Detect the Cancer-Driving Proteins — Not Just the Virus — for Clinically Meaningful Cervical Cancer Risk Stratification
Human papillomavirus (HPV) types 16 and 18 account for approximately 70% of all cervical cancers worldwide. While HPV DNA testing detects viral presence, it cannot distinguish between transient infections (which will clear spontaneously) and integrated, oncogenically active infections — the ones that actually cause cancer.
Sekbio's HPV 16/18 E7 Oncoprotein Rapid Test Kit (Colloidal Gold) detects the E7 oncoprotein — the primary carcinogenic effector of HPV — directly from female cervical swab specimens. E7 overexpression occurs specifically in high-grade lesions (CIN2/3) and invasive cervical carcinoma where the virus has integrated and is actively degrading the tumor suppressor pRb.
Alongside the ready-to-use rapid test kit, Sekbio offers matched antibody pairs for both targets: an anti-HPV 16 E7 pair (S22-HPV-W1CC + W2CC) and an anti-HPV 18 E7 pair (S22-HPV-W5CC + W7CC) — covering IgG1 and IgG2a isotypes, validated for LFA, CLIA, and ELISA platform development.
HPV E7 oncoprotein is not merely a marker of infection — it is the molecular driver of cervical carcinogenesis, making its detection clinically more meaningful than DNA-based HPV testing alone.
HPV E7 oncoprotein binds and degrades pRb (retinoblastoma protein), the master brake of the cell cycle. This releases E2F transcription factors and forces cells into uncontrolled proliferation. E7 upregulation is the key molecular event distinguishing oncogenic HPV infection from benign viral carriage.
Standard HPV DNA/RNA tests detect viral nucleic acid regardless of integration status. The majority of HPV infections — including high-risk types 16 and 18 — are transient and clear without causing disease. DNA positivity alone cannot identify which infections have progressed to active oncogenesis and require intervention.
E7 oncoprotein levels increase progressively with cervical lesion severity: low in CIN1, substantially elevated in CIN2/3, and highest in invasive carcinoma. This graded correlation makes E7 detection a direct indicator of disease severity — informing triage decisions in HPV-positive women.
The Sekbio assay was validated against 11 clinically relevant conditions including Staphylococcus aureus, Candida albicans, Neisseria gonorrhoeae, Gardnerella vaginalis, EBV, and three non-target HPV types (31, 33, 52) at 100 ng/mL — all producing negative results. No false positives observed.
The colloidal gold lateral flow format delivers a visual result from a cervical swab without laboratory instrumentation, centrifugation, or nucleic acid extraction. This makes HPV E7 oncoprotein testing accessible in primary care clinics, colposcopy units, and resource-limited settings globally.
Sekbio supplies two independently validated antibody pairs: S22-HPV-W1CC + W2CC (both IgG2a, anti-HPV 16 E7) and S22-HPV-W5CC + W7CC (IgG1 + IgG2a, anti-HPV 18 E7). Each pair enables complete sandwich immunoassay construction for its respective target across CLIA, LFA, and ELISA platforms.
Complete qualification data from three production batches (F10001, F10002, F10003), covering limit of detection, repeatability, inter-batch consistency, cross-reactivity, and endogenous interference.
Dose-response testing across five concentration levels for each target. Acceptance criteria: all replicates at LOD concentration read positive; color grade difference ≤ 0.5 across 10 replicates. Batch: F10001.
