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tooluniverse-variant-interpretation工具宇宙变体解释

Agent Skill

tooluniverse-variant-interpretation 用于查找、检索和筛选相关信息,适合在 Codex、Claude、Cursor、Gemini CLI 中需要根据关键词、任务场景或来源线索快速定位候选结果时使用。可结合来源仓库、安装命令和原始 README 继续核验具体用法。安装前建议确认权限范围、维护状态,以及是否会触发联网、命令执行或文件读写。

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安装说明

本站只整理中文说明和来源信息,不托管安装包,也不代用户安装。

GitHub

来源数

2

许可证

unknown

最后核验

2026-05-01

来源状态

来源可访问

安装方式

通过对话安装

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请帮我安装这个 Agent Skill:tooluniverse-variant-interpretation(工具宇宙变体解释)
来源仓库:https://github.com/wu-yc/labclaw
仓库路径:skills/tooluniverse-variant-interpretation
安装命令:
npx skills add https://github.com/wu-yc/labclaw --skill tooluniverse-variant-interpretation
安装前请先检查当前环境是否支持对应 CLI,并向我确认将要执行的命令、安装目录、联网范围和文件读写权限;确认后再执行。

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skills.shnpx skills
npx skills add https://github.com/wu-yc/labclaw --skill tooluniverse-variant-interpretation

简介

用于查找、检索和筛选变体解释相关信息。

  • 适合在 Codex、Claude、Cursor、Gemini CLI 中根据任务场景定位候选结果。
  • 通过 npx 命令从 GitHub 仓库安装并使用。
  • 安装前需确认权限范围和维护状态,注意可能触发联网或文件操作。
  • tooluniverse-variant-interpretation 属于研究检索类 Skill,可作为该场景下的辅助能力补充。

SKILL.md


name: tooluniverse-variant-interpretation description: Systematic clinical variant interpretation from raw variant calls to ACMG-classified recommendations with structural impact analysis. Aggregates evidence from ClinVar, gnomAD, CIViC, UniProt, and PDB across ACMG criteria. Produces pathogenicity scores (0-100), clinical recommendations, and treatment implications. Use when interpreting genetic variants, classifying variants of uncertain significance (VUS), performing ACMG variant classification, or translating variant calls to clinical actionability.

Clinical Variant Interpreter

Systematic variant interpretation skill using ToolUniverse - from raw variant calls to ACMG-classified clinical recommendations with structural impact analysis.


Problem This Skill Solves

Clinical labs and researchers face critical challenges in variant interpretation:

  1. Variant classification uncertainty - VUS (Variants of Uncertain Significance) comprise 40-60% of clinical variants
  2. Evidence aggregation burden - Must integrate data from 10+ databases per variant
  3. Structural context missing - Traditional annotation ignores 3D protein impact
  4. Clinical actionability unclear - How does classification translate to patient care?

This skill provides: A systematic workflow that combines population databases, functional predictions, structural analysis (via AlphaFold2), and literature evidence into ACMG-compliant interpretations with clear clinical recommendations.


Key Principles

  1. ACMG-Guided Classification - Follow ACMG/AMP 2015 guidelines with explicit evidence codes
  2. Structural Evidence Integration - Use AlphaFold2 for novel structural impact analysis
  3. Population Context - gnomAD frequencies with ancestry-specific data
  4. Gene-Disease Validity - ClinGen curation status for clinical relevance
  5. Actionable Output - Clear recommendations, not just classifications
  6. English-first queries - Always use English terms in tool calls (gene names, variant descriptions, disease names), even if the user writes in another language. Only try original-language terms as a fallback. Respond in the user's language

Triggers

Use this skill when users:

  • Ask about variant interpretation or classification
  • Have VCF data needing clinical annotation
  • Ask "what does this variant mean clinically?"
  • Need ACMG classification for variants
  • Want structural impact analysis for missense variants
  • Ask about pathogenicity of specific variants

