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Red Sun Medizone Launches CE-Marked HPV 5+9 Genotyping Assay Detecting 14 High-Risk HPV Types with Individual Genotyping of HPV16, 18, 52, 33 and 58 for Cervical Cancer Screening

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September 29, 2026

HPV 5+9 Genotyping Assay: Real-Time PCR Detection of 14 High-Risk HPV Types with Individual Genotyping of HPV16, 18, 52, 33 and 58 for Primary Cervical Cancer Screening and Triage

HONG KONG, China — September 29, 2026 — Red Sun Medizone today announced the availability of a CE-marked in vitro diagnostic (IVD) real-time PCR kit that detects 14 high-risk human papillomavirus (HPV) types in a single analysis. The assay individually identifies HPV16, HPV18, HPV52, HPV33 and HPV58 while concurrently detecting the remaining nine high-risk types — HPV31, 35, 39, 45, 51, 56, 59, 66 and 68 — as a group, from cervical exfoliated cells collected in cell preservation solution. A β-globin internal control monitors the entire process from extraction to amplification. In a comparative study of 1,000 samples across three provincial hospitals using HPV L1 region DNA sequencing as the reference method, the assay achieved a kappa value of 1, with 100% positive, 100% negative and 100% total coincidence.
Molecular diagnostics laboratory bench with a 96-well real-time PCR plate, PCR tube strips in a rack and liquid cytology sample vials containing preservation fluid for high-risk HPV genotyping in cervical cancer screening

Key facts at a glance

  • Analytes: 14 high-risk HPV types in one analysis — individually genotyped: HPV16, HPV18, HPV52, HPV33, HPV58; detected as a group: HPV31, HPV35, HPV39, HPV45, HPV51, HPV56, HPV59, HPV66, HPV68
  • Specimen: cervical exfoliated cells collected with an endocervical brush into cell preservation solution
  • Method: real-time PCR amplification of HPV type-specific and β-globin target sequences with fluorescent-labelled oligonucleotide probes, detected across four dyes
  • Two-tube design: Tube A — HPV16 (VIC), HPV18 (ROX), HPV52 (FAM), β-globin (CY5); Tube B — HPV33 (VIC), HPV58 (ROX), the nine pooled high-risk types (FAM), β-globin (CY5)
  • Internal control: β-globin monitors extraction, amplification and inhibition across the whole test process
  • Limit of detection: ≤ 100 copies per test for all 14 high-risk types in the panel
  • Reproducibility: Ct coefficient of variation ≤ 5% across ten repeats at 100 and 500 copies per test
  • Clinical verification: 1,000 samples across three provincial hospitals against HPV L1 DNA sequencing — kappa 1, 100% positive coincidence, 100% negative coincidence, 100% total coincidence
  • Timing: same-day reporting; two PCR reactions per specimen
  • Instrumentation: any open real-time PCR platform with FAM, VIC/HEX, ROX and CY5 channels, such as the Applied Biosystems 7500 or Roche LightCycler 480
  • Kit configuration: 48 tests per kit
  • Regulatory status: CE-marked in vitro diagnostic device, and registered with China's National Medical Products Administration (NMPA) for cervical cancer screening

