Molecular epidemiology of infectious laryngotracheitis: a review

<div><p>Infectious laryngotracheitis (ILT) is an economically important respiratory disease of poultry that affects the poultry industry worldwide. The disease is caused by <i>gallid herpesvirus I</i> (GaHV-1), a member of the genus <i>Iltovirus</i>, family <i>Herpesviridae</i>, subfamily <i>Alphaherpesvirinae</i>. The current incidence of the disease is heavily influenced by live attenuated vaccines, which have been used extensively since their introduction in the mid-twentieth century. The capability of current live attenuated vaccine viruses to revert to virulence and spread from bird to bird has shaped the molecular epidemiology of ILT. Because of the antigenic homogeneity among GaHV-1 strains, differentiation of strains has been achieved by targeting genomic differences between outbreak-related isolates and vaccine strains. Numerous genes and genomic regions have been utilized in the development of DNA-based diagnostic assays to differentiate outbreak-related isolates from vaccine strains in countries where ILT outbreaks have occurred. More recently, full genome sequences have allowed determination of the origin of some of the outbreak-related isolates circulating in some poultry production countries. Overall, molecular typing data collected worldwide have identified live attenuated vaccine-related isolates as the primary source for outbreaks of the disease.</p></div

Evaluation of the transcriptional status of host cytokines and viral genes in the trachea of vaccinated and non-vaccinated chickens after challenge with the infectious laryngotracheitis virus

<p>Infectious laryngotracheitis is a highly contagious disease of chickens responsible for significant economic losses for the poultry industry worldwide. The disease is caused by <i>Gallid herpesvirus-1</i> (GaHV-1) commonly known as the infectious laryngotracheitis virus. Although characterized by their potential to regain virulence, chicken embryo origin (CEO) vaccines are the most effective vaccines against laryngotracheitis as they significantly reduce the replication of challenge virus in the trachea and conjunctiva. Knowledge on the nature of protective immunity elicited by CEO vaccines is very limited. Therefore, elucidating the origin of the immune responses elicited by CEO vaccination is relevant for development of safer control strategies. In this study the transcription levels of key host immune genes (IFN-γ, IFN-β, IL-1β, IL-6, IL-8, IL-18) and viral genes (ICP4, ICP27, UL46, UL49), as well as viral genome loads in trachea were quantified at 6 and 12 hours post-challenge of CEO vaccinated and non-vaccinated chickens. Immediately after challenge a significant increase in IFN-γ gene expression was followed by a significant reduction in viral replication. In contrast to the rapid induction of IFN-γ, expression of the pro-inflammatory cytokines (IL-1β, IL-6, IL-8) and type I IFN β was either slightly reduced or remained at basal levels. These suggest that the former cytokines may not play important roles during immediate early responses induced by ILTV challenge in either vaccinated or non-vaccinated chickens. Overall, these results suggest that the rapid expression of IFN-γ may induce pathways of antiviral responses necessary for blocking early virus replication.</p