Workflow Overview

┌─────────────────────────────────────────────────────────────────┐
│                    VARIANT INTERPRETATION                        │
├─────────────────────────────────────────────────────────────────┤
│                                                                  │
│  Phase 1: VARIANT IDENTITY                                       │
│  ├── Normalize variant notation (HGVS)                          │
│  ├── Map to gene, transcript, protein                           │
│  └── Get consequence type (missense, nonsense, etc.)            │
│                                                                  │
│  Phase 2: CLINICAL DATABASES                                     │
│  ├── ClinVar: Existing classifications                          │
│  ├── gnomAD: Population frequencies (all + ancestry)            │
│  ├── OMIM: Gene-disease associations                            │
│  ├── ClinGen: Gene validity + dosage sensitivity (ENHANCED)     │
│  │   └─ ClinGen_search_gene_validity, ClinGen_search_dosage     │
│  └── SpliceAI: Splice variant prediction (NEW)                  │
│                                                                  │
│  Phase 2.5: REGULATORY CONTEXT (NEW - for non-coding variants)  │
│  ├── ChIPAtlas: TF binding at position                          │
│  ├── ENCODE: Regulatory elements (enhancers, promoters)         │
│  ├── Conservation in regulatory regions                         │
│  └── Functional annotation of regulatory impact                 │
│                                                                  │
│  Phase 3: COMPUTATIONAL PREDICTIONS                              │
│  ├── SIFT/PolyPhen: Damaging predictions                        │
│  ├── CADD: Deleteriousness score                                │
│  ├── SpliceAI: Splice impact (if applicable)                    │
│  └── Conservation: Cross-species alignment                      │
│                                                                  │
│  Phase 4: STRUCTURAL ANALYSIS (for VUS/novel missense)          │
│  ├── Get protein structure (PDB or AlphaFold2)                  │
│  ├── Map variant to structure                                   │
│  ├── Assess domain/functional site impact                       │
│  └── Predict structural destabilization                         │
│                                                                  │
│  Phase 4.5: EXPRESSION CONTEXT (NEW)                            │
│  ├── CELLxGENE: Cell-type specific expression                   │
│  ├── Tissue relevance to phenotype                              │
│  └── Expression validation                                       │
│                                                                  │
│  Phase 5: LITERATURE EVIDENCE                                    │
│  ├── PubMed: Functional studies                                 │
│  ├── BioRxiv/MedRxiv: Recent preprints (NEW)                   │
│  ├── Case reports: Phenotype correlations                       │
│  └── Segregation data (if in literature)                        │
│                                                                  │
│  Phase 6: ACMG CLASSIFICATION                                    │
│  ├── Apply evidence codes (PVS1, PM2, PP3, etc.)               │
│  ├── Calculate classification                                   │
│  ├── Identify limiting factors                                  │
│  └── Generate clinical recommendations                          │
│                                                                  │
└─────────────────────────────────────────────────────────────────┘

Phase Details

Phase 1: Variant Identity & Normalization

Goal: Standardize variant notation and determine molecular consequence

Tools:

ToolPurpose
myvariant_queryGet variant annotations from MyVariant.info
Ensembl_get_variant_infoVariant effect predictor data
NCBI_gene_searchGene information

Key Information to Capture:

  • HGVS notation (c. and p.)
  • Gene symbol and Ensembl ID
  • Transcript (canonical/MANE Select)
  • Consequence type
  • Amino acid change (for missense)
  • Exon/intron location

Phase 2: Clinical Database Queries

Goal: Aggregate existing clinical knowledge

Tools:

ToolPurposeKey Data
clinvar_searchExisting classificationsClassification, review status, submissions
gnomad_searchPopulation frequencyAF, ancestry-specific AFs, homozygotes
OMIM_search, OMIM_get_entryGene-diseaseInheritance, phenotypes
ClinGen_gene_validityCuration statusGene-disease validity level
COSMIC_search_mutationsSomatic mutations (NEW)Cancer frequency, histology
DisGeNET_search_geneGene-disease associations (NEW)Evidence scores, sources

2.1 COSMIC for Somatic Context (NEW)

For cancer variants, check COSMIC for somatic mutation frequency:

def get_somatic_context(tu, gene_symbol, variant_aa):
    """Get somatic mutation context from COSMIC."""

    # Search for specific mutation
    cosmic = tu.tools.COSMIC_search_mutations(
        operation="search",
        terms=f"{gene_symbol} {variant_aa}",
        max_results=20,
        genome_build=38
    )

    # Get all gene mutations for context
    gene_mutations = tu.tools.COSMIC_get_mutations_by_gene(
        operation="get_by_gene",
        gene=gene_symbol,
        max_results=100
    )

    # Determine if it's a hotspot
    mutation_counts = Counter(m['MutationAA'] for m in gene_mutations.get('results', []))
    is_hotspot = variant_aa in [m[0] for m in mutation_counts.most_common(10)]

    return {
        'cosmic_hits': cosmic.get('results', []),
        'is_somatic_hotspot': is_hotspot,
        'cancer_types': [m['PrimarySite'] for m in cosmic.get('results', [])],
        'total_cosmic_count': cosmic.get('total_count', 0)
    }

2.2 OMIM Gene-Disease Context (NEW)

def get_omim_context(tu, gene_symbol):
    """Get OMIM gene-disease associations."""