The clinical problem: the primary screening test has changed

Cervical cancer remains one of the most common cancers in women worldwide, and persistent infection with a high-risk HPV type is its necessary cause [1,2]. Because the causal agent is a virus, cervical screening has been able to move from looking at cells to looking for the virus — and the World Health Organization's 2021 guideline formalised that shift by recommending HPV DNA testing as the preferred primary screening method for cervical cancer prevention [15].
The performance case for that shift is well documented. A Cochrane systematic review of 40 studies covering more than 140,000 women aged 20 to 70 compared HPV testing with cytology for the detection of cervical intraepithelial neoplasia grade 2 or worse: pooled sensitivity was 89.9% for hybrid capture 2 versus 62.5% for conventional cytology and 72.9% for liquid-based cytology at the ASCUS threshold, with pooled specificity of 89.9%, 96.6% and 90.3% respectively [6]. The clinical consequence of that sensitivity difference was demonstrated by long-term follow-up of four European randomised controlled trials, in which HPV-based screening reduced the rate of invasive cervical carcinoma (rate ratio 0.60, 95% CI 0.40–0.89), with the benefit concentrated after the first 2.5 years of follow-up (rate ratio 0.45, 95% CI 0.25–0.81) and reaching a rate ratio of 0.30 (95% CI 0.15–0.60) among women who had a negative screening test at entry [7].
Two further developments shape how such a test is deployed. First, self-collection is now a credible route: a 2025 meta-analysis found that pooled sensitivity for CIN2 or worse was 87% (95% CI 76–93) for clinician-collected cytology, 90% for HPV testing on self-collected specimens and 93% for HPV testing on clinician-collected specimens, when restricted to PCR-based HPV assays — supporting the use of the same screening intervals for negative self-collected HPV results as for negative cytology [11]. Second, international validation frameworks exist: the widely used 2020 list of HPV assays suitable for primary cervical cancer screening identified seven hrHPV DNA tests that consistently fulfilled all validation criteria across multiple studies [10]. Laboratories and programme managers now have an explicit benchmark against which to qualify an assay.

Why extended genotyping matters more than HPV16/18 alone

Once HPV DNA testing is the primary screen, the question becomes what the report should say. The global evidence on type attribution is unambiguous and, importantly, geographically uneven. A 2024 systematic analysis in The Lancet, covering 1,174 studies with 111,902 HPV-positive invasive cervical cancer cases and 2,755,734 normal cytology results, quantified the causal attribution of individual genotypes: HPV16 accounted for 61.7% of invasive cervical cancers, HPV18 for 15.3%, HPV45 for 4.8%, HPV33 for 3.8%, HPV58 for 3.5%, HPV31 for 2.8% and HPV52 for 2.8%, with the remaining ten causal genotypes contributing 5.3% combined [4]. HPV16 and HPV18 together accounted for 71.9% of cases in Africa but 83.2% in central, western and southern Asia; adding HPV31, 33, 45, 52 and 58 raised coverage to 92.1% in Africa and 95.9% in central, western and southern Asia [4]. In other words, a substantial and region-dependent share of cervical cancers is attributable to types that a 16/18-only assay does not name.
The type-specific risk data explain why. A study of type-specific HPV natural history found that risks of progression to CIN3 or worse differ substantially by genotype: HPV16 conveyed uniquely elevated risk (representing 26% of infections, with a seven-year CIN3+ risk of 22%), while the other carcinogenic types fell into three distinct risk groups — HPV18 and HPV45 (13% of infections, seven-year risk above 5%), HPV31, 33, 35, 52 and 58 (39% of infections, seven-year risk above 5%), and HPV39, 51, 56, 59 and 68 (23% of infections, seven-year risk below 5%). In the absence of progression, clearance was similar by type, with 80% of infections no longer detected within three years; the authors concluded that type and persistence are the major predictors of progression, and that separating out the higher-risk types is clinically important [5].
The same principle was demonstrated prospectively in the ATHENA study, which recruited 47,208 women during routine screening: women positive for HPV16 or HPV18 had an absolute risk of CIN2 or worse of 24.4%, compared with 14.0% for women positive for pooled high-risk HPV types and 0.8% for women who were high-risk HPV negative — establishing that HPV16/18 genotyping identifies women at highest risk and can be used in formulating management decisions [8].
The argument is strongest in Asian populations, and the reason is empirical. In a cross-sectional study of 125,604 women in Yueyang, China, the most prevalent high-risk types were, in descending order, HPV52 (5.1%), HPV16 (2.7%), HPV58 (2.6%), HPV53 (2.4%) and HPV51 (1.7%) — HPV52 ranking first, ahead of HPV16 [13]. In a series of 101,621 samples in Fujian, China, 24.5% tested positive for HPV, and among single infections 71.4% were non-16/18 high-risk types; most strikingly, in the cancer group, HPV52 (21.8%) and HPV58 (18.6%) were the predominant types, ahead of HPV33 and HPV31 [12]. An assay that genotypes only HPV16 and HPV18 and pools everything else would therefore report the two most important cancer-associated types in this population without naming either of them.
Finally, extended genotyping has been shown to improve the efficiency of the downstream pathway. In a study of 8,000 women with 83 CIN2+ and 33 CIN3+ outcomes, agreement between extended and partial HPV genotyping was 92.66%, and a risk-based triage strategy built on extended genotyping achieved higher specificity for CIN2+ (94.84% versus 92.46%) and CIN3+ (96.05% versus 91.92%) than conventional HPV primary screening, while requiring fewer colposcopies to detect one cervical disease [9].
DNA double helix with highlighted genotype segments and virus particles overlaid on a semi-transparent illustration of the cervix and female reproductive anatomy, illustrating individual genotyping of HPV16, 18, 52, 33 and 58 in cervical cancer screening

