RESUMEN
Drug abuse is a common method of human immunodeficiency virus type 1 transmission, but the role of opiates on lentivirus disease progression is not well understood. The feline immunodeficiency virus (FIV)/cat system was used to model the weekend opiate abuser: the nondependent, nonaddicted, and nontolerant person. Sixteen cats were placed into 4 groups: FIV only, morphine only, morphine/FIV, and controls. Multiple acute morphine exposure did not increase the severity of early lentivirus infection. On the contrary, it delayed or moderated the FIV-induced disease progression. Although the animals were exposed to only 1 injection of morphine per day for 2 consecutive days per week, the morphine-treated FIV-infected animals had a delayed onset of the FIV-induced lymphadenopathy, did not develop or had a significant delay in the FIV-induced effects on brain stem auditory evoked potentials, and demonstrated a trend toward decreased virus load.
Asunto(s)
Modelos Animales de Enfermedad , Síndrome de Inmunodeficiencia Adquirida del Felino/fisiopatología , Morfina/toxicidad , Trastornos Relacionados con Sustancias/complicaciones , Animales , Gatos , Progresión de la Enfermedad , Infecciones por VIH/transmisión , Hidrocortisona/sangre , Drogas Ilícitas/efectos adversos , Virus de la Inmunodeficiencia Felina/genética , Virus de la Inmunodeficiencia Felina/aislamiento & purificación , Morfina/administración & dosificación , Dependencia de Morfina/complicaciones , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Factor de Necrosis Tumoral alfa/análisis , Factor de Necrosis Tumoral alfa/líquido cefalorraquídeo , Viremia/diagnósticoRESUMEN
Feline immunodeficiency virus (FIV), a lentivirus, causes progressive immunosuppression and neurologic dysfunction in cats. Glucocorticoids are common therapeutic agents that are also immunosuppressive, and their use might enhance the pathogenic effects of lentivirus infections. Methylprednisolone acetate, a long-acting glucocorticoid, was administered to cats before FIV inoculation, and the course of early infection was monitored. The humoral immune response to FIV was not affected by corticosteroid treatment, but CD8+ cell-mediated antiviral activity was poor in cultures from FIV-infected cats treated with methylprednisolone. Steroid-treated cats had higher plasma viral RNA levels than untreated cats during acute viremia. In contrast, FIV-associated changes in brain stem auditory-evoked potentials were slow to develop in the methylprednisolone-treated cats. Methylprednisolone treatment of cats with established FIV infections appeared to reverse these neurophysiologic changes. These results emphasize the complexity of host-lentivirus interactions and suggest potential advantages and drawbacks of using glucocorticoids in lentivirus infections.