    # Search OMIM for gene
    search = tu.tools.OMIM_search(
        operation="search",
        query=gene_symbol,
        limit=5
    )

    omim_data = []
    for entry in search.get('data', {}).get('entries', []):
        mim = entry.get('mimNumber')

        # Get detailed entry
        details = tu.tools.OMIM_get_entry(
            operation="get_entry",
            mim_number=str(mim)
        )

        # Get clinical synopsis
        synopsis = tu.tools.OMIM_get_clinical_synopsis(
            operation="get_clinical_synopsis",
            mim_number=str(mim)
        )

        omim_data.append({
            'mim_number': mim,
            'title': details.get('data', {}).get('titles', {}),
            'inheritance': synopsis.get('data', {}).get('inheritance'),
            'clinical_features': synopsis.get('data', {})
        })

    return omim_data

2.3 DisGeNET Gene-Disease Evidence (NEW)

def get_disgenet_context(tu, gene_symbol, variant_rsid=None):
    """Get gene-disease associations from DisGeNET."""

    # Gene-disease associations
    gda = tu.tools.DisGeNET_search_gene(
        operation="search_gene",
        gene=gene_symbol,
        limit=20
    )

    # Variant-disease associations (if rsID available)
    vda = None
    if variant_rsid:
        vda = tu.tools.DisGeNET_get_vda(
            operation="get_vda",
            variant=variant_rsid,
            limit=20
        )

    return {
        'gene_associations': gda.get('data', {}).get('associations', []),
        'variant_associations': vda.get('data', {}).get('associations', []) if vda else []
    }

2.4 ClinGen Gene Validity & Dosage Sensitivity (NEW)

ClinGen provides authoritative curation of gene-disease relationships:

def get_clingen_evidence(tu, gene_symbol):
    """
    Get ClinGen gene validity and dosage sensitivity data.
    CRITICAL for ACMG classification - establishes gene-disease validity.
    """

    # 1. Gene-disease validity (Definitive/Strong/Moderate/Limited)
    validity = tu.tools.ClinGen_search_gene_validity(gene=gene_symbol)

    validity_data = []
    if validity.get('data'):
        for entry in validity.get('data', []):
            validity_data.append({
                'disease': entry.get('Disease Label'),
                'classification': entry.get('Classification'),  # Definitive, Strong, etc.
                'inheritance': entry.get('Inheritance'),
                'mondo_id': entry.get('Disease ID (MONDO)')
            })

    # 2. Dosage sensitivity (haploinsufficiency, triplosensitivity)
    dosage = tu.tools.ClinGen_search_dosage_sensitivity(gene=gene_symbol)

    dosage_data = {}
    if dosage.get('data'):
        for entry in dosage.get('data', []):
            dosage_data = {
                'haploinsufficiency_score': entry.get('Haploinsufficiency Score'),
                'triplosensitivity_score': entry.get('Triplosensitivity Score'),
                'disease': entry.get('Disease')
            }
            break  # Usually one entry per gene

    # 3. Clinical actionability (for incidental findings context)
    actionability = tu.tools.ClinGen_search_actionability(gene=gene_symbol)

    return {
        'gene_validity': validity_data,
        'dosage_sensitivity': dosage_data,
        'actionability': actionability.get('data', {}),
        'has_definitive_validity': any(v['classification'] == 'Definitive' for v in validity_data),
        'is_haploinsufficient': dosage_data.get('haploinsufficiency_score') == '3'
    }

ClinGen Validity Levels (for ACMG PM1/PP4):

ClassificationMeaningACMG Impact
DefinitiveMultiple concordant studiesStrong gene-disease support
StrongExtensive evidenceModerate-strong support
ModerateSome evidenceModerate support
LimitedMinimal evidenceWeak support, use caution
DisputedConflicting evidenceDo not use for classification
RefutedEvidence againstGene NOT associated

Dosage Sensitivity Scores (for CNV interpretation):

ScoreMeaningInterpretation
3Sufficient evidenceHaploinsufficiency/triplosensitivity established
2Emerging evidenceSome support, not definitive
1Little evidenceMinimal support
0No evidenceUnknown

2.5 SpliceAI Splice Variant Prediction (NEW)

~15% of pathogenic variants affect splicing. SpliceAI is the gold standard for splice prediction:

def get_spliceai_prediction(tu, chrom, pos, ref, alt, genome="38"):
    """
    Get SpliceAI splice effect predictions.