What the assay reports

Reporting modeHPV typesClinical rationale
Individually genotypedHPV16, HPV18, HPV52, HPV33, HPV58Types with the highest attributable fractions and the highest type-specific progression risk; HPV52 and HPV58 are the dominant high-risk types in several Asian populations
Detected as a groupHPV31, HPV35, HPV39, HPV45, HPV51, HPV56, HPV59, HPV66, HPV68Broad coverage of the remaining carcinogenic types in a single channel, so that no high-risk infection in the panel goes undetected
Total high-risk coverage14 types in a single analysisComplete high-risk coverage without requiring a separate assay
Internal controlβ-globinConfirms DNA extraction, amplification and absence of PCR inhibition across the entire process
Source: type lists and reporting design as stated in the product instructions for use, version V2.3. All 14 types are detected; five are reported by name and nine are reported as a group.

How the assay works

HPV DNA is extracted from cervical exfoliated cells collected in cell preservation solution. The master mix contains primer pairs and probes specific for the 14 high-risk HPV types together with β-globin, and amplification is performed with real-time detection of fluorescent-labelled oligonucleotide probes across four dyes. The two-tube design distributes the panel so that the five highest-priority genotypes each receive their own dedicated signal, while the nine remaining high-risk types are detected together:
  • Tube A: HPV16 in VIC, HPV18 in ROX, HPV52 in FAM, β-globin in CY5
  • Tube B: HPV33 in VIC, HPV58 in ROX, the nine pooled high-risk types (31, 35, 39, 45, 51, 56, 59, 66, 68) in FAM, β-globin in CY5
Result interpretation is threshold-based: a channel signal at or below the Ct threshold is called positive, and β-globin must be detected for the result to be valid. A specimen is reported positive for the named genotype where the corresponding dedicated channel is positive; where only the pooled channel is positive, the specimen is reported as positive for the group of nine high-risk types. If β-globin is not detected, the result is invalid and the original specimen must be re-tested. Ct determination settings, baseline window and threshold values are specified per instrument in the instructions for use, and the passive reference is set to "None" on the Applied Biosystems 7500.
A practical safeguard is stated in the instructions for use: a specimen returning a Ct at or below 5 should be reported as positive, or re-tested after 100-fold dilution — a control against the very high viral loads that can suppress a channel.

