A 2-Year Prospective Study of Human Papillomavirus Persistence Among Women With a Cytological Diagnosis of Atypical Squamous Cells of Undetermined Significance or Low-Grade Squamous Intraepithelial Lesion

Plummer, Martyn; Schiffman, Mark; Castle, PE; Maucort‐Boulch, Delphine; Wheeler, CM

doi:10.1097/01.lgt.0000305247.00437.26

Cited by 138 publications

(211 citation statements)

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“…Up to 25% of infections are due to multiple HPV genotypes as is shown by HPV typing regularly. Multiple genotypes have an effect on the probability of underlying pre-cancerous lesions and make clinical data interpretation very complex Plummer et al, 2007). Multiple HPV infections have been found among women with mild or moderately abnormal lesions but their persistence and progression are unclear (Rousseau et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

High-risk Human Papillomavirus Genotype Detection by Electrochemical DNA Chip Method

Chansaenroj

Theamboonlers²,

Chinchai³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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According to a cohort study, HPV cumulative incidence rates are associated with younger women, certain ethnic groups and high frequency of alcohol consumption. Forty-three percent of women, who had attended at least one follow-up visit, were HPV negative. The incidence tended to decrease by 20% in the first year, 14% and 9% in the second and third years, respectively. The median duration of HPV infection was 8 months. 70% of women were no longer infected one year after the incident and 9% continued to be infected for two years. The longest median duration of infection was established for HPV 16, 18, 61, 73 and AE7. In developed countries, the highest rates of HPV infection have been observed among 15-25-year old women who might reflect transmission during their first sexual intercourse whereas the infection rate Jira Chansaenroj et al

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Section: Introductionmentioning

confidence: 99%

High-risk Human Papillomavirus Genotype Detection by Electrochemical DNA Chip Method

Chansaenroj

Theamboonlers²,

Chinchai³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…Overall, our results show that NK cells could participate in the high rate of spontaneous regression of HPV-associated preneoplastic lesions. Indeed, HPV infections are cleared in $90% of women within 2 years [8]. NK cells present in these preneoplastic lesions could be activated by L1 viral particles and kill HPVinfected cells.…”

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confidence: 99%

“…Consequently, most studies aiming to investigate interactions between virus and host cells have used virus-like particles (VLPs), which result from HPV L1 major capsid protein self-assembly and which are morphologically and immunologically [5,6]. Yet, these vaccines have no therapeutic efficacy and it has been estimated that there will be no measurable decline of HPVassociated tumors before 2040 [7].HPV infection can be controlled by the host immune response and the vast majority of HPV-infected women clear the virus within two years [8]. Moreover, the prevalence of HPV-induced tumors is higher in immunodeficient patients [9].…”

mentioning

confidence: 99%

Human papillomavirus entry into NK cells requires CD16 expression and triggers cytotoxic activity and cytokine secretion

et al. 2011

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Human papillomavirus (HPV) infections account for more than 50% of infection-linked cancers in women worldwide. The immune system controls, at least partially, viral infection and around 90% of HPV-infected women clear the virus within two years. However, it remains unclear which immune cells are implicated in this process and no study has evaluated the direct interaction between HPVs and NK cells, a key player in host resistance to viruses and tumors. We demonstrated an NK-cell infiltration in HPVassociated preneoplastic cervical lesions. Since HPVs cannot grow in vitro, virus-like particles (VLPs) were used as a model for studying the NK-cell response against the virus. Interestingly, NK cells displayed higher cytotoxic activity and cytokine production (TNF-a and IFN-c) in the presence of HPV-VLPs. Using flow cytometry and microscopy, we observed that NK-cell stimulation was linked to rapid VLP entry into these cells by macropinocytosis. Using CD16 1 and CD16 À NK-cell lines and a CD16-blocking antibody, we demonstrated that CD16 is necessary for HPV-VLP internalization, as well as for degranulation and cytokine production. Thus, we show for the first time that NK cells interact with HPVs and can participate in the immune response against HPV-induced lesions. IntroductionHigh-risk human papillomaviruses (HPVs) are the causative agents of uterine cervical cancer and are also etiologically associated with other anogenital tumors and with head and neck carcinomas [1].Among the 100 HPV genotypes already characterized, 15 are oncogenic and more than 50% of uterine cervical cancers are associated with HPV16 [2]. Because of their keratinocyte differentiation-dependent life cycle, virus production in vitro has required complex cell culture systems and only low virus titers can be obtained [3]. Consequently, most studies aiming to investigate interactions between virus and host cells have used virus-like particles (VLPs), which result from HPV L1 major capsid protein self-assembly and which are morphologically and immunologically [5,6]. Yet, these vaccines have no therapeutic efficacy and it has been estimated that there will be no measurable decline of HPVassociated tumors before 2040 [7].HPV infection can be controlled by the host immune response and the vast majority of HPV-infected women clear the virus within two years [8]. Moreover, the prevalence of HPV-induced tumors is higher in immunodeficient patients [9]. However, it remains unclear which immune cells are implicated in this process and no study has been performed evaluating the direct interaction between HPVs and NK cells, although these cells play a key role in host resistance to viruses [10] (Fig. 1A and B), but not in squamous cell carcinoma (SCC) (Fig. 1D) despite the presence of more numerous NK cells in the surrounding stroma (Supporting Information Fig. 1). Interestingly, virus particles have been detected mainly in SILs and not in SCC [19] where the virus is usually integrated into the host genome [20]. Our results thus suggest that NK cells could...

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“…B. von der Sensitivität der verwendeten Nachweismethode (potenzieller Nachweis auch latenter Infektionen), der Länge der Intervalle zwischen 2 Tests (je kürzer, um so eher 2-fach positiv) und dem Zeitpunkt des Eintritts in die Testung (kurz vor, während oder nach Infektion) abhängig ist [34], ist dies aus prognostischer Sicht im Rahmen einer HR-HPV-Infektion bislang der mit Abstand zuverlässigste Risikofaktor für die Entstehung einer mäßig-oder schwergradigen zervikalen intraepithelialen Neoplasie (CIN 2/3). So nimmt mit fortschreitender Dauer der Infektion die Wahrscheinlichkeit eines spontanen Verschwindens des Virus ab, und es steigt gleichzeitig das Risiko der Entstehung einer Präkanzero-se [19].…”

Section: Hpv-persistenzunclassified

Die Infektion mit humanen Papillomaviren

Sotlar

2008

Pathologe

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A 2-Year Prospective Study of Human Papillomavirus Persistence Among Women With a Cytological Diagnosis of Atypical Squamous Cells of Undetermined Significance or Low-Grade Squamous Intraepithelial Lesion

Cited by 138 publications

References 0 publications

High-risk Human Papillomavirus Genotype Detection by Electrochemical DNA Chip Method

High-risk Human Papillomavirus Genotype Detection by Electrochemical DNA Chip Method

Human papillomavirus entry into NK cells requires CD16 expression and triggers cytotoxic activity and cytokine secretion

Die Infektion mit humanen Papillomaviren

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