| Target & Concentration | n | Color Grade Range | Max Grade Diff | Result |
|---|---|---|---|---|
| Negative Control (0 ng/mL) | 10 | B0 | 0 | All Negative |
| HPV 16 E7 — 5 ng/mL (LOD) | 10 | B2 to B2− | ≤ 0.5 | All Positive ✓ |
| HPV 16 E7 — 10 ng/mL | 10 | B3 to B3− | ≤ 0.5 | All Positive |
| HPV 16 E7 — 50 ng/mL | 10 | B4 to B4+ | ≤ 0.5 | All Positive |
| HPV 16 E7 — 500 ng/mL | 10 | B6 to B6− | ≤ 0.5 | All Positive |
| HPV 16 E7 — 1000 ng/mL | 10 | B7 to B7+ | ≤ 0.5 | All Positive |
| HPV 18 E7 — 0.5 ng/mL (LOD) | 10 | B1+ to B2− | ≤ 0.5 | All Positive ✓ |
| HPV 18 E7 — 1 ng/mL | 10 | B3 to B3− | ≤ 0.5 | All Positive |
| HPV 18 E7 — 10 ng/mL | 10 | B4 to B4+ | ≤ 0.5 | All Positive |
| HPV 18 E7 — 50 ng/mL | 10 | B6 to B6− | ≤ 0.5 | All Positive |
| HPV 18 E7 — 100 ng/mL | 10 | B7 to B7− | ≤ 0.5 | All Positive |
| Color grade B0 = negative. B1–B7+ = positive with increasing intensity. Grade difference ≤ 0.5 at LOD confirms stable, reproducible signal at the detection threshold. Batch F10001. | ||||
Intra-batch repeatability (10 replicates per concentration per lot) and inter-batch consistency were assessed across production lots F10001, F10002, and F10003. Acceptance criteria: color grade difference ≤ 0.5 within each batch; difference between batches ≤ 0.5 at the same concentration.
| Target & Concentration | Lot F10001 Range | Lot F10002 Range | Lot F10003 Range | Inter-Lot Diff | Status |
|---|---|---|---|---|---|
| HPV 16 E7 — 5 ng/mL | B2 to B2− | B2 to B2− | B2 to B2− | ≤ 0.5 | PASS |
| HPV 16 E7 — 10 ng/mL | B3 to B3− | B3 to B3− | B3 to B3− | ≤ 0.5 | PASS |
| HPV 18 E7 — 1 ng/mL | B3 to B3− | B3 to B3− | B3 to B3− | ≤ 0.5 | PASS |
| HPV 18 E7 — 10 ng/mL | B4 to B4+ | B4 to B4+ | B4 to B4+ | ≤ 0.5 | PASS |
| All intra-batch and inter-batch color grade differences ≤ 0.5 grade. Repeatability and inter-batch precision meet acceptance criteria across all three production lots. | |||||
Interference testing assessed common co-pathogens of the female reproductive tract, systemic infection agents, and non-target HPV types at clinical or supraphysiological concentrations. No false-positive results were observed in any condition. Batch: F10001, 2 replicates per agent.
| Interference Agent / Condition | Category | Concentration | Result (n=2) | Conclusion |
|---|---|---|---|---|
| Staphylococcus aureus | Bacterial pathogen | Clinical | Negative (−) | No interference |
| Escherichia coli | Bacterial pathogen | Clinical | Negative (−) | No interference |
| Ureaplasma urealyticum | Urogenital pathogen | Clinical | Negative (−) | No interference |
| Candida albicans | Fungal pathogen | Clinical | Negative (−) | No interference |
| Neisseria gonorrhoeae | STI pathogen | Clinical | Negative (−) | No interference |
| Gardnerella vaginalis | Urogenital pathogen | Clinical | Negative (−) | No interference |
| Mycoplasma hominis | Urogenital pathogen | Clinical | Negative (−) | No interference |
| EBV (Epstein-Barr Virus) | Viral pathogen | Clinical | Negative (−) | No interference |
| HPV type 31 E7 | Non-target HPV (high-risk) | 100 ng/mL | Negative (−) | No cross-reactivity |
| HPV type 33 E7 | Non-target HPV (high-risk) | 100 ng/mL | Negative (−) | No cross-reactivity |
| HPV type 52 E7 | Non-target HPV (high-risk) | 100 ng/mL | Negative (−) | No cross-reactivity |
| Non-target HPV types 31, 33, and 52 tested at 100 ng/mL — 20× above the HPV 16 E7 LOD of 5 ng/mL. No cross-reactivity observed, confirming assay specificity for HPV 16 and 18 E7 oncoproteins exclusively. | ||||
Two matched antibody pairs — one targeting HPV 16 E7 (W1CC + W2CC) and one targeting HPV 18 E7 (W5CC + W7CC) — available for OEM integration into LFA, CLIA, and ELISA platforms. Covering IgG1 and IgG2a isotypes for flexible capture/detection configuration.