Specimen collection, transport and storage

Because at least one half to two thirds of false-negative HPV results arise from conditions present at collection and from the technique of the person obtaining the specimen, the instructions for use specify the collection conditions: sampling approximately 10–18 days after the first day of the last menstrual period; no douching, tampons, vaginal creams or vaginal medications for 48 hours before the test; and no intercourse for 48 hours before the test. Collection uses a sterile single-use speculum without lubricant and an endocervical brush inserted into the endocervical canal, rotated 45–90° and withdrawn into cell preservation solution.
Once collected in preservation solution, the specimen is stable for 7 days at room temperature, 2 months at 2–8 °C and 6 months at ≤ –20 °C, and tolerates up to five freeze–thaw cycles. Specimens may be transported at room temperature or on dry ice at 2–8 °C for 4 days. Reagents are stored at ≤ –20 °C for up to 6 months, tolerate no more than five freeze–thaw cycles, may be transported at 2–8 °C for no longer than 4 days, and are valid for 7 days at 2–8 °C once opened. The endocervical brush, cell preservation solution and nucleic acid extraction kit are supplied separately as accessories; where a laboratory prefers its own preservation solution or extraction kit, the instructions for use require an equivalence check beforehand.

Analytical performance

  • National reference panel. The kit was evaluated against the complete HPV genome genotyping national reference panel, including HPV51 and HPV56 as positive controls; product appearance, internal control Ct value, positive and negative control coincidence, reproducibility, limit of detection and control performance all conformed with regulatory requirements.
  • Positive control coincidence. Using the national genotyping reference panel or standardised enterprise controls at 500 copies per test, all 14 HPV types within the detection range were reported positive with the correct type assignment.
  • Negative control coincidence. With out-of-range genotypes, no cross-reaction occurred among high-risk HPV genotypes, and the permitted cross-reaction rate for low-risk types is stated as no higher than 10.0%; with the national negative reference panel, all HPV types were reported negative.
  • Reproducibility. References for HPV16, HPV18 and HPV45 at 100 and 500 copies per test were each detected ten times; all results were positive for the corresponding type with a Ct coefficient of variation ≤ 5%.
  • Limit of detection. ≤ 100 copies per test for each of the 14 high-risk types within the detection range.
  • Extraction-kit equivalence. DNA nucleic acid extraction kits from different suppliers showed no distinct difference in results.
  • Interference and specificity. Fourteen pathogen-positive samples from similar sampling sites — including Mycoplasma urealyticum, Chlamydia trachomatis, Candida albicans, Neisseria gonorrhoeae, trichomonas, mildew and Gardnerella vaginalis — were all negative for HPV. Thirty-eight homologous HPV types outside the detection range (including HPV6, 11, 26, 40, 42, 43, 44, 53, 55, 61, 81, 82, 83, 54, 70, 72, 73, 67, 71, 69, 78, 2, 3, 13, 27, 57, 75, 74, 77, 84 and 94) were all negative. Samples containing vaginal lotions and suppositories, HPV-positive samples spiked with peripheral blood, and HPV-positive fester samples all gave correct results, supporting the kit's resistance to interference from drugs, blood and inflammatory material.
  • Dye cross-interference. Mixed HPV16, HPV18 and HPV45 positive samples showed a Ct coefficient of variation ≤ 5% against single positive samples, indicating no mutual interference among the four fluorescence dyes.

Clinical performance: the 1,000-sample comparison

Study elementAs documented
Reference methodDNA sequencing using HPV L1 region type-specific primers
DesignComparative study in three provincial hospitals
Samples1,000 cervical samples, all analysed by both methods
Discordant samplesSubjected to third-party verification before statistical analysis
AgreementKappa 1; positive coincidence rate 100%; negative coincidence rate 100%; total coincidence rate 100% for all types
Secondary comparison200 samples compared with a 27-genotype assay: kappa 1, positive coincidence 100%, negative coincidence 100%, total coincidence 100%
Source: product instructions for use, version V2.3, section "Specific performance characteristics — Clinical verification". Study hospital names, specimen-level records and the complete technical dossier are available to qualified laboratories on request and are deliberately omitted from this communication.
Two points should be read carefully. First, the reference method was HPV L1 region DNA sequencing with type-specific primers — an appropriate reference for a genotyping assay, because it resolves the type rather than merely detecting or not detecting high-risk HPV. Second, and this is the honest qualifier: kappa 1 establishes analytical agreement with the reference method on these samples. It does not establish clinical sensitivity or specificity for detecting CIN2+ or cancer, which requires outcome-based studies of the kind conducted for the assays in the international validation list [10]. Laboratories qualifying this assay for a screening programme should treat the concordance data as the analytical foundation and request the outcome data separately.

