Laryngotracheitis (gallid-1) herpesvirus infection in the chicken 4. Latency establishment by wild and vaccine strains of ilt virus

Abstract

Tracheal organ culture (TOC) techniques utilising multiple-well plastic trays were used to detect and assay latent infection established by infectious laryngotracheitis (ILT) herpesvirus in clinically normal chickens. Between 3 and 16 months after tracheal exposure to wild strain (CSW-1, haemorrhagic tracheitis) ILT virus and 2 to 10 months after exposure to vaccine strain ILT (SA-2), groups of chickens were examined for evidence of infection. Neither the examination of tracheal swabbings in monolayer cell cultures nor the inoculation of tracheal tissue suspensions detected virus, and this result was not influenced by preliminary immunosuppressive treatment of the birds with cyclophosphamide or dexamethasone. Latent infection was detected, however, by TOC in 6 (38%) of 16 chickens 100 days to 15 months after exposure to wild strain ILT virus and in 4 (44%) of 9 chickens 2 to 10 months after exposure to the vaccine strain. These data provide the first proof that both wild and vaccine strains of ILT virus regularly establish long term latent infections. Sites of establishment of latent infection in the trachea were highly focal in distribution. Virus reactivation was demonstrated in only 20 (8.3%) of the TOC preparations established from previously infected chickens and usually from only one or two sites in each trachea. Both strains of ILT virus exhibited characteristics of latency in vitro in that virus was not detectable in supernatant fluids until 5 to 6 days after establishment of TOC. Virus shedding then usually continued for 1 to 2 weeks 102 to 104PFU/ml being produced each 2 to 3 days. In some preparations, virus production continued for up to 30 days. are caused by infectious laryngotracheitis (ILT) virus, currently designated Gallid herpes-1 virus (Roizman, 1982). While ILT is generally controlled by the use of infectious attenuated vaccines, site quarantine and sanitation (Hanson, 1984), outbreaks tend to recur on commercial poultry sites, especially in multi-age operations. Outbreaks are more likely to occur on sites which formerly have housed infected flocks than on farms with no previous experience of the disease, and for reasons other than mechanical persistence of virus in the physical environment (Zellen et al., 1984). Soon after the first recognition of ILT in the USA, reports appeared (Komarov and Beaudette, 1932; Gibbs 1933) of the detection of long-term, tracheal ‘carriers’ among convalescent birds in field flocks. These pioneering studies, which indicated approximately 2% of carriers amongst flocks which had recovered from acute ILT virus infection, still constitute the major evidence (Hanson, 1984) that establishment of latency may be a significant factor in the long-term survival of the virus. While reviewing prospects for the control of ILT, Hitchner (1975) specifically urged determination of whether the current vaccine viruses produce a carrier state, but his question has remained unanswered. This paper details investigations undertaken into the putative establishment of latency by both wild and vaccine strains of ILT viruses. A preliminary report on some of the findings was presented elsewhere (Bagust, 1985). © 1986, Taylor & Francis Group, LLC. All rights reserved.