    Delta scores:
    - DS_AG: Acceptor gain
    - DS_AL: Acceptor loss
    - DS_DG: Donor gain
    - DS_DL: Donor loss

    Thresholds:
    - ≥0.8: High pathogenicity (strong PP3)
    - 0.5-0.8: Moderate (supporting PP3)
    - 0.2-0.5: Low (weak evidence)
    - <0.2: Likely benign
    """

    # Format variant for SpliceAI
    variant = f"chr{chrom}-{pos}-{ref}-{alt}"

    # Get full splice predictions
    result = tu.tools.SpliceAI_predict_splice(
        variant=variant,
        genome=genome
    )

    if result.get('data'):
        max_score = result['data'].get('max_delta_score', 0)
        interpretation = result['data'].get('interpretation', '')

        # Determine ACMG support
        if max_score >= 0.8:
            acmg = 'PP3 (strong) - high splice impact'
        elif max_score >= 0.5:
            acmg = 'PP3 (supporting) - moderate splice impact'
        elif max_score >= 0.2:
            acmg = 'PP3 (weak) - possible splice impact'
        else:
            acmg = 'BP7 (if synonymous) - splice benign'

        return {
            'max_delta_score': max_score,
            'interpretation': interpretation,
            'acmg_support': acmg,
            'scores': result['data'].get('scores', [])
        }
    return None

def quick_splice_check(tu, variant, genome="38"):
    """Quick triage using max delta score only."""

    result = tu.tools.SpliceAI_get_max_delta(
        variant=variant,
        genome=genome
    )

    return result.get('data', {})

When to Use SpliceAI:

  • Intronic variants near splice sites (±50bp)
  • Synonymous variants (may still affect splicing)
  • Exonic variants near splice junctions
  • Variants creating cryptic splice sites

Report Section for Splice Variants:

### Splice Impact Analysis (SpliceAI)

| Score Type | Value | Position | Interpretation |
|------------|-------|----------|----------------|
| DS_AG | 0.02 | +15 | Acceptor gain unlikely |
| DS_AL | 0.85 | -2 | **High acceptor loss** |
| DS_DG | 0.01 | +8 | Donor gain unlikely |
| DS_DL | 0.03 | +1 | Donor loss unlikely |

**Max Delta Score**: 0.85 (DS_AL)
**Interpretation**: High impact - likely disrupts acceptor site
**ACMG Support**: PP3 (strong) for splice-altering effect

*Source: SpliceAI via `SpliceAI_predict_splice`*

ClinVar Classification Map:

ClinVarInterpretation
PathogenicDisease-causing
Likely pathogenic90%+ confidence pathogenic
VUSUncertain significance
Likely benign90%+ confidence benign
BenignNot disease-causing
ConflictingMultiple interpretations

gnomAD Thresholds (for rare disease):

FrequencyACMG CodeInterpretation
AbsentPM2_SupportingAbsent from controls
<0.00001PM2_SupportingExtremely rare
<0.0001-Rare (use with caution)
>0.01BS1/BA1Too common for rare disease

COSMIC Somatic Evidence (NEW):

COSMIC FindingInterpretationACMG Support
Recurrent hotspot (>100 samples)Known oncogenic driverPS3 (functional)
Moderate frequency (10-100)Likely oncogenicPM1 (hotspot)
Rare somatic (<10)Unknown significanceNo support

DisGeNET Score Interpretation (NEW):

GDA ScoreEvidence LevelACMG Support
>0.7StrongPP4 (phenotype)
0.4-0.7ModerateSupporting
<0.4WeakInsufficient

Phase 2.5: Regulatory Context (NEW - for Non-Coding Variants)

Goal: Assess regulatory impact for non-coding, intronic, and promoter variants

When to Apply:

  • Intronic variants (not splice site)
  • Promoter variants
  • 5'UTR / 3'UTR variants
  • Intergenic variants near disease genes

Tools:

ToolPurposeKey Data
ChIPAtlas_enrichment_analysisTF binding at positionBound TFs, cell types
ChIPAtlas_get_peak_dataChIP-seq peaksPeak coordinates, scores
ENCODE_search_experimentsRegulatory elementsEnhancers, promoters, DHS
ENCODE_get_experimentExperiment detailsAssay type, targets

Regulatory Impact Assessment:

def assess_regulatory_impact(tu, variant_position, gene_symbol):
    """Assess regulatory impact of non-coding variant."""

