RESUMO
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.
Assuntos
Transformação Celular Viral , Neoplasias Pulmonares/virologia , Papillomaviridae/fisiologia , Transformação Celular Viral/genética , Humanos , Pulmão/patologia , Pulmão/virologia , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/patologia , Infecções por Papillomavirus/complicações , Internalização do VírusRESUMO
The aim of this study was to examine the prevalence and genetic variability of the capsid L1 gene of rare HPV genotypes that were found in the cervical lesions of women from North-East Brazil. A total number of 263 patients were included in this study. HPV detection was performed using PCR followed by direct sequencing of MY09/11, as well as type-specific PCR to detect the Alpha-9 species. Epitope prediction was performed to determine whether or not the genetic variants are inserted in B-cell and T-cell epitopes. The prevalence of rare HPV types in cervical lesions was found to be 9.47%. The rare HPV genotypes that were detected were HPV-53, 54, 56, 61, 62, 66, 70, and 81. The genetic variability in the L1 gene of rare HPV types involved thirty nucleotide changes, eight of which were detected for the first time in this study. Moreover, some of these variants are embedded in B-cell or T-cell epitope regions. The results of this research suggest that rare HPV types might be involved in cervical lesions and some of these variants can be found in B-cell and T-cell epitopes. Data on the prevalence and variability of rare HPV types will assist in clarifying the role of these viruses in carcinogenesis.
Assuntos
Proteínas do Capsídeo/genética , Variação Genética , Papillomaviridae/genética , Neoplasias do Colo do Útero/virologia , Adolescente , Adulto , Idoso , Sequência de Aminoácidos , Aminoácidos/genética , Sequência de Bases , Brasil/epidemiologia , Proteínas do Capsídeo/química , Epitopos de Linfócito B/química , Epitopos de Linfócito T/química , Feminino , Humanos , Pessoa de Meia-Idade , Dados de Sequência Molecular , Prevalência , Adulto Jovem , Displasia do Colo do Útero/virologiaRESUMO
Cervical cancer is the second most common cancer in females worldwide. It is well-established that Human Papillomavirus (HPV) infections play a critical role in the development of cervical cancer. However, a large number of women infected with oncogenic HPV types will never develop cervical cancer. Thus, there are several external environment and genetic factors involved in the progression of a precancerous lesion to invasive cancer. In this review article, we addressed possible susceptible phenotypes to cervical cancer, focusing on host genome and HPV DNA variability, multiple HPV infections, co-infection with other agents, circulating HPV DNA and lifestyle.
