Hyperproliferative action of bovine papillomavirus: genetic and histopathological aspects

Abstract

ABSTRACT. The bovine papillomavirus (BPV) causes papillomas that regress spontaneously, but can also progress to malignancy. This study evaluated the role of BPV in oncogenesis. Twenty-four samples from uninfected calves and the papillomas of BPV infected cattle were subjected to molecular diagnosis, as well as histopathological and immunohistochemical analyses. The comet assay (CA) was used to evaluate the clastogenic potential of BPV. The results confirmed the presence of BPV-2, 3, 5, and 9 in infected samples. Histopathological analysis revealed acanthosis, koilocytosis, hypergranulosis, hyperkeratosis, and transformed fibroblasts. E7 and L1 BPV proteins were detected in the epithelium, as well as in the connective tissues, indicating productive infection at different sites. CA 12943 Genetics and histopathological aspects of BPV ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (4): 12942-12954 (2015) results showed that BPV-2, 5, and 9 exhibit the same level of clastogenicity. These findings support the oncogenic action of BPV in establishing a favorable microenvironment for oncogenesis.

Bos taurus papillomavirus activity in peripheral blood mononuclear cells: demonstrating a productive infection

“…However, these clues into the transformation of fibroblasts are a result of the synergistic actions of the E5, E6 and E7 oncoproteins (DeMasi et al, 2007). Although preliminary data, it is suggested that papillomaviruses in the stroma can migrate to peripheral blood, establishing a latent infection (Araldi et al, 2015b).…”

“…The alterations observed in the epithelium resulted from the synergistic action of the E5, E6 and E7 oncoproteins (Araldi et al, 2015b). These proteins induce S phase entry, leading to a mitogenic stimulus, which results in the observed acanthosis and parakeratosis.…”

“…E7 promotes the phosphorylation of retinoblastoma protein (pRb), leading to S phase entry (White and Howley, 2013), and is related to centrosome duplication and numeric aberrations (Duensing et al, 2000). The combined action of oncoproteins E5, E6, and E7 leads to genomic instability and malignancy (Araldi et al, 2013a;Araldi et al, 2015b).…”

Genetics and metabolic deregulation following cancer initiation: A world to explore

“…Hypoxia is a consequence of cell hyperproliferation, which reduces the oxygen supply by the blood vessels distancing. This process is verified in both benign and malignant neoplasia [74]. Hypoxia promotes hypoxia inducible factor 1 (HIF-1) stabilization, process dependent of mitochondrial ROS generation [39,75].…”

“…For this reason, mutagen identification has been explored [13][14][15][16], since to avoid the long term exposure to these mutagens can be considered a protective method against cancer. Currently, it is known that several drugs [16][17][18], organic [19][20][21][22] and inorganic chemical compounds [23,24] and biological agents, including viruses [12,[25][26][27][28][29][30][31][32][33] are able to induce DNA damage.…”