Peer-reviewed evidence retrievable on PubMed

Every study below is retrievable on PubMed under the identifier given, and full citations with DOIs appear in the reference list.

HPV testing as the primary screening method

  • A Cochrane systematic review of 40 studies including more than 140,000 women found pooled sensitivity for CIN2+ of 89.9% for hybrid capture 2 versus 62.5% for conventional cytology and 72.9% for liquid-based cytology at the ASCUS threshold, with corresponding specificities of 89.9%, 96.6% and 90.3%. Results did not differ by age or in studies with verification bias. (PMID 28796882) [6]
  • Follow-up of four European randomised controlled trials showed that HPV-based screening reduced the rate of invasive cervical carcinoma versus cytology (rate ratio 0.60, 95% CI 0.40–0.89), with the benefit emerging after 2.5 years (rate ratio 0.45, 95% CI 0.25–0.81) and a rate ratio of 0.30 (95% CI 0.15–0.60) in women whose entry screening test was negative. The cumulative incidence of invasive cervical carcinoma in women with negative entry tests was 4.6 and 8.7 per 100,000 at 3.5 and 5.5 years in the HPV arm, versus 15.4 and 36.0 per 100,000 in the control arm. (PMID 24192252) [7]
  • A 2025 meta-analysis comparing self-collected HPV testing with clinician-collected HPV testing and cytology found pooled sensitivity for CIN2+ of 87% (95% CI 76–93) for cytology, 90% for HPV testing on self-collected specimens and 93% for HPV testing on clinician-collected specimens, restricted to PCR-based HPV assays — information that matters for programmes extending screening beyond clinic-based sampling. (PMID 40643571) [11]
  • The 2020 list of HPV assays suitable for primary cervical cancer screening assessed candidate tests against international validation criteria and identified seven hrHPV DNA tests that consistently fulfilled all criteria across multiple studies, providing the benchmark framework against which a new assay is now judged. (PMID 33975008) [10]
  • The epidemiological basis for the causal role of high-risk HPV types in cervical cancer was established by the IARC-led international case–control study, which classified HPV types by their carcinogenic risk. (PMID 12571259) [2]
  • In women with normal cervical cytology worldwide, pooled HPV prevalence across 157,879 women was 10.4% (95% CI 10.2–10.7), ranging from 8.0% in Asia and 8.1% in Europe to 22.1% in Africa; prevalence was highest below age 35 and showed a second peak at 45 years or older in Africa, the Americas and Europe. Approximately 291 million women worldwide were estimated to carry HPV DNA. (PMID 17597569) [3]

Type-specific risk and the value of genotyping

  • The 2024 global attribution analysis quantified causal attribution of individual genotypes to invasive cervical cancer across 111,902 HPV-positive cases: HPV16 61.7%, HPV18 15.3%, HPV45 4.8%, HPV33 3.8%, HPV58 3.5%, HPV31 2.8%, HPV52 2.8%, with ten further causal genotypes contributing 5.3% combined. HPV16/18 coverage ranged from 71.9% in Africa to 83.2% in central, western and southern Asia, rising to 92.1% and 95.9% respectively when HPV31, 33, 45, 52 and 58 were included. (PMID 39097395) [4]
  • A study of type-specific HPV natural history grouped carcinogenic types by seven-year risk of CIN3+: HPV16 uniquely elevated (26% of infections, seven-year risk 22%); HPV18 and HPV45 (13% of infections, risk above 5%); HPV31, 33, 35, 52 and 58 (39% of infections, risk above 5%); and HPV39, 51, 56, 59 and 68 (23% of infections, risk below 5%). Approximately 80% of infections were no longer detected within three years in the absence of progression. (PMID 32510043) [5]
  • In the ATHENA study of 47,208 women screened routinely, women positive for HPV16 or HPV18 had an absolute risk of CIN2 or worse of 24.4%, versus 14.0% for women positive for pooled high-risk HPV types and 0.8% for high-risk HPV-negative women. (PMID 21350104) [8]
  • A study of 8,000 women found 92.66% agreement between extended and partial HPV genotyping, and showed that a risk-based triage strategy using extended genotyping achieved higher specificity for CIN2+ (94.84% versus 92.46%) and CIN3+ (96.05% versus 91.92%) than conventional HPV primary screening, while requiring fewer colposcopies to detect one cervical disease. (PMID 37441737) [9]
  • Molecular approaches that improve HPV screening and genotyping for cervical cancer prevention were reviewed in Expert Review of Molecular Diagnostics. (PMID 28277144) [14]