    # Check TF binding at position
    tf_binding = tu.tools.ChIPAtlas_enrichment_analysis(
        gene=gene_symbol,
        cell_type="all"
    )

    # Get ChIP-seq peaks overlapping variant
    peaks = tu.tools.ChIPAtlas_get_peak_data(
        gene=gene_symbol,
        experiment_type="TF"
    )

    # Search ENCODE for regulatory annotations
    encode_data = tu.tools.ENCODE_search_experiments(
        assay_title="ATAC-seq",
        biosample="all"
    )

    # Assess if variant disrupts TF binding
    binding_disrupted = check_motif_disruption(variant_position, peaks)

    return {
        'tf_binding': tf_binding,
        'regulatory_peaks': peaks,
        'encode_annotations': encode_data,
        'likely_regulatory': binding_disrupted
    }

Regulatory Impact Categories:

CategoryCriteriaACMG Support
High impactDisrupts known TF binding motifPP3 (supporting)
Moderate impactIn active regulatory regionConsider context
Low impactNo regulatory annotationNo support

Output for Report:

### 2.5 Regulatory Context (for Non-Coding Variants)

| Feature | Finding | Significance |
|---------|---------|--------------|
| Variant location | Intron 5, 120bp from exon 6 | Not canonical splice |
| TF binding site | CTCF binding peak (ChIPAtlas) | May affect insulation |
| ENCODE annotation | Active enhancer (H3K27ac) | Regulatory function |
| Conservation | PhyloP = 2.8 | Moderate conservation |

**Regulatory Interpretation**: Variant overlaps CTCF binding site in active enhancer region. Potential impact on gene regulation.

*Source: ChIPAtlas, ENCODE*

Phase 3: Computational Predictions (ENHANCED)

Goal: Assess in silico pathogenicity predictions using state-of-the-art models

Tools:

ToolPurposeScore Range
CADD_get_variant_scoreDeleteriousness score (NEW API)PHRED 0-99
AlphaMissense_get_variant_scoreDeepMind pathogenicity (NEW)0-1
EVE_get_variant_scoreEvolutionary pathogenicity (NEW)0-1
myvariant_queryAggregated predictionsSIFT, PolyPhen
Ensembl_get_variant_infoVEP predictionsSIFT, PolyPhen

3.1 CADD Deleteriousness Scoring (NEW)

def get_cadd_score(tu, chrom, pos, ref, alt):
    """Get CADD deleteriousness score for a variant."""

    result = tu.tools.CADD_get_variant_score(
        chrom=str(chrom),
        pos=pos,
        ref=ref,
        alt=alt,
        version="GRCh38-v1.7"
    )

    if result.get('status') == 'success':
        phred = result['data'].get('phred_score')
        return {
            'score': phred,
            'interpretation': result['data'].get('interpretation'),
            'acmg_support': 'PP3' if phred >= 20 else ('BP4' if phred < 15 else 'neutral')
        }
    return None

3.2 AlphaMissense Pathogenicity (NEW)

DeepMind's AlphaMissense provides state-of-the-art missense pathogenicity prediction:

def get_alphamissense_score(tu, uniprot_id, variant):
    """
    Get AlphaMissense pathogenicity score.
    variant format: 'R123H' or 'p.R123H'

    Thresholds:
    - Pathogenic: score > 0.564
    - Ambiguous: 0.34-0.564
    - Benign: score < 0.34
    """

    result = tu.tools.AlphaMissense_get_variant_score(
        uniprot_id=uniprot_id,
        variant=variant
    )

    if result.get('status') == 'success' and result.get('data'):
        score = result['data'].get('pathogenicity_score')
        classification = result['data'].get('classification')

        # Map to ACMG
        if classification == 'pathogenic':
            acmg = 'PP3 (strong)'  # AlphaMissense has high accuracy
        elif classification == 'benign':
            acmg = 'BP4 (strong)'
        else:
            acmg = 'neutral'

        return {
            'score': score,
            'classification': classification,
            'acmg_support': acmg
        }
    return None

3.3 EVE Evolutionary Prediction (NEW)

EVE uses unsupervised learning on evolutionary data:

def get_eve_score(tu, chrom, pos, ref, alt):
    """
    Get EVE evolutionary pathogenicity score.

    Threshold: >0.5 indicates likely pathogenic
    """

    result = tu.tools.EVE_get_variant_score(
        chrom=str(chrom),
        pos=pos,
        ref=ref,
        alt=alt
    )

    if result.get('status') == 'success':
        eve_scores = result['data'].get('eve_scores', [])
        if eve_scores:
            best_score = eve_scores[0]
            return {
                'score': best_score.get('eve_score'),
                'classification': best_score.get('classification'),
                'gene': best_score.get('gene_symbol'),
                'acmg_support': 'PP3' if best_score.get('eve_score', 0) > 0.5 else 'BP4'
            }
    return None

