Dynamics of papillomavirus in vivo disease formation &amp; susceptibility to high-level disinfection—Implications for transmission in clinical settings

Egawa, Nagayasu; Shiraz, Aslam; Crawford, Robin; Saunders-Wood, Taylor; Yarwood, Jeremy; Rogers, Marc; Sharma, Ankur; Eichenbaum, Gary; Doorbar, John

doi:10.1016/j.ebiom.2020.103177

Cited by 22 publications

(26 citation statements)

References 33 publications

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“…In addition to ethanol, we also detected a strong reduction in HPV16 pseudovirus titer after incubation with disinfectants based on GTA, DPTA, or OPA. The virucidal activity of OPA found in our study is in accordance with Egawa et al ( 2021), who have recently shown that OPA inactivates HPV16 pseudovirus and HPV18 native virions [27]. In the study by Meyers et al (2016), OPA was not effective against HPV16 and HPV18 native viruses, pointing also at differences in the preparation of native viruses used in different studies [28].…”

Section: Discussionsupporting

confidence: 91%

Inactivation of Polyomavirus SV40 as Surrogate for Human Papillomaviruses by Chemical Disinfectants

Hufbauer

Wieland

Gebel

et al. 2021

Viruses

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Human papillomaviruses (HPV) are non-enveloped DNA viruses infecting cutaneous and mucosal squamous epithelia. Sexually transmitted HPV-types that are carcinogenic to humans such as HPV16 can induce cervical and other anogenital cancers. Virus transmission through fomites such as inadequately disinfected gynecological equipment is a further potential transmission route. Since HPV cannot be easily grown in cell culture, polyomavirus SV40 has been used as a surrogate virus when testing the virucidal activity of chemical disinfectants. So far, studies that have compared the virucidal activity of different disinfectants against HPV and SV40 are lacking. Here, we evaluated the susceptibility of HPV16 pseudovirus and SV40 to seven active biocidal substances using quantitative suspension tests. Ethanol, glutaraldehyde (GTA), dodecyldipropylentriamin (DPTA), and ortho-phthalaldehydes (OPA) were able to reduce the infectivity of HPV16 pseudovirus >99.99% after 5 min. In contrast, isopropanol, peracetic acid (PAA), and quaternary ammonium compounds with alkylamines (QAC) only led to a slight or no reduction in infectivity. Concerning SV40, only GTA (60 min contact time), PAA, and OPA had virus-inactivating effects. In conclusion, the virucidal activity of three out of seven disinfectants tested was different for HPV16 pseudovirus and SV40. In this study, SV40 was shown to be a reliable surrogate virus for HPV when testing isopropanol-, GTA-, QAC-, and OPA-based disinfectants.

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Section: Discussionsupporting

confidence: 91%

Inactivation of Polyomavirus SV40 as Surrogate for Human Papillomaviruses by Chemical Disinfectants

Hufbauer

Wieland

Gebel

et al. 2021

Viruses

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“…In order to investigate whether MmuPV1-induced PI3K signaling is regulated by IQGAP1, we again turned to our isogenic NOKs and NOKs IQGAP1 KO cells based upon the prior observation that MmuPV1 can infect human keratinocytes [ 49 ]. We first confirmed that human NOKs and NOKs IQGAP1 KO cells could be infected by MmuPV1 ( Figure S1B ).…”

Section: Resultsmentioning

confidence: 99%

Role of IQGAP1 in Papillomavirus-Associated Head and Neck Tumorigenesis

Tao

Choi

Buehler

et al. 2021

Cancers

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Approximately 25% of head and neck squamous cell carcinomas (HNSCC) are associated with human papillomavirus (HPV) infection. In these cancers as well as in HPV-associated anogenital cancers, PI3K signaling is highly activated. We previously showed that IQ motif-containing GTPase activating protein 1 (IQGAP1), a PI3K pathway scaffolding protein, is overexpressed in and contributes to HNSCC and that blocking IQGAP1-mediated PI3K signaling reduces HPV-positive HNSCC cell survival and migration. In this study, we tested whether IQGAP1 promotes papillomavirus (PV)-associated HNSCCs. IQGAP1 was necessary for optimal PI3K signaling induced by HPV16 oncoproteins in transgenic mice and MmuPV1 infection, a mouse papillomavirus that causes HNSCC in mice. Furthermore, we found that, at 6 months post-infection, MmuPV1-infected Iqgap1−/− mice developed significantly less severe tumor phenotypes than MmuPV1-infected Iqgap1+/+ mice, indicating a role of IQGAP1 in MmuPV1-associated HNSCC. The tumors resulting from MmuPV1 infection showed features consistent with HPV infection and HPV-associated cancer. However, such IQGAP1-dependent effects on disease severity were not observed in an HPV16 transgenic mouse model for HNC. This may reflect that IQGAP1 plays a role in earlier stages of viral pathogenesis, or other activities of HPV16 oncogenes are more dominant in driving carcinogenesis than their influence on PI3K signaling.

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“…The work by Egawa and colleagues established a clear correlation between viral titers obtained in vitro and the pathogenic potential in vivo, and presented a detailed analysis of inactivation of PVs particles by the HDLs mentioned above, confirming the efficacy of these compounds [6]. They also presented interesting results showing that OPAglycine, but not OPA-lysine, was also able to inhibit PVs infectivity in vitro and this correlated with the capacity of the former to interact with virus particles.…”

mentioning

confidence: 80%

“…In two articles of EBioMedicine, the authors presented a very detailed and controlled set of experiments to determine the efficacy of ortho-phthalaldehyde (OPA), hypoclorite and hydrogen peroxide in inactivating PVs particles from experimental models, including quasivirions, xenografts, raft cultures and Mus musculus PV type 1 (MmuPV1) induced-lesions in mice. Besides, they included the analysis of HPVs virions retrieved from recurrent respiratory papillomas, anal warts and cervical lesions from patients with hrHPV [5,6].…”

mentioning

confidence: 99%

New approaches for infective HPV detection, quantification and inactivation: Preventing accidental virus transmission in medical settings

Boccardo

2021

EBioMedicine

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Dynamics of papillomavirus in vivo disease formation & susceptibility to high-level disinfection—Implications for transmission in clinical settings

Cited by 22 publications

References 33 publications

Inactivation of Polyomavirus SV40 as Surrogate for Human Papillomaviruses by Chemical Disinfectants

Inactivation of Polyomavirus SV40 as Surrogate for Human Papillomaviruses by Chemical Disinfectants

Role of IQGAP1 in Papillomavirus-Associated Head and Neck Tumorigenesis

New approaches for infective HPV detection, quantification and inactivation: Preventing accidental virus transmission in medical settings

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