Association of Human Papillomavirus Infection and Inflammation in Cervical Cancer

Author(s):  
Nima Hemmat ◽  
Hossein Bannazadeh Baghi

Abstract Human papillomavirus (HPV) associated cancers, and in particular cervical cancer, are considered to be directly stimulated by HPV oncogenes. Alternatively, these types of cancers could also be indirectly stimulated by HPV-induced chronic inflammations, which in turn are also caused by HPV oncogenes activity. Chronic inflammation is associated with repeated tissue injury and development of mutations in the vital tumor suppressor genes. Thus, it is important to understand that the persistent HPV infection and its associated chronic inflammation is responsible for the progression of HPV-induced cancers. HPV E5, E6, and E7 could upregulate the expression of cyclooxygenase (COX)-2 and prostaglandin (PG) E2 followed by the activation of the COX-PG pathway. This pathway is assumed to be the main cause of HPV-induced inflammation. Additionally, HPV oncogenes could have an impact on the upregulation of pro-inflammatory cytokines in HPV-positive patients. The upregulation of such cytokines accelerates the incidence of inflammation following HPV infection. Other factors such as microRNAs, which are involved in the inflammation pathways and aging, give rise to the increased level of pro-inflammatory cytokines and could also be responsible for the acceleration of HPV-induced inflammation and consequent cervical cancer. In this review, the exact roles of HPV oncogenes in the occurrence of inflammation in cervical tissue, and the effects of other factors in this event are evaluated.

2004 ◽  
Vol 14 (2) ◽  
pp. 293-303 ◽  
Author(s):  
C. Duttagupta ◽  
S. Sengupta ◽  
M. Roy ◽  
D. Sengupta ◽  
P. Bhattacharya ◽  
...  

Muslim women are known to have lower incidences of cervical cancer and/or human papillomavirus (HPV) infection. Here we aim to determine any association that may be present between the oncogenic HPV16/18 infections and abnormal cytological lesions along with demographic and other attributes among Indian Muslim women (n = 478) and compare with the neighboring Hindus (n = 534) from a prospective cohort study. Agewise distribution of both subject-groups is similar. HPV16/18 infection is present in 9.6% Muslims and 7.5% Hindu women. Jointly atypical cells of undetermined significance (a typical cells of undetermined significance) and HPV16/18 are present in seven Muslim and two Hindu women. No high squamous intraepithelial lesions or cervical cancer is detected at the baseline. HPV16/18 infections show trends that varied with age, a nonlinear trend among Muslim women. In Hindu women the prevalence is highest at age ≤24 years, which linearly drops with increasing age. Abnormal cytology increases significantly in both religion-groups with increasing age. The data show that these Indian Muslim women are equally susceptible to HPV16/18 infection and for the development of abnormal cytology. There is a paucity in epidemiological data, which justifies the need to screen women of all religions for cervical cancer (that includes oncogenic HPV testing).


Sexual Health ◽  
2010 ◽  
Vol 7 (3) ◽  
pp. 368 ◽  
Author(s):  
David G. Regan ◽  
David J. Philp ◽  
Edward K. Waters

Mathematical transmission models are widely used to forecast the potential impact of interventions such as vaccination and to inform the development of health policy. Effective vaccines are now available for the prevention of cervical cancer and other diseases attributable to human papillomavirus (HPV). Considerable uncertainties remain regarding the characterisation of HPV infection and its sequelae, infectivity, and both vaccine-conferred and naturally-acquired immunity. In this review, we discuss the key knowledge gaps that impact on our ability to develop accurate models of HPV transmission and vaccination.


2021 ◽  
Vol 9 ◽  
Author(s):  
Luyao Pan ◽  
Bingxin Li ◽  
Jiahua Chen ◽  
Haofeng Zhang ◽  
Xi Wang ◽  
...  

Persistent human papillomavirus (HPV) infection will eventually lead to clinical problems, varying from verrucous lesions to malignancies like cervical cancer, oral cancer, anus cancer, and so on. To address the aforementioned problems, nanotechnology-based strategies have been applied to detect the virus, prevent the interaction between virus and mammalian cells, and treat the virus-infected cells, due mainly to the unique physicochemical properties of nanoparticles. In this regard, many nanotechnology-based chemotherapies, gene therapy, vaccination, or combination therapy have been developed. In this Minireview, we outline the pathogenesis of HPV infection and the recent advances in nanotechnology-based weapons that can be applied in combating HPV-associated diseases.


2004 ◽  
Vol 6 (9) ◽  
pp. 1-21 ◽  
Author(s):  
Joakim Dillner ◽  
Darron R. Brown

Human papillomavirus (HPV) infection is the cause of squamous cell carcinoma of the uterine cervix. This causative relationship has provided the rationale and incentive for development of a prophylactic vaccine. Such a vaccine, if found to be effective, could reduce the need for cervical cancer screening and have a profound effect on the incidence of cervical and other anogenital cancers. This review begins by examining the basic biological and epidemiological principles relevant to the development of HPV preventative vaccines. It then summarises studies examining the use of vaccines to prevent HPV infection in animals and humans, and, finally, discusses some of the unanswered issues surrounding vaccine development against HPV infection and cervical cancer.


