Human Papillomavirus: Biology and Pathogenesis

Fernandes, José Veríssimo; Fernandes, Thales Allyrio Araújo de Medeiros

doi:10.5772/27154

Cited by 6 publications

(5 citation statements)

References 170 publications

(157 reference statements)

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“…HPVs belonging to the Papillomaviridae family cause various benign and malignant lesions, most commonly in the skin and mucous membranes. HPV can convert a non-permissive cell to an oncogenic one, facilitating lytic viral infections in permissive cell types 8 , 9 . Currently, data indicate that HPV has more than 200 genotypes, and the whole genome sequence is known for about 100 genotypes.…”

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confidence: 99%

“…HPV genotypes are divided into low-risk, high-risk and possible high-risk types according to their oncogenic potential 10 , 11 . The fifteen high-risk HPV genotypes (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73 and 82) are known to be responsible for 99 per cent of cervical cancer cases 9 . Worldwide, HPV type 16 is found in 50-60 per cent of cervical cancers, and HPV type 18 in 10-12 per cent 9 , 12 - 14 .…”

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confidence: 99%

“…The fifteen high-risk HPV genotypes (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73 and 82) are known to be responsible for 99 per cent of cervical cancer cases 9 . Worldwide, HPV type 16 is found in 50-60 per cent of cervical cancers, and HPV type 18 in 10-12 per cent 9 , 12 - 14 . Furthermore, in addition to cervical cancer, HPV types 16 and 18 are also associated with other cancer types, including vulvar, anal vaginal, oral and oropharyngeal cancers 9 .…”

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confidence: 99%

“…Worldwide, HPV type 16 is found in 50-60 per cent of cervical cancers, and HPV type 18 in 10-12 per cent 9 , 12 - 14 . Furthermore, in addition to cervical cancer, HPV types 16 and 18 are also associated with other cancer types, including vulvar, anal vaginal, oral and oropharyngeal cancers 9 .…”

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confidence: 99%

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High-risk human papillomavirus in Turkish patients with clinically suspicious cervical lesions analyzed by multiplex-PCR

Gorur¹,

Dolanbay²,

Öztürk³

et al. 2022

Indian Journal of Medical Research

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Background & objectives: Human papillomavirus (HPV) infection is known to be the main cause of cervical cancer. This study aimed to determine the prevalence of high-risk HPV genotypes in smear specimens taken from women who had normal or abnormal cytology using a multiplex PCR method. Methods: The study included 270 women aged between 19 and 69 yr with or without suspicious cervical abnormalities. A Pap smear sample from each patient was cytologically examined, and HPV typing was performed using a multiplex fluorescent PCR method. Those who were high-risk HPV positive and had a normal or abnormal cytology were further evaluated by colposcopy and biopsy. Results: The total HPV positivity was 43 per cent (116/270). HPV positivity in the patients with an abnormal cytology was 77 per cent (33/43), whereas it was only 37 per cent (83/227) in women with normal cytology, which showed a significant difference ( P <0.05). HPV positivity was also related to the age group when all the subjects were considered ( P <0.05), and the highest prevalence of HPV infection was in the 30-39 yr age group. High-risk HPV types 16, 18, 31, 35, 51 and 56 were more common in the normal cytology patients, whereas high-risk HPV types 16, 31, 35, 45, 58 and 68 were commonly found in the abnormal cytology patients. Interpretation & conclusions: The determination of high-risk HPV genotypes in women with clinically suspicious cervical lesions should be conducted during an annual follow-up, irrespective of a normal or abnormal cytology by the age of 30 years or above.

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High-risk human papillomavirus in Turkish patients with clinically suspicious cervical lesions analyzed by multiplex-PCR

Gorur¹,

Dolanbay²,

Öztürk³

et al. 2022

Indian Journal of Medical Research

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“…HPV virions are approximately 55 nm in diameter. The HPV genome consists of circular double-stranded DNA approximately 8kb in size enclosed in an icosahedral capsid composed of 72 capsomeres (Veressimo Fernandes & Fernandes, 2012). The viral genome consists of the functional early (E) genes E1, E2, E4, E5, E6 and E7, and the structural late (L) genes, L1, and L2 (Figure 5).…”