3.4 Integrated Prediction Strategy

For VUS (Variants of Uncertain Significance), combine multiple predictors:

def comprehensive_pathogenicity_assessment(tu, variant_info):
    """
    Combine all prediction tools for robust classification.
    """
    chrom = variant_info['chrom']
    pos = variant_info['pos']
    ref = variant_info['ref']
    alt = variant_info['alt']
    uniprot_id = variant_info.get('uniprot_id')
    aa_change = variant_info.get('aa_change')  # e.g., 'R123H'

    predictions = {}

    # 1. CADD (works for all variant types)
    cadd = get_cadd_score(tu, chrom, pos, ref, alt)
    if cadd:
        predictions['cadd'] = cadd

    # 2. AlphaMissense (missense only, requires UniProt ID)
    if uniprot_id and aa_change:
        am = get_alphamissense_score(tu, uniprot_id, aa_change)
        if am:
            predictions['alphamissense'] = am

    # 3. EVE (missense only)
    eve = get_eve_score(tu, chrom, pos, ref, alt)
    if eve:
        predictions['eve'] = eve

    # Consensus assessment
    damaging_count = sum(1 for p in predictions.values()
                         if 'PP3' in p.get('acmg_support', ''))
    benign_count = sum(1 for p in predictions.values()
                       if 'BP4' in p.get('acmg_support', ''))

    if damaging_count >= 2 and benign_count == 0:
        consensus = 'likely_damaging'
        acmg = 'PP3 (multiple predictors concordant)'
    elif benign_count >= 2 and damaging_count == 0:
        consensus = 'likely_benign'
        acmg = 'BP4 (multiple predictors concordant)'
    else:
        consensus = 'uncertain'
        acmg = 'neutral (discordant predictions)'

    return {
        'predictions': predictions,
        'consensus': consensus,
        'acmg_recommendation': acmg
    }

Prediction Interpretation (Updated):

PredictorDamagingBenign
AlphaMissense>0.564<0.34
CADD PHRED≥20 (top 1%)<15
EVE>0.5≤0.5
SIFT<0.05≥0.05
PolyPhen2>0.85 (probably)<0.15 (benign)

ACMG Application (Enhanced):

  • PP3: Multiple concordant damaging predictions (AlphaMissense + CADD + EVE agreement = strong PP3)
  • BP4: Multiple concordant benign predictions
  • Note: AlphaMissense alone achieves ~90% accuracy on ClinVar pathogenic variants

Phase 4: Structural Analysis

Goal: Assess protein structural impact (especially for VUS)

Tools:

ToolPurpose
PDB_search_by_uniprotFind experimental structures
NvidiaNIM_alphafold2Predict structure if no PDB
alphafold_get_predictionGet AlphaFold DB structure
InterPro_get_protein_domainsDomain annotations
UniProt_get_protein_functionFunctional sites

Structural Impact Categories:

Impact LevelDescriptionACMG Support
CriticalActive site, catalytic residuePM1 (strong)
HighBuried residue, disulfide, structural corePM1 (moderate)
ModerateDomain interface, binding sitePM1 (supporting)
LowSurface, flexible regionNo support

Using AlphaFold2 for VUS:

1. Get wildtype structure (PDB or AlphaFold)
2. Identify residue location:
   - pLDDT at position (confidence)
   - Solvent accessibility
   - Secondary structure
3. Assess structural context:
   - Distance to functional sites
   - Interaction partners
   - Conservation in structure
4. Predict impact:
   - Side chain burial
   - Hydrogen bond disruption
   - Charge changes in buried positions

Phase 4.5: Expression Context (NEW)

Goal: Validate gene expression in disease-relevant tissues/cells

Tools:

ToolPurposeKey Data
CELLxGENE_get_expression_dataCell-type specific expressionTPM per cell type
CELLxGENE_get_cell_metadataCell type annotationsTissue, disease state
GTEx_get_median_gene_expressionTissue expressionTPM per tissue

Expression Validation:

def validate_expression_context(tu, gene_symbol, phenotype_tissues):
    """Validate gene is expressed in phenotype-relevant tissues."""

    # Single-cell expression
    sc_expression = tu.tools.CELLxGENE_get_expression_data(
        gene=gene_symbol,
        tissue=phenotype_tissues[0] if phenotype_tissues else "all"
    )

    # Bulk tissue expression (GTEx)
    gtex = tu.tools.GTEx_get_median_gene_expression(
        gene=gene_symbol
    )

    # Check expression in relevant tissues
    relevant_expression = {
        tissue: gtex.get(tissue, 0)
        for tissue in phenotype_tissues
    }

    return {
        'single_cell': sc_expression,
        'gtex': relevant_expression,
        'expressed_in_phenotype_tissue': any(v > 1 for v in relevant_expression.values())
    }

Why it matters:

  • Confirms gene is expressed where disease manifests
  • Supports PP4 (phenotype-specific) if highly restricted expression
  • Can challenge classification if not expressed in affected tissue