High-risk HPV type distribution in Chinese populations

  • A cross-sectional study of 125,604 women in Yueyang, China reported an overall HPV prevalence of 20.5% (high-risk 17.5%); among high-risk subtypes the top five, in descending order, were HPV52 (5.1%), HPV16 (2.7%), HPV58 (2.6%), HPV53 (2.4%) and HPV51 (1.7%). Most infections (74.3%) were single-subtype. (PMID 37601194) [13]
  • A series of 101,621 samples in Fujian, China found 24.5% HPV positivity (17.3% single, 7.2% multiple). The predominant non-16/18 high-risk types were HPV52, 58, 53, 51 and 81, and 71.4% of single infections were non-16/18 high-risk types. In the cancer group, HPV52 (21.8%) and HPV58 (18.6%) were the predominant types, followed by HPV33 and HPV31. (PMID 38903575) [12]

Clinical use scenarios and who the test is for

Primary cervical cancer screening

As the primary screening test in a programme that has adopted HPV DNA testing, reporting 14 high-risk types with five reported by name. Where a programme's protocol requires HPV16/18 genotyping with a pooled result for other high-risk types, this assay maps directly onto that algorithm.

Risk-based triage and reflex testing

Where a positive primary screen must be stratified into immediate colposcopy referral versus surveillance. Because HPV16 and HPV18 carry the highest absolute risk of CIN2+, and HPV52, 33 and 58 fall into the elevated type-specific risk group [4,5,8], naming these types supports the risk-based strategies that have been shown to reduce unnecessary colposcopy [9].

ASC-US and equivocal cytology triage

Where a cytology result is equivocal and high-risk HPV testing is used to decide who needs colposcopy — the use case validated prospectively in the ATHENA study, in which HPV16/18 genotyping identified the subgroup at highest risk [8].

Populations where HPV52 and HPV58 dominate

In settings where HPV52 and HPV58 are the leading high-risk types — as documented in large Chinese series [12,13] — an assay that genotypes only HPV16 and HPV18 reports the dominant cancer-associated types without naming them. This panel names them individually.

Programmes extending to self-collection

Where self-collected specimens are being introduced. A PCR-based HPV assay run on a self-collected specimen achieved 90% sensitivity for CIN2+ in a 2025 meta-analysis, supporting the same screening intervals as for negative cytology [11]. Laboratories should validate their own self-collection device and specimen-transport path before reporting.
Who this test is for. The kit is intended for laboratory directors and molecular pathology managers, clinical virologists, gynaecologists and colposcopy services, cytopathology laboratories, cervical screening programme managers in public health, health-check centres, hospital procurement teams and in-vitro diagnostics distributors. It is a laboratory test for professional use.

