RESUMO
Herpes simplex virus (HSV)-specified RNA transcript has been detected by in situ hybridization and by RNA blot analyses in latently infected peripheral nerve ganglia in experimentally infected mice and humans. Physical analysis of the nucleotide sequence, approximately 2,500, indicates possible splicing of the transcript into two overlapping open reading frames (ORF) and the presence of potential promoter elements. The latency-associated transcript, probably, is involved in the maintenance of latent herpes simplex virus infection; however, recent findings indicate that latent-phase transcription is involved in some in vivo reactivation.
Assuntos
Simplexvirus/genética , Transcrição Gênica , Animais , Genes Virais , Humanos , Camundongos , RNA Viral/análise , Simplexvirus/patogenicidade , Fatores de Tempo , Ativação ViralRESUMO
Latent herpes simplex virus type 1 (HSV-1) infection was induced in human embryonic lung cells in vitro by using a combination of viral replication inhibitors and elevated temperature. Under reactivating conditions (superinfection by human cytomegalovirus or temperature manipulation), a nonantiviral thymidine kinase inhibitor (L-653,180) was found to suppress or delay reactivation of HSV-1 from latently infected human embryonic lung cells. L-653,180 alone or in combination with interferon was ineffective as a primary or acute viral replication inhibitor and was unable to induce latent HSV-1 infection in cell culture. These data suggest that initial or acute virus replication and replication resulting from reactivation from latency are separate events.
Assuntos
Antivirais/farmacologia , Guanina/análogos & derivados , Simplexvirus/efeitos dos fármacos , Células Cultivadas , Feminino , Guanina/farmacologia , Humanos , Gravidez , Simplexvirus/crescimento & desenvolvimento , Simplexvirus/fisiologia , Superinfecção , Ativação Viral/efeitos dos fármacos , Replicação Viral/efeitos dos fármacosRESUMO
In an attempt to elucidate the role of viruses in certain neuroendocrine disorders, we have demonstrated that infection of endocrine cells (GH-3 and Y-1) in vitro by moloney murine leukemia virus (M-MuLV) resulted in diminution of cell-specific secretory function, hormone secretion into culture. In GH-3 (rat anterior pituitary gland) active (initial) and persistent infection by M-MuLV resulted in approximately 80% reduction in prolactin and growth hormone secretion. The adrenal cortex tumor cell line (Y-1), when actively infected with the same virus, showed a transient increase in fluorogenic steroid secretion; however, on subsequent passages of infected cell cultures, steroid secretion was markedly reduced to about 10% of the uninfected Y-1 cells. The virus yield from M-MuLV-infected cultures of Y-1 and GH-3 cells produced a significantly lower amount of virus than the control NIH-3T3-infected cell cultures.