Dexamethasone-induced reactivation of bovine herpesvirus type 5 latent infection in experimentally infected rabbits results in a broader distribution of latent viral DNA in the brain

Bovine herpesvirus type 5 (BHV-5) is a major agent of meningoencephalitis in cattle and establishes latent infections mainly in sensory nerve ganglia. The distribution of latent BHV-5 DNA in the brain of rabbits prior to and after virus reactivation was studied using a nested PCR. Fifteen rabbits inoculated intranasally with BHV-5 were euthanized 60 days post-inoculation (group A, N = 8) or submitted to dexamethasone treatment (2.6 mg kg-1 day-1, im, for 5 days) and euthanized 60 days later (group B, N = 7) for tissue examination. Two groups of BHV-1-infected rabbits (C, N = 3 and D, N = 3) submitted to each treatment were used as controls. Viral DNA of group A rabbits was consistently detected in trigeminal ganglia (8/8), frequently in cerebellum (5/8), anterior cerebral cortex and pons-medulla (3/8) and occasionally in dorsolateral (2/8), ventrolateral and posterior cerebral cortices, midbrain and thalamus (1/8). Viral DNA of group B rabbits showed a broader distribution, being detected at higher frequency in ventrolateral (6/7) and posterior cerebral cortices (5/7), pons-medulla (6/7), thalamus (4/7), and midbrain (3/7). In contrast, rabbits inoculated with BHV-1 harbored viral DNA almost completely restricted to trigeminal ganglia and the distribution did not change post-reactivation. These results demonstrate that latency by BHV-5 is established in several areas of the rabbit's brain and that virus reactivation leads to a broader distribution of latent viral DNA. Spread of virus from trigeminal ganglia and other areas of the brain likely contributes to this dissemination and may contribute to the recrudescence of neurological disease frequently observed upon BHV-5 reactivation.

Seguimiento de siete años de 20 pacientes hemofílicos infectados con VIH / Seven-year follow-up of 20 HIV positive hemophilic patients

El 1986 detectamos que veinticuatro pacientes (28.3 por ciento) del grupo de hemofílicos de grado moderado a grave de nuestro hospital, tenían anticuerpos séricos contra el virus de la inmunodeficiencia humana; veinte estaban asintomáticos. Después de siete años de seguimiento, encontramos que sólo tres de los 20 (15 por ciento) permanecían asintomáticos y diecisiete (85 por ciento) habían desarrollado el síndrome de inmunodeficiencia adquirida; el tiempo medio de desarrollo de SIDA fue de cuatro años ocho meses. Catorce pacientes (70 por ciento) habián fallecido al cierre del estudio; el tiempo medio entre el desarrollo del síndrome de inmunodeficiencia adquirida y la muerte fue de 11 meses. Sólo cuatro de los pacientes que fallecieron recibieron zidovudina, y en ellos se observó que la sobrevida media fue de dos años ocho meses