RESUMO
Actualmente se sabe que el 20 por ciento de los cánceres humanos están asociados con virus oncogénicos. El virus papiloma humano con cáncer anogenital, los virus de la hepatitis B y C con carcinoma hepatocelular, el virus Epstein Barr con carcinomas nasofaríngeos y linfomas, el virus de la leucemia-linfoma T con leucemias en el adulto. Un rasgo común en todos los tumores asociados con infección viral es el largo período de latencia entre la infección y la aparición de la neoplasia y la baja proporción de individuos infectados que desarrollan un tumor maligno. Estas observaciones indican que los virus oncogénicos son necesarios pero no suficientes para inducir cáncer, otros factores podrían estar involucrados. Esta actualización resume informaciones recientes acerca de los mecanismos de carcinogénesis viral, en particular, la interacción de oncoproteínas virales y proteínas supresoras tumorales. La inactivación de estas proteínas supresoras podría representar una estrategia común a través de la cual los virus tumorales pueden contribuir a la transformación maligna de la célula
Assuntos
Humanos , Adenovírus Humanos , Carcinoma Hepatocelular/fisiopatologia , Causalidade , Vírus da Hepatite B/genética , Infecções por HTLV-I/complicações , Infecções por HTLV-II/complicações , Papillomaviridae/genética , Polyomavirus/genética , Proteínas Oncogênicas Virais/efeitos adversos , Vírus Oncogênicos/patogenicidade , Adenovírus Humanos/patogenicidade , Adenovírus Humanos/fisiologia , Linfoma de Burkitt/genética , Testes de Carcinogenicidade , Carcinoma Hepatocelular/etiologia , Vírus de DNA/patogenicidade , Genes Supressores/fisiologia , Vírus da Hepatite B/patogenicidade , Vírus da Hepatite B/fisiologia , Herpesviridae/patogenicidade , Herpesviridae/fisiologia , Herpesvirus Humano 4/genética , Herpesvirus Humano 4/patogenicidade , Infecções por HTLV-I/etiologia , Infecções por HTLV-II/etiologia , Interferons/uso terapêutico , Papillomaviridae/patogenicidade , Papillomaviridae/fisiologia , Polyomavirus/patogenicidade , Polyomavirus/fisiologia , Replicação Viral/genética , Retroviridae/patogenicidade , Sarcoma de Kaposi/virologia , Vacinas Virais , Vírus Oncogênicos/fisiologiaRESUMO
A genital infection with human papillomavirus (HPV) of a high risk type is necessary for the development of cervical carcinoma. HPV viral distribution among diverse world populations is not homogeneous, viral reservoirs having been detected in particular regions that can interact when humans engage in active contacts. Such viral dynamics alters the population cervical cancer relative risk, particularly when the prevalence of HPV oncogenic risk types is high. We have compared women exposed to different social, cultural and environmental conditions regarding cervical HPV infection, analyzing two populations from Misiones, Argentina: White urban women and--Guarani indian women living in the rain forest. Demographic, clinical and sexual behavior data were collected and cytological, colposcopical and virological analysis performed. Detection and genotypification of HPV was performed by PCR-RFLP. The prevalence for generic HPV infection found was high in both populations, urban women: 43
, with a statistically significant difference. These values were positively associated to age of first intercourse, number of male partners and smoking history. HPV type-specific prevalences showed a relative homogeneity between populations when the main representatives of the high risk (16 and 18: 23
) types were grouped together. However, the presence of other viral types was notoriously different, representing only 9
in urban women and 29
in Guarani indians with particularly high risk HPV types (33, 35, 39, 45, 51, 52, 58, 67, 68). This situation might be of importance for future viral dynamics, phylogenetic and vaccine formulation studies.
) and low risk (6 y 11: 12