scholarly journals Some issues in pathogenesis of premalignant lesions of the uterine cervix

2021 ◽  
pp. 26-34
Author(s):  
V.V. Rachkovskaya ◽  
◽  
A.P. Gorbunov ◽  
V.D. Anokhova ◽  
A.I. Pashov ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
Uterine Cervix ◽  
Host Cells ◽  
Premalignant Lesions ◽  
Cancer Development ◽  
Viral Agent ◽  
Scientific Review ◽  
Persistent Viral Infection ◽  
Cellular And Humoral Immunity ◽  
Cervical Cancer Development

Aetiological and pathogenetic aspects in uterine cervix pathology associated with persistent viral infection by the high-risk human papillomavirus (HR HPV) are considered in this scientific review. The article provides a concise description of the biological structure and life processes of the virus. The main stages of uterine cervix impairment by the viral agent crucial for cancer development are described. Additionally, some mechanisms in the escape of viral progression from the immune control are given insight into. It is considered that, alongside with the aggression of the virus toward the host cells, there is a decline of cellular and humoral immunity in the female’s genitourinary tract, which may determine the growth and development of the neoplasm as well. The article puts a large emphasis on the defensive mechanisms appearing in the female organism as a response to the invasion and the persistence of the human papillomavirus. It is assumed that complete knowledge of pathogenetic mechanisms in development of oncogenic potential of the virus would imply the absence of rampant CIN and cervical cancer development induced by invasion of the agent into the organism

scholarly journals Human Papillomavirus 16 Oncoproteins Downregulate the Expression of miR-148a-3p, miR-190a-5p, and miR-199b-5p in Cervical Cancer

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Mi-Soon Han ◽  
Jae Myun Lee ◽  
Soo-Nyung Kim ◽  
Jae-Hoon Kim ◽  
Hyon-Suk Kim
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
High Risk ◽  
Expression Profiles ◽  
Normal Group ◽  
Cancer Development ◽  
Hybridization Method ◽  
Cancer Group ◽  
Cervical Cancer Development ◽  
High Risk Hpv

Almost all cervical cancers are associated with human papillomavirus (HPV); however, the majority of women infected with this virus do not develop cervical cancer. Therefore, new markers are needed for reliable screening of cervical cancer, especially in relation to HPV infection. We aimed to identify potential microRNAs that may serve as diagnostic markers for cervical cancer development in high-risk HPV-positive patients. We evaluated the microRNA expression profiles in 12 cervical tissues using the hybridization method and verified them by quantitative polymerase chain reaction (qPCR). Finally, we evaluated the effects of HPV16 oncoproteins on the expression of selected microRNAs using cervical cancer cells (CaSki and SiHa) and RNA interference. With the hybridization method, eight microRNAs (miR-9-5p, miR-136-5p, miR-148a-3p, miR-190a-5p, miR-199b-5p, miR-382-5p, miR-597-5p, and miR-655-3p) were found to be expressed differently in the HPV16-positive cervical cancer group and HPV16-positive normal group (fold change ≥ 2). The results of qPCR showed that miR-148a-3p, miR-190a-5p, miR-199b-5p, and miR-655-3p levels significantly decreased in the cancer group compared with the normal group. Upon silencing of HPV16 E5 and E6/E7, miR-148a-3p levels increased in both cell lines. Silencing of E6/E7 in SiHa cells led to the increase in miR-199b-5p and miR-190a-5p levels. Three HPV16 oncoproteins (E5, E6, and E7) downregulate miR-148a-3p, while E6/E7 inhibit miR-199b-5p and miR-190a-5p expression in cervical carcinoma. The three microRNAs, miR-148a-3p, miR-199b-5p, and miR-190a-5p, may be novel diagnostic biomarkers for cervical cancer development in high-risk HPV-positive patients.