Section: Human Papilloma Virusesmentioning

confidence: 99%

The Role of HPV16 E1 in Cervical Carcinogenesis

Baedyananda

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Objectives: This study aimed to determine the expression profile of HPV-16 E1 in cervical samples and the role of E1 in cervical carcinogenesis. In addition, this work also aimed to determine whether the HPV-16 E1 63bp duplication is present in the Thai population. Methods: One-hundred and twenty-four HPV16 positive cervical samples ranging from normal, CIN1, CIN2/3, and SCC lesions were studied. E1 mRNA expression was determined by ddPCR. Methylation of promoters p97 and p670 was quantified by pyrosequencing, while PCR and sequencing were used to determine the physical state and variations of HPV16 E1 genome. HEK 293T cells were transfected with pEGFP-C1 containing HPV16 E1. Cell proliferation of transfected cells was measured using cell viability count and cell metabolism assay. Apoptosis and necrosis was determined in transfected cells treated with or without QVD-OPH (pan-caspase inhibitor) by Annexin V and propidium iodide staining and quantitated using flow cytometry. RNA expression Microarray analysis was performed on FACS sorted HPV16 transfected cells. RNA expression was confirmed by Real-time reverse transcription (RT) PCR. Plasmid containing pEGFP-C1 was used as a vector control throughout the experiments. Results: Increased E1mRNA expression related to disease progression (normal 0.18, CIN 1 0.41, CIN 2/3 0.65 and SCC 0.79) was demonstrated with significant positive correlation (r = 0.661, p =0.019). No association between physical state and E1 expression was found.� Methylation of p97and p670 promoters showed significant elevation in SCC compared to normal samples. Only 4.2% showed genomic variations of HPV16 E1 63 bp duplication. HPV16 E1 transfected HEK293T cells showed a significant decrease in number of viable cells and cell proliferation 24 h post-transfection (p < 0.0001). HPV16 E1 significantly induced both apoptotic and necrotic cell death 48 h post-transfection. Treatment of HPV16 E1 transfected cells with QVD-OPH showed a decreasing trend without statistical significance. Microarray and real-time RT PCR results revealed that E1 dysregulated genes involved in protein synthesis (RPL36A), metabolism (ALDOC), cell proliferation (CREB5, HIF 1A, JMJD1C, FOXO3, NFKB1, PIK3CA, TSC22D3), DNA damage (ATR, BRCA1 and CHEK1), and immune response (ISG20) pathways. Kinetic host gene expression in HPV16 E1 transfected cells indicated that most genes were downregulated after 48 h post-transfection. Conclusion: Detection of E1 mRNA and p97 methylation were beneficial as cancer prognostic markers. The presence of 63 bp duplication in HPV16 E1 was observed in the Thai population and related to low grade lesions. The presence of HPV16 E1 protein alone was able to dysregulate many cellular pathways in a time dependent manner. Notable genes disrupted by HPV16 E1 included genes involved in cell proliferation and host DNA damage response. This study suggests that E1 may play a role in cancer development however HPV16 E1 transfection experiments did not provide a definite carcinogenic pathway which warrants further studies.

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Telomeres and Telomerase During Human Papillomavirus-Induced Carcinogenesis

2018

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Human papillomaviruses (HPVs) belong to a small spherical virus family and are transmitted through direct contact, most often through sexual behavior. More than 200 types of HPV are known, a dozen or so of which are classified as high-risk viruses (HR HPV) and may contribute to the development of cervical cancer. HPV is a small virus with a capsid composed of L1 and L2 proteins, which are crucial for entry to the cell. The infection begins at the basal cell layer and progresses to involve cells from higher layers of the cervical epithelium. E6 and E7 viral proteins are involved in the process of carcinogenesis. They interact with suppressors of oncogenesis, including p53 and Rb proteins. This leads to DNA replication and intensive cell divisions. The persistent HR HPV infection leads to the development of dysplasia and these changes may progress to invasive cancer. During the initial stage of carcinogenesis, telomeres shorten until telomerase activates. The activation of telomerase, the enzyme necessary to extend chromosome ends (telomeres) is the key step in cell immortalization. Analyzing the expression level of hTERT and hTERC genes encoding telomerase and telomere length measurement may constitute new markers of the early carcinogenesis.

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Human Papillomavirus: Biology and Pathogenesis

Cited by 6 publications

References 170 publications

High-risk human papillomavirus in Turkish patients with clinically suspicious cervical lesions analyzed by multiplex-PCR

High-risk human papillomavirus in Turkish patients with clinically suspicious cervical lesions analyzed by multiplex-PCR

The Role of HPV16 E1 in Cervical Carcinogenesis

Telomeres and Telomerase During Human Papillomavirus-Induced Carcinogenesis

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