ABStRACt. Bovine papillomavirus (BPV) DNA sequences were detected in different tissues, in addition to epithelium. Cytogenetic abnormalities were observed in blood lymphocytes. The presence of more than one virus in a single tissue is a difficult aspect to evaluate, especially when the DNA sequences are detected in tissues that are not specifically targeted by the virus. BPV and bovine leukemia virus (BLV) are clastogenic, causing chromosome aberrations in peripheral blood lymphocytes. In the present study, we investigated the simultaneous presence of DNA sequences of both viruses and the possibility of vertical transmission and compared the types of chromosome aberrations related to viral action. BPV 1, 2, and 4 DNA sequences were found in three females of the herd and in their offspring. BLV DNA sequences were not detected in their progeny. A newborn calf that was negative for BLV infection showed specific chromosome rearrangements possibly related to the effect of infection with BPV.
This study has detected BPV-1 DNA sequences in wart, blood and plasma samples collected from animals affected by papillomatosis, suggesting viral presence inside the cell. We sellected an animal in which we could detect BPV-1 DNA sequences in wart, blood, placenta and amniotic liquid samples and her offspring which presented BPV-1 DNA sequences in blood sample collected immediately after birth. These results show a possible vertical transmission of BPV-1.
The immune response is a key factor in the fight against HPV infection and related cancers, and thus, HPV is able to promote immune evasion through the expression of oncogenes. In particular, the E5 oncogene is responsible for modulation of several immune mechanisms, including antigen presentation and inflammatory pathways. Moreover, E5 was suggested as a promising therapeutic target, since there is still no effective medical therapy for the treatment of HPV-related pre-neoplasia and cancer. Indeed, several studies have shown good prospective for E5 immunotherapy, suggesting that it could be applied for the treatment of pre-cancerous lesions. Thus, insofar as the majority of cervical, oropharyngeal and anal cancers are caused by high-risk HPV (hrHPV), mainly by HPV16, the aim of this review is to discuss the immune pathways interfered by E5 oncoprotein of hrHPV highlighting the various aspects of the potential immunotherapeutic approaches.
Cervical cancer and cervical intraepithelial neoplasia (CIN) are well-known outcomes of a human papillomavirus (HPV) infection. Viral oncogenes expressions like E6, E7, and, recently recognized E5, lead to HPV-related malignant progression. Although HPV prevention by powerful vaccines against most frequent and oncogenic genotypes is feasible, current treatment against cervical neoplasia is distant from an ideal one. In addition, late diagnosis is commonly associated with a poor prognosis. On top of that, radiotherapy, chemotherapy, or surgery are less effective in high-grade lesions. Areas covered: Due to their peculiarities, HPV oncogenes represent an excellent target for cancer immunotherapy. Safety, efficacy, and potential immunogenicity are features achieved by DNA vaccines targeting HPV. The literature search has indicated that genetic immunotherapy is becoming a pharmacological tool and therapeutic option against cervical disease, as more and more DNA vaccines are reaching clinical trial phases. Expert commentary: Among some of the promising results, a phase II randomized trial showed a clinical activity of a nucleic acid-based vaccine in HPV16 or HPV18 positive CIN patients. The concept of a synergic combination of anti-HPV DNA vaccines with radiotherapy, chemotherapy, sophisticated delivery methods, immunomodulators or immune adjuvants opens a new and interesting perspective in cervical malignancy treatment.
Lung cancer is the most common cause of cancer deaths worldwide. Although tobacco smoking is considered to be the main risk factor and the most well-established risk factor for lung cancer, a number of patients who do not smoke have developed this disease. This number varies between 15 % to over one-half of lung cancer cases, and the deaths from lung cancer in non-smokers are increasing every year. There are many other agents that are thought to be etiological, including diesel exhaust exposure, metals, radiation, radon, hormonal factors, cooking oil, air pollution and infectious diseases, such as human papillomavirus (HPV). Studies in various parts of the world have detected HPV DNA at different rates in lung tumors. However, the role of HPV in lung cancer is still unclear. Thus, in this review, we investigated some molecular mechanisms of HPV protein activity in host cells, the entry of HPV into lung tissue and the possible route used by the virus to reach the lung cells.
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