Five 13- to 18-month old Belgian Blue bulls were used in this experiment. Whereas HSV-1 periodically reactivates in the TGs, VZV reactivates very rarely. The mechanisms responsible, however, are not so clear. In this report, we demonstrate that QM7 cells were susceptible to infection with either MDV or herpesvirus of turkey (HVT; also known as Meleagrid herpesvirus 1, MDV-3). HIF is classically activated posttranscriptionally with hypoxia, leading to increased protein stability of HIF1α and/or HIF2α. Fifteen 1-day-old chicks were inoculated by intraperitoneal inoculation with 2000 plaque forming units of strain FC126 HVT. At day 50 post-reactivation (pr), the animals were euthanized and regional tissues were collected for PCR and virus isolation.
The dominant immunogenic region of orf 65 is within the carboxyterminal 80 aminoacids, a region with little sequence similarity to the related Epstein-Barr virus, suggesting that orf 65 is a KSHV specific antigen. 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. At 21 days PI, gB expression was present in the thymus, spleen, and bursa. The late-onset neurological disease, after acute infection or Dx treatment, was probably a consequence of spontaneous virus reactivation. At 70 days PI, gB expression was detected only in the spleen, and at 105 days PI, gB expression was not detected in any of the lymphoid tissue (thymus, spleen, or bursa). Although most adults harbor multiple herpesviruses, severe disease attributable to herpesvirus infection is rare in immune competent individuals. Parasitic worms may influence control of pathogens, including Mycobacterium tuberculosis, HIV, and Plasmodium species in humans, but there are few studies elucidating the mechanisms behind this immunomodulation(13).
However, HVT was demonstrated in all other tissues from 21 to 105 days PI. Progression from a productive HVT infection to a latent HVT infection results in the loss of gB expression. However, no clear correlation of a KSHV subtype with a particular disease or disease progression has been identified.