Absence of <i>in situ</i> hybridization evidence for latent ‐ or lytic‐phase Epstein‐Barr virus infection of preinvasive squamous lesions of the cervix

Payne, Simon; Kernohan, N. M.; Walker, F.

doi:10.1002/path.1711760303

Cited by 21 publications

(19 citation statements)

References 35 publications

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“…In addition, recent reports indicate that EBV-specific PCR data need to be confirmed by morphological techniques. 28,29 The discrepancy between our present study and previous reports may therefore reflect differences in analytical methods.…”

Section: Discussioncontrasting

confidence: 99%

Prevalence of Epstein-Barr virus in oral squamous cell carcinoma

et al. 1999

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Forty‐six samples of oral squamous cell carcinoma (OSCC) were evaluated for the prevalence of Epstein–Barr virus (EBV) infection by the polymerase chain reaction (PCR), Southern blot hybridization, and in situ hybridization (ISH). EBV DNA was detected in 7 (15·2 per cent) out of 46 samples by a combination of PCR and Southern blot hybridization methods. All seven positive samples showed well‐differentiated carcinoma, thus suggesting a possible relationship between EBV infection and the degree of differentiation of carcinoma tissue. Latent infection membrane protein 1 (LMP1) was detected immunohistochemically in six of the EBV‐positive OSCCs. However, no signal of the EBV‐encoded small RNA (EBER)‐1 was demonstrated by the ISH method. No significant relationship was observed between EBV infection and lymph node metastasis. A follow‐up study (range from 4·4 to 79 months; mean 34·9 months) showed no recurrence or death to occur in the EBV‐positive patients, which thus suggested a good prognosis for EBV‐positive OSCC patients. Copyright © 1999 John Wiley & Sons, Ltd.

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Section: Discussioncontrasting

confidence: 99%

Prevalence of Epstein-Barr virus in oral squamous cell carcinoma

et al. 1999

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“…In a ® rst attempt using in situ hybridization 5 biopsies from patients with detectable EBV DNA in cervical cell samples were examined but EBER positive cells were neither identi® ed in epithelial cells nor in B-lymphocytes. Similar negative results in cervical cancer and dysplasia have recently been published 20,22 . These results are contradictory to a previously published study by Landers and co-workers, who demonstrated EBV DNA in 43% in biopsies from cervical cancer by in situ hybridization technique 23 .…”

Section: Discussionsupporting

confidence: 75%

“…Since positive EBV analysis with PCR may derive from immortalized B-lymphocytes in the tissue, it is necessary to con® rm data from PCR analysis by morphological techniques, such as in situ hybridization, to show in which cells EBV is present 20 . Two short viral transcripts known as EBERs have been found to be expressed at high levels in most latent EBV infection 21 , although the absence of EBER does not exclude an EBV infection.…”

Section: Discussionmentioning

confidence: 99%

Are acetowhite lesions of the cervix correlated to the presence of Epstein-Barr virus DNA?

Voog

Ricksten²,

Stenglein³

et al. 1997

Int J STD AIDS

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The purpose of this study was to investigate whether Epstein-Barr virus (EBV) is associated with acetowhite lesions of the portio cervix, demonstrating koilocytosis and/or cervical intraepithelial neoplasia (CIN) I-III. The study group comprised 37 women admitted to the Department of Gynaecology and Obstetrics, Sahlgrenska University Hospital, Göteborg because of pathological colposcopy or cytology of the portio cervix. Colposcopically, all exhibited acetowhite lesions of the portio cervix. Cells were sampled with a cytobrush for examination for EBV and human papillomavirus (HPV) DNA by polymerase chain reaction (PCR) and a biopsy was taken for histopathology. Biopsies from 5 patients positive for EBV by PCR in cervical cell samples were examined by an in situ hybridization technique for EBER (Epstein-Barr virus encoded RNA), RNAs expressed in latent EBV infection. The control group consisted of women attending the Department of Dermato-Venereology at the same hospital for STD check-up. These had a normal cytology and no signs of acetowhiteness of the portio cervix. In the study group, EBV DNA was found in 30% and HPV DNA in 51%. In the control group 57% exhibited EBV DNA and 23% HPV DNA. EBV was not found to be a predictive factor in the development of koilocytosis and/or CIN I-III. HPV was a predictive factor in acetowhite, koilocytotic lesions. No expression of EBER was found in the 5 biopsies examined by in situ hybridization.

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“…A low EBV copy number less than 1 copy per cell was observed in cervical tumors, and EBER ISH positive cells were only detected in a subset of tumor nests (Sasagawa et al, 2000). Furthermore, EBV has been detected in normal squamous and glandular epithelial tissue adjoining the tumor and in B lymphocytes infiltrating the tumor or the stroma, and not in dysplastic or tumor cells, questioning whether EBV has any role in cervical cancer or is merely a passenger (Payne et al, 1995; Shoji et al, 1997). However, EBV may play an indirect role by interfering with the immune response to HPV-transformed cells through the production of the viral BCRF1 gene product, an interleukin-10 homolog (Al-Daraji and Smith, 2009; Polz-Dacewicz et al, 2016).…”

Section: Hpv and Herpesvirusesmentioning

confidence: 99%

The interaction between human papillomavirus and other viruses

2017

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The etiological role of human papillomavirus (HPV) in anogenital tract and head and neck cancers is well established. However, only a low percentage of HPV-positive women develop cancer, indicating that HPV is necessary but not sufficient in carcinogenesis. Several biological and environmental cofactors have been implicated in the development of HPV-associated carcinoma that include immune status, hormonal changes, parity, dietary habits, tobacco usage, and co-infection with other sexually transmissible agents. Such cofactors likely contribute to HPV persistent infection through diverse mechanisms related to immune control, efficiency of HPV infection, and influences on tumor initiation and progression. Conversely, HPV co-infection with other factors may also harbor anti-tumor effects. Here, we review epidemiological and experimental studies investigating human immunodeficiency virus (HIV), herpes simplex virus (HSV) 1 and 2, human cytomegalovirus (HCMV), Epstein-Barr virus (EBV), BK virus (BKV) JC virus (JCV), and adeno-associated virus (AAV) as viral cofactors in or therapeutic factors against the development of genital and oral HPV-associated carcinomas.

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Absence of in situ hybridization evidence for latent ‐ or lytic‐phase Epstein‐Barr virus infection of preinvasive squamous lesions of the cervix

Cited by 21 publications

References 35 publications

Prevalence of Epstein-Barr virus in oral squamous cell carcinoma

Prevalence of Epstein-Barr virus in oral squamous cell carcinoma

Are acetowhite lesions of the cervix correlated to the presence of Epstein-Barr virus DNA?

The interaction between human papillomavirus and other viruses

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