RESUMO
Infections with human papillomaviruses (HPV) are a common occurrence in both men and women. In contrast HPV-associated neoplasias are relatively rare and occur only in certain areas of the body. The virus has obviously developed efficient mechanisms for its persistence without inducing too much damage to the host. The formation of neoplasia seems to be more an exception. Epigenetic mechanisms play an important role in the regulation of viral gene expression. Investigations have indicated that exactly the transition from the permissive infection stage to a transformation stage, where neoplastic alterations can occur due to expression of the viral oncogenes, is associated with certain methylation patterns of the viral genome which promote the expression of the oncogenes E6 and E7. The transforming stage is seen as the actual carcinogenic event and can be immunohistochemically detected by the biomarker p16(INK4a).
Assuntos
Transformação Celular Neoplásica/genética , Genoma Viral/genética , Papillomavirus Humano 16/genética , Infecções por Papillomavirus/genética , Infecções por Papillomavirus/virologia , Neoplasias do Colo do Útero/genética , Neoplasias do Colo do Útero/virologia , Carcinoma de Células Escamosas/genética , Carcinoma de Células Escamosas/patologia , Carcinoma de Células Escamosas/virologia , Proliferação de Células , Transformação Celular Neoplásica/patologia , Transformação Celular Viral/genética , Colo do Útero/patologia , Colo do Útero/virologia , Inibidor p16 de Quinase Dependente de Ciclina/genética , Metilação de DNA/genética , DNA Viral/genética , Epigênese Genética/genética , Feminino , Regulação Neoplásica da Expressão Gênica/genética , Humanos , Estadiamento de Neoplasias , Proteínas Oncogênicas Virais/genética , Infecções por Papillomavirus/patologia , Doenças por Vírus Lento/genética , Doenças por Vírus Lento/patologia , Doenças por Vírus Lento/virologia , Neoplasias do Colo do Útero/patologia , Ativação Viral/genética , Displasia do Colo do Útero/genética , Displasia do Colo do Útero/patologia , Displasia do Colo do Útero/virologiaRESUMO
The symptoms associated with slow viral or prion diseases of the central nervous system tend to have multiple neurologic symptoms, and different patients may present with different symptoms. This review discusses the most common slow virus infections and their imaging findings.
Assuntos
Doenças Priônicas/diagnóstico , Doenças por Vírus Lento/diagnóstico , Humanos , Imageamento por Ressonância Magnética , Neurorradiografia , Doenças Priônicas/virologia , Doenças por Vírus Lento/virologia , Tomografia Computadorizada por Raios XRESUMO
Classification, structure and characteristics of neurotropic viruses are briefly summarized. Neurotropic viruses causing acute infection include Japanese, Venezuelan equine, and California encephalitis viruses, polio, coxsackie, echo, mumps, measles, influenza, and rabies viruses as well as members of the family Herpesviridae such as herpes simplex, varicella-zoster, cytomegalo and Epstein-Barr viruses. Those causing latent infection include herpes simplex and varicella-zoster viruses. Those causing slow virus infection include measles, rubella and JC viruses, and retroviruses such as human T-lymphotropic virus 1 and human immunodeficiency virus. Prion, which is not a virus but a host-derived non-physiological protein, causes transmissible spongiform encephalopathy such as kuru and Creutzfeldt-Jakob disease that resemble slow virus infection.
Assuntos
Doenças do Sistema Nervoso/virologia , Doenças por Vírus Lento/virologiaAssuntos
Príons/patogenicidade , Animais , Humanos , Doenças Priônicas/etiologia , Doenças Priônicas/genética , Doenças Priônicas/patologia , Príons/genética , Doenças por Vírus Lento/etiologia , Doenças por Vírus Lento/genética , Doenças por Vírus Lento/patologia , Doenças por Vírus Lento/virologiaRESUMO
Sporadic amyotrophic lateral sclerosis may be an aetiologically heterogenous disease. We confirmed elevated circulating IgG immune complexes, and altered IgG seroreactivities against human retroviral antigens (HIV-2 and HTLV immunoblots) in overlapping subgroups of patients. Together with preliminary findings of a positive polymerase chain reactivity for human T-lymphotropic virus (HTLV.tax/rex) in blood leukocytes of 5 out of 14 sALS patients, we interpret this as evidence for a retroviral involvement in this relentlessly progressive, often asymmetrically spreading neurodegeneration. The possibility of a secondary phenomenon seems unlikely, yet cannot be completely ruled out.