What this test is not

Any laboratory or programme evaluating this assay should weigh its deliberate limits, which are stated in the instructions for use and reflected in the clinical literature.
  • It is not a test for cancer, and a positive result is not a diagnosis. It detects HPV DNA. Most HPV infections are transient: in a large natural-history analysis, 80% of infections were no longer detected within three years in the absence of progression, and clearance rates were similar across types [5]. A positive result indicates infection and warrants triage according to the programme's protocol, not treatment. Conversely, a positive result in a young woman may reflect a transient infection that would clear without intervention.
  • A negative result does not preclude HPV infection — this is stated explicitly in the instructions for use, and it is a property of all HPV DNA tests, not a specific deficiency of this one. Results depend on adequate specimen collection, absence of inhibitors and sufficient DNA to be detected. At least one half to two thirds of false negatives have been attributed to patient conditions at collection and to sampling technique, which is why the collection conditions in the instructions for use are not optional.
  • Nine of the 14 high-risk types are reported as a group, not individually. A positive pooled channel reports only that one or more of HPV31, 35, 39, 45, 51, 56, 59, 66 or 68 is present. Where type-specific risk stratification is required for those types — noting that HPV45 sits in a higher risk group than HPV39, 51, 56, 59 and 68 [5] — reflex genotyping of the pooled-positive sample is needed.
  • It detects high-risk types only. The panel covers 14 high-risk types. It does not report low-risk types such as HPV6 and HPV11 and is not a test for genital warts or for benign HPV disease. Thirty-eight homologous HPV types outside the detection range were confirmed negative in the analytical validation, which is the expected behaviour of a high-risk screening assay but also defines what it does not report.
  • The permitted cross-reactivity limit for low-risk types is 10%. The instructions for use state that with out-of-range genotypes there should be no cross-reaction among high-risk genotypes and that the cross-reaction rate for low-risk types should be no higher than 10.0%. In the validation performed with the 38 out-of-range types, no cross-reactivity was observed — but the stated acceptance criterion is a limit, and laboratories should verify local performance on their own specimen mix.
  • The concordance data are analytical, not outcome-based. Kappa 1 against HPV L1 DNA sequencing on 1,000 samples demonstrates genotyping agreement. It does not establish clinical sensitivity and specificity for CIN2+ or cancer, which come from outcome studies. Programme-level qualification should reference the international validation framework [10] and request outcome data.
  • It does not replace cytology in every protocol, and it does not replace colposcopy or biopsy. Some programmes use co-testing or cytology triage after a positive HPV result. A positive HPV result does not itself establish the presence of a lesion, and histological confirmation remains the reference standard for a high-grade lesion.
  • Instrument and reporting settings are specific. Ct thresholds, baseline windows and instrument-specific settings are defined in the instructions for use; a channel returning a Ct at or below 5 should be reported positive or re-tested after 100-fold dilution, and a specimen without a valid β-globin signal must be re-tested rather than reported negative.

Regulatory status, formats and availability

The kit is a CE-marked in vitro diagnostic device and is registered with China's National Medical Products Administration (NMPA) for cervical cancer screening. It is supplied as 48 tests per kit, together with positive control A (containing HPV16, HPV18 and HPV52 target sequences with human genome), positive control B (containing HPV33, HPV58 and HPV45 target sequences with human genome), a negative control and the two master mixes. Full technical documentation — including the instructions for use, analytical performance data and the clinical verification dossier — is available to qualified laboratories on request.

