving NF-κB signaling.
Your gene is connected to a viral protein through a documented regulatory chain. For instance, a viral protein activates gene X, and gene X is known to regulate your gene Y. Cascades are limited to 2 steps to minimize false positives.
This layer detects tissue-level imbalances between what a virus damages and what your genes are supposed to maintain. It is not a direct interaction. Instead, it uses 12 functional damage categories to identify where viral damage overwhelms gene function. Genes are displayed as UP (overexpressed, contributing to damage), DOWN (underexpressed, failing to protect), or NORMAL (cannot keep up with damage rate).
Unlike layers 1-3, this layer does not map what a virus does to your genes. It maps the reverse: how your genetic variants change the cellular environment in ways that benefit a virus. A gene with reduced function may remove a natural brake on viral activity, while a gain-of-function variant may amplify a pathway the virus exploits. Genes are displayed as LOSS (reduced function favors virus), GAIN (increased function favors virus), or PROTECTIVE (variant protects against viral mechanism). Example: MAML3 loss-of-function reduces competition for RBP-Jk, letting EBNA2 dominate and amplify TLR7, KDM6A, DDX3X, IRAK1, MECP2, IKBKG, BTK, IL2RG, CD40LG, and FOXP3.
| Category | What the virus does | Gene function overwhelmed |
|---|---|---|
| Extracellular Matrix Degradation | MMP1/3/9/13 degrade collagen and aggrecan | Cartilage/ECM synthesis and repair |
| Barrier Disruption | Tight junction breakdown (claudins, occludins) | Epithelial/endothelial barrier maintenance |
| Oxidative Stress | ROS and superoxide generation | Antioxidant defense |
| Debris Accumulation | Apoptotic debris, nucleosomes, dsDNA, DAMPs | Autophagy and debris clearance |
| Immune Overactivation | Chronic IFN-I, B-cell proliferation | Immune tolerance and resolution |
| Fibrosis Induction | TGFB1-driven fibroblast activation | Anti-fibrotic tissue remodeling |
| Aberrant Vascularization | VEGF/bFGF/PDGF overexpression | Vascular homeostasis |
| DNA Damage | p53/RB degradation, genotoxicity | DNA repair and cell cycle control |
| Neuroinflammation | Microglial activation, myelin damage | Neuronal protection and repair |
| Protein Aggregation | Beta-amyloid, alpha-synuclein induction | Proteostasis and aggregate clearance |
| Immune Complex Deposition | Antibody-virus complex deposition | Renal/hepatic IC clearance |
| Cell Death | Lytic infection, apoptosis induction | Cell survival programs |
48 human viruses with documented protein-level interactions. Each entry includes effectors, damage categories, and PubMed references.
Have a list of GWAS risk genes for a disease with unknown etiology? The Atlas identifies which viruses target those genes, providing mechanistic hypotheses you can validate experimentally.
If your disease genes are targeted by EBV, existing antivirals (valacyclovir, ganciclovir) or NF-κB inhibitors become testable treatment candidates.
The Atlas detects when two viruses cooperate: one disables a pathway while another exploits it. For example, one virus suppresses interferon while a second drives inflammation unchecked.
Combine the Atlas with your own RNA-seq or microarray data. If your disease genes are targeted by a specific virus, check whether the viral signature markers (receptors, immune evasion, pathway activation) match your differential expression patterns.
Any list of human gene symbols: GWAS risk genes, differentially expressed genes from RNA-seq, candidate genes from linkage studies. Paste them comma-separated, one per line, or space-separated. The tool normalizes everything automatically.
Every interaction is manually curated from peer-reviewed literature. Protein-level evidence only (binding, cleavage, ubiquitination, phosphorylation, transcriptional regulation). No predicted or inferred interactions.
Yes. ViralGene Atlas is free, open science, independent research. No paywalls, no registration, no data collection.
No. The Atlas is a research tool for hypothesis generation, not a diagnostic device. Results suggest testable mechanisms. They do not constitute medical advice or clinical evidence.
STRING and IntAct are general protein-protein interaction databases. ViralGene Atlas focuses specifically on virus-to-human interactions, includes regulatory cascades, adds functional damage and genetic susceptibility layers, and is optimized for disease gene queries rather than single-protein lookups.