Output for Report:

### 4.5 Expression Context

| Tissue | Expression (TPM) | Relevance |
|--------|------------------|-----------|
| Heart | 45.2 | ✓ Primary disease tissue |
| Skeletal muscle | 38.7 | ✓ Secondary involvement |
| Liver | 2.1 | Low expression |
| Brain | 0.5 | Not expressed |

**Single-Cell Analysis (CELLxGENE)**:
- **Cardiomyocytes**: High expression (TPM=85)
- **Cardiac fibroblasts**: Low expression (TPM=5)

**Interpretation**: Gene highly expressed in cardiomyocytes, supporting cardiac phenotype association.

*Source: GTEx, CELLxGENE Census*

Phase 5: Literature Evidence (ENHANCED)

Goal: Find functional studies, case reports, and cutting-edge preprints

Tools:

ToolPurposeCoverage
PubMed_searchPeer-reviewed studiesComprehensive
EuropePMC_searchAdditional literatureEurope PMC
BioRxiv_search_preprintsBiology preprintsRecent findings
MedRxiv_search_preprintsClinical preprintsClinical studies
openalex_search_worksCitation analysisImpact metrics
SemanticScholar_search_papersAI-ranked searchRelevance

Search Strategies:

def comprehensive_literature_search(tu, gene, variant, phenotype):
    """Search across all literature sources."""

    # 1. PubMed: Peer-reviewed
    pubmed = tu.tools.PubMed_search(
        query=f'"{gene}" AND ("{variant}" OR functional)',
        max_results=30
    )

    # 2. BioRxiv: Recent preprints
    biorxiv = tu.tools.BioRxiv_search_preprints(
        query=f"{gene} {phenotype}",
        limit=10
    )

    # 3. MedRxiv: Clinical preprints
    medrxiv = tu.tools.MedRxiv_search_preprints(
        query=f"{gene} variant {phenotype}",
        limit=10
    )

    # 4. Citation analysis
    key_papers = pubmed[:5]  # Top papers
    for paper in key_papers:
        citations = tu.tools.openalex_search_works(
            query=paper['title'],
            limit=1
        )
        paper['citation_count'] = citations[0].get('cited_by_count', 0) if citations else 0

    return {
        'pubmed': pubmed,
        'preprints': biorxiv + medrxiv,
        'key_papers_with_citations': key_papers
    }

Search Queries:

# Gene + variant specific
"{GENE} AND ({HGVS_p} OR {AA_change})"

# Functional studies
"{GENE} AND (functional OR functional study OR mutagenesis)"

# Clinical reports
"{GENE} AND (case report OR patient) AND {phenotype}"

# Preprint-specific
"{GENE} genetics 2024" (for recent preprints)

⚠️ Preprint Warning: Always flag preprints as NOT peer-reviewed in reports.

Evidence Types:

EvidenceACMG CodeWeight
Functional study (null)PS3Strong
Functional study (reduced)PS3_ModerateModerate
Case reports with segregationPP1Supporting to Moderate
Co-occurrence with pathogenicBP2Supporting against

Phase 6: ACMG Classification

Goal: Systematic classification with explicit evidence

ACMG Evidence Codes:

Pathogenic:

CodeStrengthDescription
PVS1Very StrongNull variant in gene where LOF is mechanism
PS1StrongSame amino acid change as known pathogenic
PS3StrongWell-established functional studies
PM1ModerateMutational hot spot / functional domain
PM2ModerateAbsent from controls
PM5ModerateDifferent missense at same residue as pathogenic
PP3SupportingMultiple computational predictions
PP5SupportingReputable source reports pathogenic

Benign:

CodeStrengthDescription
BA1Stand-aloneMAF >5%
BS1StrongMAF greater than expected
BS3StrongFunctional studies show no effect
BP4SupportingMultiple computational predictions benign
BP7SupportingSynonymous with no splice impact

Classification Algorithm:

ClassificationEvidence Required
Pathogenic1 Very Strong + 1 Strong; OR 2 Strong; OR 1 Strong + 3 Moderate
Likely Pathogenic1 Very Strong + 1 Moderate; OR 1 Strong + 2 Moderate; OR 1 Strong + 2 Supporting
Likely Benign1 Strong + 1 Supporting; OR 2 Supporting
Benign1 Stand-alone; OR 2 Strong
VUSCriteria not met

Output Structure

Report Sections

# Variant Interpretation Report: {GENE} {VARIANT}

## Executive Summary
- **Variant**: {HGVS notation}
- **Gene**: {gene symbol}
- **Classification**: {Pathogenic/Likely Pathogenic/VUS/Likely Benign/Benign}
- **Evidence Strength**: {strong/moderate/limited}
- **Key Finding**: {one-sentence summary}