2019 ◽  
Vol 8 (1) ◽  
pp. 23-32
Author(s):  
Paulina Rosa Evriarti ◽  
Andi Yasmon

AbstractCervical cancer is the most common cancer among women in the world. The main cause of the development of cervical cancer is due to persistent infection of a high-risk type (HR) - Human Papillomavirus (HPV). The mechanisms of HPV in causing cervical cancer are discussed in this article that collected from current information published in a scientific journal. The main target of HPV infection is the basal layer of cervical epithelia and the virus could reach its target when there is a microabrasion of epithelial cells. The HPV binds to its specific receptor on the host cellular surface and followed by the entering virus into the cytoplasm through the endocytosis process. After successfully entering the cell, the virus will uncoat and begin the replication process by hijacking the transcription and translation system of host cells. E6 and E7 proteins play an important role in the inactivation of tumor suppressor proteins p53 and pRb, causing the cells to uncontrolled divide (immortal). If the immune response failed to interfere with the replication process and eliminates HPV-infected cells, the HPV infection will lead to cervical cancer. In conclusion, the mechanism of HPV causing cervical cancer is complex and involves important proteins of HPV. AbstrakKanker serviks merupakan kanker paling banyak kedua yang diderita oleh perempuan di dunia. Penyebab utama dari perkembangan kanker serviks yakni adanya infeksi yang persisten tipe high risk (HR) – Human Papillomavirus (HPV). Artikel ini disusun untuk mengetahui mekanisme HPV dalam menimbulkan kanker serviks. Uraian dan tulisan mengenai isi artikel ini diperoleh dengan melakukan beberapa studi literatur yang terkait dengan HPV dalam menyebabkan kanker serviks. HPV dalam perannya menimbulkan kanker serviks diawali dengan masuknya HPV ke dalam lapisan sel epitel pejamu karena adanya mikroabrasi atau luka kecil. Bila berhasil melakukan pelekatan pada sel epitel serviks melalui reseptornya, virus akan diendositosis dan masuk ke dalam sel. Setelah berhasil masuk sel, virus akan mengalami uncoating, kemudian virus akan memulai proses replikasinya dengan cara mengambil alih sistem transkripsi dan translasi sel pejamu. Protein E6 dan E7 berperan penting dalam hal ini karena adanya kedua protein tersebut menghalangi kerja dari protein supressor tumor p53 dan pRb sehingga sel menjadi imortal dan pembelahan sel menjadi tidak terkendali. Apabila proses ini terakumulasi tanpa berhasil dieliminasi oleh sistem imun, infeksi oleh virus HPV dapat menjadi persisten dan timbul suatu keganasan berupa kanker serviks. Dari paparan tersebut, dapat ditarik kesimpulan bahwa mekanisme HPV dalam menyebabkan kanker serviks merupakan mekanisme yang cukup kompleks dan melibatkan protein-protein penting yang ada dalam genom HPV.


2015 ◽  
Vol 4 (1) ◽  
pp. 21-25
Author(s):  
Meichang Ai

Abstract Cervical cancer is one of the most common malignant tumors that threaten women’s life and health in both developed and developing countries. Diet and smoking are independent etiological factors of cervical cancer. Among many independent etiological factors, human papillomavirus (HPV) infection is the most important one. HPV infection is universal among women of appropriate ages, and only persistent HPV infection is considered necessary to cause cervical cancer.


2021 ◽  
Vol 11 ◽  
Author(s):  
Wenkui Dai ◽  
Hui Du ◽  
Shuaicheng Li ◽  
Ruifang Wu

Persistent high-risk human papillomavirus (hrHPV) infection is the highest risk to cervical cancer which is the fourth most common cancer in women worldwide. A growing body of literatures demonstrate the role of cervicovaginal microbiome (CVM) in hrHPV susceptibility and clearance, suggesting the promise of CVM-targeted interventions in protecting against or eliminating HPV infection. Nevertheless, the CVM-HPV-host interactions are largely unknown. In this review, we summarize imbalanced CVM in HPV-positive women, with or without cervical diseases, and the progress of exploring CVM resources in HPV clearance. In addition, microbe- and host-microbe interactions in HPV infection and elimination are reviewed to understand the role of CVM in remission of HPV infection. Lastly, the feasibility of CVM-modulated and -derived products in promoting HPV clearance is discussed. Information in this article will provide valuable reference for researchers interested in cervical cancer prevention and therapy.


Author(s):  
Kun Lee ◽  
Jingyi Si ◽  
Ricai Han ◽  
Wei Zhang ◽  
Bingbing Tan ◽  
...  

There are more supports for the view that human papillomavirus (HPV) infection might be an etiological factor in the development of cervical cancer when the association of persistent condylomata is considered. Biopsies from 318 cases with squamous cell carcinoma of uterine cervix, 48 with cervical and vulvar condylomata, 14 with cervical intraepithelial neoplasia (CIN), 34 with chronic cervicitis and 24 normal cervical epithelium were collected from 5 geographic regions of China with different cervical cancer mortalities. All specimens were prepared for Dot blot, Southern blot and in situ DNA-DNA hybridizations by using HPV-11, 16, 18 DNA labelled with 32P and 3H as probes to detect viral homologous sequences in samples. Among them, 32 cases with cervical cancer, 27 with condyloma and 10 normal cervical epitheliums were randomly chosen for comparative EM observation. The results showed that: 1), 192 out of 318 (60.4%) cases of cervical cancer were positive for HPV-16 DNA probe (Table I)


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