Frequently asked questions

What does the test detect? DNA from 14 high-risk HPV types in a single analysis, from cervical exfoliated cells. HPV16, HPV18, HPV52, HPV33 and HPV58 are reported individually; HPV31, HPV35, HPV39, HPV45, HPV51, HPV56, HPV59, HPV66 and HPV68 are detected and reported as a group.
What sample is required? Cervical exfoliated cells collected with an endocervical brush into cell preservation solution. Sampling is best scheduled 10–18 days after the first day of the last menstrual period, with no douching, tampons, vaginal medications or intercourse for 48 hours beforehand.
How is the specimen handled? In preservation solution the specimen is stable for 7 days at room temperature, 2 months at 2–8 °C and 6 months at ≤ –20 °C, and tolerates up to five freeze–thaw cycles. Transport is at room temperature or on dry ice at 2–8 °C for up to 4 days.
What equipment is needed? An open real-time PCR platform with FAM, VIC/HEX, ROX and CY5 channels, such as the Applied Biosystems 7500 or Roche LightCycler 480. Two PCR reactions are performed per specimen.
What is the limit of detection? ≤ 100 copies per test for each of the 14 high-risk types, with a Ct coefficient of variation of ≤ 5% across ten repeats.
Why individual genotyping of HPV52 and HPV58, and not just HPV16 and HPV18? Because attribution and risk are type-specific and geographically uneven. Globally, HPV16 and HPV18 account for 71.9% of invasive cervical cancers in Africa but 83.2% in central, western and southern Asia, rising to 95.9% when HPV31, 33, 45, 52 and 58 are added (PMID 39097395). In large Chinese series, HPV52 and HPV58 are among the leading high-risk types (PMID 37601194) and the predominant types in the cancer group (PMID 38903575). An assay reporting only HPV16 and HPV18 would not name them.
How was the assay validated? Against HPV L1 region DNA sequencing in a comparative study of 1,000 samples across three provincial hospitals, with discordant samples verified by a third party: kappa 1, and 100% positive, negative and total coincidence. A secondary comparison of 200 samples against a 27-genotype assay also returned kappa 1 and 100% coincidence.
Is it CE-marked? Yes — it is a CE-marked in vitro diagnostic device and is registered with China's NMPA for cervical cancer screening.

References

Citation format: Vancouver (ICMJE). PubMed identifiers are given for every reference retrievable through PubMed.
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  • [8] Stoler MH, Wright TC Jr, Sharma A, et al. High-risk human papillomavirus testing in women with ASC-US cytology: results from the ATHENA HPV study. Am J Clin Pathol. 2011;135(3):468-475. doi:10.1309/AJCPZ5JY6FCVNMOT. PMID 21350104.
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Note on sources: references [1]–[14] are independent, publicly retrievable peer-reviewed publications; reference [15] is a World Health Organization guideline document. All analytical performance figures, the type and reporting design, specimen handling conditions and the 1,000-sample clinical verification data are taken from the product's own instructions for use, version V2.3 (effective November 2024), which is product technical documentation held on file and is not independently peer reviewed; this is stated where those figures appear. Manufacturer names, trademarks, catalogue codes, certificate numbers, study hospital names, accessory product codes and authorised-representative details are deliberately omitted from this communication.

About Red Sun Medizone

Red Sun Medizone (RED SUN MEDI ZONE LIMITED) is a Hong Kong-based supplier of medical devices and in vitro diagnostic products serving hospitals, laboratories and distributors internationally. Its portfolio spans molecular diagnostics for oncology, critical-care and surgical equipment, patient monitoring, and laboratory instrumentation. The HPV 5+9 genotyping assay complements the company's existing cervical cancer portfolio, which includes a CE-marked PAX1 and JAM3 dual-gene methylation assay for cervical cancer triage in HPV-positive women. Together the two assays address the two stages of HPV-based cervical screening — detecting the viral genotype, and resolving which HPV-positive women require colposcopy. The company also supplies DNA methylation PCR assays for lung-cancer triage, a methylated SEPT9 blood test for colorectal cancer screening, and targeted EGFR, KRAS and BRAF V600E mutation detection kits built on a common real-time PCR platform.

Media and technical enquiries

Red Sun Medizone — Sales and Technical Enquiries
Mr. Matt Hou, Sales Manager
Email: [email protected]
Web: www.redsunmedizone.com
Unit 18, 8/F, Peter Leung Industrial Building, 103 Wai Yip Street, Kwun Tong, Hong Kong, China
This press release describes an in vitro diagnostic device intended for professional laboratory use. It is not a statement of clinical efficacy for any individual patient, and every performance figure quoted is drawn from the sources cited. The product is manufactured in accordance with CE-marked in vitro diagnostic requirements; manufacturing, regulatory and technical documentation is available to qualified purchasers on request.
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