Co-Expression of p53 and Bcl-2 Proteins in Human Papillomavirus-Induced Premalignant Lesions of the Uterine Cervix: Correlation with Progression to Malignancy

Tumor Biology ◽  
2009 ◽  
Vol 30 (5-6) ◽  
pp. 276-285 ◽  
Author(s):  
Madhulika Singh ◽  
Smita Srivastava ◽  
Uma Singh ◽  
Neeraj Mathur ◽  
Yogeshwer Shukla
Keyword(s):  
Human Papillomavirus ◽  
Uterine Cervix ◽  
Premalignant Lesions

scholarly journals Role of Epstein-Barr Virus and Human Papillomavirus Coinfection in Cervical Cancer: Epidemiology, Mechanisms and Perspectives

Pathogens ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 685
Author(s):  
Rancés Blanco ◽  
Diego Carrillo-Beltrán ◽  
Julio C. Osorio ◽  
Gloria M Calaf ◽  
Francisco Aguayo
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Uterine Cervix ◽  
Epstein Barr Virus ◽  
Indirect Pathway ◽  
Barr Virus ◽  
Local Immunosuppression ◽  
Epstein Barr ◽  
Cervical Cancer Development ◽  
Infiltrating Lymphocytes

High-risk human papillomavirus (HR-HPV) is etiologically associated with the development and progression of cervical cancer, although other factors are involved. Epstein-Barr virus (EBV) detection in premalignant and malignant tissues from uterine cervix has been widely reported; however, its contribution to cervical cancer development is still unclear. Here, a comprehensive analysis regarding EBV presence and its potential role in cervical cancer, the frequency of EBV/HR-HPV coinfection in uterine cervix and EBV infection in tissue-infiltrating lymphocytes were revised. Overall, reports suggest a potential link of EBV to the development of cervical carcinomas in two possible pathways: (1) Infecting epithelial cells, thus synergizing with HR-HPV (direct pathway), and/or (2) infecting tissue-infiltrating lymphocytes that could generate local immunosuppression (indirect pathway). In situ hybridization (ISH) and/or immunohistochemical methods are mandatory for discriminating the cell type infected by EBV. However, further studies are needed for a better understanding of the EBV/HR-HPV coinfection role in cervical carcinogenesis.

scholarly journals E7 properties of mucosal human papillomavirus types 26, 53 and 66 correlate with their intermediate risk for cervical cancer development

Virology ◽  
2007 ◽  
Vol 367 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Mariam Mansour ◽  
Majid Touka ◽  
Uzma Hasan ◽  
Angelica Bellopede ◽  
Anouk Smet ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Cancer Development ◽  
Intermediate Risk ◽  
Cervical Cancer Development

scholarly journals SARS-CoV-2 Entry: At the Crossroads of CD147 and ACE2

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1434
Author(s):  
Claudio Fenizia ◽  
Silvia Galbiati ◽  
Claudia Vanetti ◽  
Riccardo Vago ◽  
Mario Clerici ◽  
...  
Keyword(s):  
Underlying Mechanism ◽  
Membrane Receptors ◽  
Host Cells ◽  
Viral Agent ◽  
Blocking Antibody ◽  
Angiotensin Converting Enzyme 2 ◽  
Host Membrane ◽  
B Virus ◽  
Immunodeficiency Virus

In late 2019, the betacoronavirus SARS-CoV-2 was identified as the viral agent responsible for the coronavirus disease 2019 (COVID-19) pandemic. Coronaviruses Spike proteins are responsible for their ability to interact with host membrane receptors and different proteins have been identified as SARS-CoV-2 interactors, among which Angiotensin-converting enzyme 2 (ACE2), and Basigin2/EMMPRIN/CD147 (CD147). CD147 plays an important role in human immunodeficiency virus type 1, hepatitis C virus, hepatitis B virus, Kaposi’s sarcoma-associated herpesvirus, and severe acute respiratory syndrome coronavirus infections. In particular, SARS-CoV recognizes the CD147 receptor expressed on the surface of host cells by its nucleocapsid protein binding to cyclophilin A (CyPA), a ligand for CD147. However, the involvement of CD147 in SARS-CoV-2 infection is still debated. Interference with both the function (blocking antibody) and the expression (knock down) of CD147 showed that this receptor partakes in SARS-CoV-2 infection and provided additional clues on the underlying mechanism: CD147 binding to CyPA does not play a role; CD147 regulates ACE2 levels and both receptors are affected by virus infection. Altogether, these findings suggest that CD147 is involved in SARS-CoV-2 tropism and represents a possible therapeutic target to challenge COVID-19.

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