Efficacy of Recombinant HVT-IBD Vaccines Administered to Broiler Chicks from a Single Breeder Flock at 30 and 60 Weeks of Age.

The efficacy of commercially available recombinant herpesvirus of turkeys-infectious bursal disease (rHVT-IBD) virus vaccines was studied in broiler chickens derived from an IBDV-vaccinated breeder flock at 30 wk of age (Trial 1) and 60 wk of age (Trial 2). In parallel, specific-pathogen-free (SPF) white leghorn chickens were used to evaluate vaccine efficacy to control for the effects of maternally derived antibodies (MDA) associated with the broiler chickens. Broilers and SPF leghorns were vaccinated subcutaneously in the neck at 1 day of age with Vaxxitek® HVT+IBD or Vectormune® HVT-IBD vaccines and were placed in isolators. On 10, 14, 18, 22, and 26 days postvaccination (DPV), vaccinated and nonvaccinated broilers and SPF leghorns were bled prior to challenge via the oral-nasal route with infectious bursal disease (IBD) reference strains ST-C, Delaware variant E (Del E), or contemporary field isolates DMV/5038/07 or FF6. Microscopic lesion assessment of the bursa was useful for assessing IBDV challenge in both rHVT-IBD-vaccinated broiler and SPF leghorn chickens. In general, rHVT-IBD vaccines induced greater protection as the time between vaccination and challenge increased. Based on incidence of microscopic lesions (IML) of bursa tissue, Vaxxitek HVT+IBD vaccination of SPF leghorns induced protection by 18 DPV and continued to protect 22 DPV and 26 DPV in Trials 1 and 2. Vectormune HVT-IBD vaccine induced protection of SPF leghorns by 18 or 22 DPV in Trial 1, depending upon the IBDV challenge strain. However, the onset of protection was delayed until 22 or 26 DPV in Trial 2. With either commercial vaccine, rHVT-IBD vaccination of broiler chickens was not as effective as was observed in SPF leghorns, based on IML of bursa tissue. However, Vaxxitek HVT+IBD vaccination protected broilers following challenge with ST-C in both Trial 1 (30-wk-old breeder progeny) and Trial 2 (60-wk-old breeder progeny). Partial protection against FF6 (Trial 1) and DMV/5038/07 (Trial 2) challenges was observed. Vectormune HVT-IBD vaccination protected broilers vs. FF6 challenge in Trial 1. In Trial 2, the vaccine did not offer protection on the basis of IML of bursa tissue. The results indicate that 1) bursa/body weight ratios were not consistently useful as a tool for assessing IBDV challenge in broiler chickens with anti-IBDV MDA compared to assessment by IML of bursa tissue, though were useful for assessing protection in SPF leghorns; and 2) both vaccines may offer some protection to older broilers; however, a window of susceptibility exists between the waning of MDA and the development of vaccine-induced antibodies. The SPF studies showed that some vaccinated chickens were not protected from an IBDV challenge earlier than 14 DPV while broiler studies showed that MDA was not fully protective beyond 10 DPV. Because these vaccines did not protect chickens from an IBDV challenge during this window of susceptibility, our data show that breeder vaccination programs for IBDV must aim to maximize anti-IBDV MDA in progeny to protect against early IBDV challenge.

Biocharacteristics shared by highly protective vaccines against Marek's disease.

Attenuated serotype 1 Marek's disease virus strains vary widely in their protection properties. This study was conducted to elucidate which biocharacteristics of serotype 1 MDV strains are related with protection. Three pairs of vaccines, each one including a higher protective (HP) vaccine and a lower protective (LP) vaccine originating from the same MDV strain, were studied. Two other highly protective vaccines (RM1 and CVI988/BP5) were also included in the study. Comparison within pairs of vaccines showed that marked differences existed between the HP and the LP vaccines. Compared with LP vaccines, HP vaccines replicated better in vivo. Also, they induced a significant expansion of total T cells and of the helper and cytotoxic T cell lineages (CD45(+)CD3(+), CD4(+)CD8(-), CD4(-)CD8(+)) as well as a marked increase in the expression of the antigens of MhcI and MhcII on T cells. Thus, our results show that in vivo replication and early stimulation of the T-cell lineage are two characteristics shared by HP vaccines. However, comparison among the four HP vaccines that provided protection equal to that of CVI988 (RM1, CVI988/BP5, CVI988 and 648A80) revealed variability, especially regarding in vivo replication. Strains RM1 and CVI988/BP5 showed much stronger replication in vivo than the other two vaccine strains (CVI988 and 648A80). Thus, no single set of characteristics could be used to identify the most protective Marek's disease vaccines, implying, perhaps, that multiple mechanisms may be involved.

Marek's disease: an update on oncogenic mechanisms and control.

Marek's disease (MD) is a common lymphoproliferative disease of poultry caused by a highly contagious and oncogenic herpesvirus. In spite of the widespread use of highly effective MD vaccines, recently there have been worrying trends in the evolution of MD virus pathotypes towards greater virulence. In the last few years, there has been significant progress in determining the molecular structure of MD virus and several genes that map within the repeat regions of the virus, such as Bam HI-H family, ICP 4, meq and pp38, which are potentially associated with the latency and transformation have been identified. The functions of some of these genes have provided insights into the mechanisms of MD virus-induced oncogenesis. This review summarises some of these oncogenic mechanisms and the progress in the control of MD.