## 1. Variant Identity
{gene, transcript, protein change, consequence}

## 2. Population Data
{gnomAD frequencies, ancestry breakdown}

## 3. Clinical Database Evidence
{ClinVar, ClinGen, OMIM}

## 4. Computational Predictions
{SIFT, PolyPhen, CADD scores}

## 5. Structural Analysis
{Domain location, functional site proximity, AlphaFold confidence}

## 6. Literature Evidence
{Functional studies, case reports}

## 7. ACMG Classification
{Evidence codes applied, classification rationale}

## 8. Clinical Recommendations
{Testing, management, family screening}

## 9. Limitations & Uncertainties
{Missing data, conflicting evidence}

## Data Sources
{All tools and databases queried}

Evidence Grading

Classification Confidence

SymbolClassificationEvidence Level
★★★High confidenceMultiple independent lines
★★☆Moderate confidenceSome supporting evidence
★☆☆Limited confidenceMinimal evidence
VUSUncertainInsufficient data

Structural Impact Confidence

pLDDT RangeInterpretation
>90Very high confidence in position
70-90High confidence
50-70Moderate (often loops)
<50Low confidence (disorder)

Special Scenarios

Scenario 1: Novel Missense VUS

Additional workflow:

  1. Check if other pathogenic variants at same residue
  2. Get AlphaFold2 structure
  3. Analyze:

- Is residue buried or surface? - What secondary structure? - Proximity to active/binding sites? - Conservation across species?

  1. Apply PM1 if in functional domain
  2. Apply PP3 if predictions concordant

Scenario 2: Truncating Variant

Additional workflow:

  1. Check if LOF is mechanism for gene
  2. Determine if escapes NMD (last exon)
  3. Check for alternative isoforms
  4. Review ClinGen LOF curation

PVS1 Application:

ScenarioPVS1 Strength
Canonical LOF gene, NMD predictedVery Strong
LOF gene, last exonModerate
Non-LOF geneNot applicable

Scenario 3: Splice Variant

Additional workflow:

  1. Check SpliceAI scores (if available)
  2. Determine canonical splice site distance
  3. Review for in-frame skipping potential
  4. Check for cryptic splice activation

Quantified Minimums

SectionRequirement
Population frequencygnomAD overall + ≥3 ancestry groups
Predictions≥3 computational predictors
Literature search≥2 search strategies
ACMG codesAll applicable codes listed

NVIDIA NIM Integration

When to Use AlphaFold2 for Variants

Use Case: VUS missense variants where structural context aids interpretation

Workflow:

# 1. Get protein sequence
protein_seq = tu.tools.UniProt_get_protein_sequence(accession=uniprot_id)

# 2. Get/predict structure
try:
    pdb_hits = tu.tools.PDB_search_by_uniprot(uniprot_id=uniprot_id)
    structure = tu.tools.PDB_get_structure(pdb_id=pdb_hits[0]['pdb_id'])
except:
    # Predict with AlphaFold2
    structure = tu.tools.NvidiaNIM_alphafold2(
        sequence=protein_seq['sequence'],
        algorithm="mmseqs2"
    )

# 3. Analyze variant position
# - Extract pLDDT at residue position
# - Calculate solvent accessibility
# - Check for nearby functional sites

Structural Features to Report:

  • pLDDT at variant position
  • Secondary structure (helix/sheet/coil)
  • Solvent accessibility (buried/exposed)
  • Distance to active site (if applicable)
  • Interactions disrupted (H-bonds, salt bridges)

Report File Naming

{GENE}_{VARIANT}_interpretation_report.md

Examples:
BRCA1_c.5266dupC_interpretation_report.md
TP53_p.R273H_interpretation_report.md

Clinical Recommendations Framework

For Pathogenic/Likely Pathogenic

Disease ContextRecommendations
Cancer predispositionEnhanced screening, risk-reducing options
PharmacogenomicsDrug dosing adjustment
Carrier statusReproductive counseling
Predictive testingFamily cascade screening

For VUS

ActionDetails
Clinical managementDo not use for medical decisions
Follow-upReinterpret in 1-2 years
ResearchFunctional studies if available
FamilySegregation data valuable

For Benign/Likely Benign

ActionDetails
ClinicalNot expected to cause disease
FamilyNo cascade testing needed
DocumentationInclude in report for completeness

See Also

  • CHECKLIST.md - Pre-delivery verification
  • EXAMPLES.md - Sample interpretations
  • TOOLS_REFERENCE.md - Tool parameters and fallbacks

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