vaxZipper
Your DNA · your report · processed locally

vaxZipper

Explore vaccine-response genetics — privately, in your browser.

Drop in a 23andMe, AncestryDNA or MyHeritage export. vaxZipper reads it locally, finds the report markers, and shows the study behind each result.

Upload your DNA file
23andMe, AncestryDNA, or MyHeritage — .txt, .csv, or .zip
See how it works
.txt · .csv · .zip  •  nothing is uploaded
100% localYour DNA stays on your device.
Private by designNo account. No server-side genome processing.
Personal reportYour genotypes, coverage and cited evidence.
01
Choose your DNA fileUse your raw 23andMe, AncestryDNA or MyHeritage export.
02
vaxZipper reads it locallyThe browser checks the report markers without sending your genome anywhere.
03
See what stands outGet your genotype, coverage status and the study behind each result.
Current report areas
MMRHepatitis BDTaPHibType I IFN research
Science, scope, privacy & limitations
What this is. A browser-based reference that checks a small set of variants reported in vaccine-response research. Each section represents different biology, and each result points back to its supporting study.
What an associated finding means. The study-associated allele or genotype was found in this DNA file. The report states the exact phenotype — for example, febrile response or antibody response — rather than treating every result as one generic “risk.”
Where studies disagree. vaxZipper reports the genotype without forcing a direction. Study alleles are reconciled to the forward strand before a directional result is shown.
What this is not. Not a clinical genetic test, diagnosis, or vaccination recommendation. A marker that is not assessed is a coverage limitation, not a negative finding.
Local only. Nothing leaves this tab.
Reading your file
Finding your variants
Checking vaccine markers
Building your report
Personal reference · vaxZipper · build 15

vaxZipper

Vaccine response, zipped.
The sections below report different biology. An "associated allele detected" call in the MMR section does not mean the same thing as one in the Hep B section. Reading them uniformly leads to wrong conclusions.

MMR-specific — variant associated with a stronger febrile response after MMR. Population-level tendency, not an individual prediction.
General febrile response — variant associated with febrile-seizure susceptibility from any cause, illness or vaccine. The literature distinguishes simple from complex febrile seizures; that distinction is noted in the exclusions.
Hepatitis B — variant associated with reduced antibody response (non-response) to the vaccine series. This finding concerns antibody response; adverse reactions were not the phenotype evaluated in the cited studies. Related clinical measurement: post-vaccination anti-HBs titer.
DTaP — candidate TLR-pathway variants for pertussis-component antibody response. Direction of effect varies. The clinically important DTaP thread (SCN1A / Dravet syndrome) is in the exclusions block.
Hib — no assessable common SNPs at the consumer-array level. Related clinical measurement: post-vaccination anti-PRP antibody titer.
Type I IFN pathway (research) — common variants in the innate antiviral system. Reported as genotype observed because direction of effect is often two-sided (a variant increasing autoimmune risk may protect against viral disease, and vice versa). Rare loss-of-function variants and anti-IFN autoantibodies — the clinically consequential parts — are NOT covered by consumer arrays or by DNA at all, respectively. Details in exclusions.

How an associated allele gets assigned. Each marker stores what every cited study printed, in that study's own orientation. Those letters are mapped onto the forward strand your DNA file uses, and only then compared with each other. A marker shows an associated allele only when the studies still agree after that mapping. Where they disagree, the card says so and reports the genotype without a direction.

What the result states mean: Associated allele detected — the allele the cited studies agree on was found in this file. Each card states what it is associated with, because those directions are not interchangeable: a lower antibody titer and a stronger febrile response are different findings, not two flavours of the same "risk". Associated allele not detected — that allele was not found at this one marker. Not proof of protection. Genotype observed — the SNP was read but no associated allele is assigned, either because no cited study establishes a direction or because the cited studies disagree. Each card says which. Alleles do not match reference — the genotype in the file is not made of the alleles expected at that position, which usually means a strand or reference mismatch. The tool reports this rather than flipping the genotype to force a match. Not assessed — the SNP was not in the uploaded file. Not a negative result. No-call — the SNP was in the file but could not be read.
Some genes with the strongest published signal for vaccine response — HLA class II in particular — cannot be reliably read from consumer genotyping arrays. This report does not attempt to assess them, and a blank here is not a negative result.
Add a documented reaction for this person

Entered here, kept only for this session, and included in the report you download next. Nothing is written back into this file, so the next person to load their DNA starts with an empty history.