Anti-HPV 16 E7 Pair
Anti-HPV 18 E7 Pair
For HPV 16 E7 detection, the W1CC (capture) + W2CC (detection) configuration — both IgG2a — provides a validated sandwich pair. For HPV 18 E7 detection, the W5CC (IgG1) + W7CC (IgG2a) pairing crosses isotypes, which typically reduces steric interference at the antigen binding site and improves sandwich assay sensitivity.
All four antibodies are purified by affinity chromatography to >92% purity and supplied in PBS pH 7.4 — compatible with standard colloidal gold conjugation, CLIA tracer labeling, and ELISA plate coating protocols without buffer exchange in most applications.
HPV E7 oncoprotein detection spans clinical cervical cancer screening, triage of HPV-positive women, and IVD manufacturer raw material supply.
In women who test positive on HPV DNA screening, E7 oncoprotein positivity identifies those with active oncogenic viral expression — guiding colposcopy referral decisions. E7-negative women in the HPV DNA-positive pool are more likely to have self-clearing infections, reducing unnecessary procedures.
The test is specifically designed as an auxiliary diagnostic tool for cervical precancerous lesions (CIN2/3) and cervical carcinoma. E7 overexpression in cervical swab specimens correlates directly with histological high-grade disease, complementing cytology and colposcopy findings.
The colloidal gold format requires no laboratory equipment. Results are read visually from a cervical swab sample — enabling HPV E7 oncoprotein testing in primary care clinics, gynecology practices, community health centers, and low-resource settings where cytology or HPV PCR infrastructure is unavailable.
Sekbio supplies matched antibody pairs for both HPV 16 E7 (W1CC + W2CC, both IgG2a) and HPV 18 E7 (W5CC IgG1 + W7CC IgG2a). Each pair enables complete sandwich immunoassay construction for its respective target. Antibody concentrations of 4.9–6.1 mg/mL are optimized for direct colloidal gold conjugation, CLIA tracer labeling, and ELISA plate coating.
Understanding the molecular function of E7 oncoprotein and why its detection is more clinically informative than HPV DNA or serology alone.
HPV types 16 and 18 are the two highest-risk genotypes, responsible for the majority of HPV-attributable cancers globally. Their oncogenic activity is mediated through two viral proteins: E6 (which degrades p53) and E7 (which degrades pRb). E7 is the dominant driver of cell cycle dysregulation and uncontrolled proliferation in cervical carcinogenesis.
| HPV Type | Cervical Cancer Attribution | E7 Target | E7 LOD in Sekbio Assay |
|---|---|---|---|
| HPV 16 | ~50–60% of cervical cancers | pRb degradation, cell cycle arrest bypass | 5 ng/mL |
| HPV 18 | ~10–15% of cervical cancers | pRb degradation, cell cycle arrest bypass | 0.5 ng/mL |
| HPV 31, 33, 52 (non-target) | Additional ~15% combined | Homologous E7 proteins | No cross-reactivity at 100 ng/mL |
| HPV 16 and 18 together account for approximately 70% of all cervical cancers globally (WHO). The Sekbio assay detects both type-specifically, with no cross-reactivity to the next three most common high-risk types. | |||
Multiple HPV biomarker strategies exist. E7 oncoprotein detection occupies a unique specificity niche: it confirms active carcinogenic viral expression at the protein level — distinct from DNA presence, RNA transcription markers, or host immune response serology.
| Biomarker / Test Type | What It Detects | Confirms Active Oncogenesis? | Point-of-Care Feasible? |
|---|---|---|---|
| HPV DNA (PCR / hybrid capture) | Viral DNA presence | No — transient and persistent infections appear identical | No — requires lab |
| HPV E6/E7 mRNA (NASBA / RT-PCR) | Viral oncoprotein transcription | Partially — indicates active transcription | No — requires lab |
| p16/Ki-67 cytology | Host cell cycle dysregulation | Indirectly — host response marker | No — requires cytologist |
| Anti-HPV serology (IgG) | Past exposure / immune response | No — cannot distinguish active from resolved infection | Possible |
| HPV E7 Oncoprotein (Sekbio) | E7 protein expression — direct carcinogenic effector | Yes — protein detection confirms active expression | Yes — colloidal gold LFA |
| E7 oncoprotein testing is the only format that directly confirms active carcinogenic protein expression at point of care, without nucleic acid extraction or laboratory infrastructure. | |||
Request the rapid test datasheet, antibody panel technical data, or OEM supply information from our team.