RESUMO
Research into the biology of human immunodeficiency virus type 1 (HIV-1), the causative agent of the acquired immunodeficiency syndrome, has yielded valuable information about the replicative cycle of the virus. The steps involved are (1) attachment of the virus to a receptor protein on the surface of the target cell, (2) entry of the virus into the cell, (3) replication of the viral genome through a DNA intermediary, (4) entry of proviral DNA into the nucleus of the host cell, (5) integration of proviral DNA into the host cell genome, (6) transcription of proviral DNA to viral genomic and messenger RNA, (7) translation of viral messenger RNA to viral proteins, and (8) assembly of viral components into new virions that are released by budding from the host cell membrane. Each step in the HIV-1 replicative cycle offers a potential target for antiviral chemotherapy. Although many drugs have been developed, none appears singularly effective against all stages of HIV-1 infection. Many obstacles remain in the quest for an effective vaccine against HIV-1.
Assuntos
Humanos , HIV , Antivirais , Infecções por Retroviridae , Replicação Viral , Síndrome da Imunodeficiência Adquirida , Vacinas ViraisRESUMO
Most clinicians agree that mycosis fungoides is the prototypic cutaneous T cell lymphoma. However, certain clinical characteristics indicate that this disorder may begin as a reactive rather than a neoplastic process. The concept of a nonneoplastic etiopathogenesis of mycosis fungoides is further supported by recent data on the function of Langerhans cells, a population of epidermal cells known to play a critical role in immune surveillance and the development of contact sensitivity. It has been suggested that chronic occupational exposure to environmental allergens results in persistent antigenic stimulation, leading to a breakdown in immune surveillance and eventually, malignancy. Modern laboratory technics have enhanced the clinician's ability to diagnose and stage mycosis fungoides. Data obtained from such studies have indicated that systemic spread may occur much earlier in the course of disease than has previously been appreciated. The therapeutic implications of such knowledge are as yet uncertain.