MMR and general febrile response. Feenstra B, Pasternak B, Geller F, et al. Common variants associated with general and MMR vaccine-related febrile seizures. Nature Genetics. 2014;46(11):1274–1282.
PubMed: 25344690  ·  DOI: 10.1038/ng.3129  ·  Full text: PMC4244308
Damiano JA, Deng L, Li W, et al. SCN1A variants in vaccine-related febrile seizures: a prospective study. Ann Neurol. 2020;87(2):281–288. PMID 31755124. Reports the opposite rs6432860 allele to Feenstra once orientation is reconciled; see that marker's card.
Haralambieva IH, Ovsyannikova IG, Kennedy RB, et al. Genome-wide associations of CD46 and IFI44L genetic variants with neutralizing antibody response to measles vaccine. Hum Genet. 2017;136(4):421–435. A different phenotype from febrile response; recorded on the CD46 card as context.
Hepatitis B — vaccine-response sources. These are the studies that actually measured antibody response to the vaccine, and they are what the Hep B cards rest on.
Png E, Thalamuthu A, Ong RTH, et al. A genome-wide association study of hepatitis B vaccine response in an Indonesian population reveals multiple independent risk variants in the HLA region. Hum Mol Genet. 2011;20(19):3893–3898. PMID 21764829.
Sakai A, et al. Strong influence of HLA-DP variants on response to hepatitis B vaccine in a Japanese population. Vaccine. 2017. PMID 28882445.
Wu TW, et al. SNP rs7770370 in HLA-DPB1 as a major genetic determinant of response to booster hepatitis B vaccination: a genome-wide association study. PMID 25389088.
Association of HLA-DP variants with responsiveness to hepatitis B vaccination in Korean infants. Vaccine. 2016. PMID 27083422.
Genetic polymorphisms of CXCR5 and CXCL13 are associated with non-responsiveness to the hepatitis B vaccine. Vaccine. 2014. PMID 25077417. A single cohort of 65 people; weigh it well below the HLA-DP markers.
Hepatitis B — infection-outcome sources (background). These concern chronic HBV infection and viral clearance, not vaccine antibody response. They are kept for context and are marked as context on the marker cards; they do not support a vaccine-response call.
Nishida N, et al. Genome-wide association study confirming association of HLA-DP with protection against chronic hepatitis B and viral clearance in Japanese and Korean. 2012. PMID 22737229.
Hu Z, Liu Y, Zhai X, et al. New loci associated with chronic hepatitis B virus infection in Han Chinese. Nat Genet. 2013;45:1499–1503.
DTaP — primary sources. Kimman TG, Vandebriel RJ, Hoebee B. Genetic variation in the response to vaccination. Community Genet. 2007;10(4):201–217.
Kimman TG, Banus S, Reijmerink N, et al. Association of interacting genes in the toll-like receptor signaling pathway and the antibody response to pertussis vaccination. PLoS ONE. 2008;3(11):e3665.
McIntosh AM, McMahon J, Dibbens LM, et al. Effects of vaccination on onset and outcome of Dravet syndrome: a retrospective study. Lancet Neurol. 2010;9(6):592–598.
Hib — context sources. Slack MPE, Livesey R, et al. Haemophilus influenzae infections in the H. influenzae type b conjugate vaccine era. Clin Microbiol Rev. 2011;24(4):826–862.
Ambrosino DM, Siber GR, Chilmonczyk BA, et al. An immunodeficiency characterized by impaired antibody responses to polysaccharides. N Engl J Med. 1987;316(13):790–793.
Type I IFN pathway — primary sources. Gorman JA, Hundhausen C, Errett JS, et al. The A946T variant of the RNA sensor IFIH1 mediates an interferon program that limits viral infection but increases the risk for autoimmunity. Nat Immunol. 2017;18(7):744–752.
Boisson-Dupuis S, Ramirez-Alejo N, Li Z, et al. Tuberculosis and impaired IL-23–dependent IFN-γ immunity in humans homozygous for a common TYK2 missense variant. Sci Immunol. 2018;3(30):eaau8714.
Zhang Q, Bastard P, Liu Z, et al. Inborn errors of type I IFN immunity in patients with life-threatening COVID-19. Science. 2020;370(6515):eabd4570.
van der Made CI, Simons A, Schuurs-Hoeijmakers J, et al. Presence of genetic variants among young men with severe COVID-19. JAMA. 2020;324(7):663–673.
Bastard P, Rosen LB, Zhang Q, et al. Autoantibodies against type I IFNs in patients with life-threatening COVID-19. Science. 2020;370(6515):eabd4585.
Bastard P, Gervais A, Le Voyer T, et al. Autoantibodies neutralizing type I IFNs are present in ∼4% of uninfected individuals over 70 years old and account for ∼20% of COVID-19 deaths. Sci Immunol. 2021;6(62):eabl4340.
Effect sizes. Every odds ratio in this report is tagged with the specific comparison it came from, because the same marker can carry several different estimates depending on which groups a study compared. An odds ratio with no comparison attached is not usable evidence. The estimates here are modest, roughly 1.2 to 2.1 per copy for most loci. At the population level most people carrying these variants do not have the outcomes studied, and most outcomes happen in people without them. These are contributors to probability, not causes.
Related clinical measurements. Where a laboratory measurement corresponds to something a section reports, it is named here. For Hepatitis B, a post-vaccination anti-HBs antibody titer, which measures antibody response directly. For Hib, a post-vaccination anti-PRP antibody titer, and an IgG subclass panel where the response is low. For SCN1A, clinical sequencing ordered through a clinician, which a consumer genotyping file cannot substitute for. For febrile response there is no corresponding laboratory measurement; the record that exists is a documented prior reaction. On SCN1A specifically, McIntosh et al. (2010) reported that vaccination did not alter the onset or outcome of Dravet syndrome in their retrospective cohort; that paper is cited in the references.