Relationship between Marek's disease virus load in peripheral blood lymphocytes at various stages of infection and clinical Marek's disease in broiler chickens

Abstract

Vaccination with herpesvirus of turkey (HVT) vaccine provides protection against clinical Marek's disease (MD) but does not preclude infection with wild-type MD virus (MDV). The quantity of MDV detected in circulating lymphocytes during the early period after infection may be a useful predictor of subsequent clinical MD later in the life. A study was designed to quantify MDV and HVT copy number in peripheral blood lymphocytes (PBL) using real-time polymerase chain reaction between days 5 and 35 post-challenge and to relate this to subsequent development of gross MD lesions. Female commercial broiler chickens were vaccinated with HVT or were sham-vaccinated at hatch, then challenged with MDV strain MPF-57 at day 2 post-vaccination and reared in positive-pressure isolators up to 56 days post-challenge, when all survivors were euthanized. All dead and euthanized chickens were examined post mortem for gross MD lesions. Birds were scored for MD lesions and mortality. MDV and HVT genome copy numbers were determined for each PBL sample. There was an increase in HVT load in PBL between days 7 and 37 post-vaccination, with marked increases between days 7 and 16 and again between days 30 and 37. There was a steady increase in MDV load to 35 days post-challenge. The mean MDV copy number (log 10 ) was greater in chickens subsequently exhibiting gross MD lesions (5.059/0.21) than in those that did not (2.889/0.223), with the largest difference at 14 and 21 days post-challenge (P B/0.001). Quantification of MDV during early infection is therefore a potential tool for monitoring MD in broiler flocks.

The immune cell landscape and response of Marek’s disease resistant and susceptible chickens infected with Marek’s disease virus

“…All uninfected birds had total viral transcripts per million (TPM) under 2 (mean = 1.46; STD = 0.225). The viral load of the infected birds was more variable, as has been seen previously 34 showing four of the six infected birds had a viral TPM higher than 10, but the TPMs of the other two (63 M: TPM = 1.86; 72 M: TPM = 3.01) were closer to those of the uninfected birds than the other infected birds (for all six infected birds, mean = 14.2, STD = 9.62). However, a principal components analysis of gene expression at the sample level shows 72 M clustering with other infected birds despite its low viral TPM, with PC1 corresponding to infection status (Fig.…”

Ostreid Herpesvirus 1 Infection among Pacific Oyster (Crassostrea gigas) Spat: Relevance of Water Temperature to Virus Replication and Circulation Prior to the Onset of Mortality

“…These results suggest that prior to the onset of mortality, the virus replicated and circulated widely among the oysters, infecting a large number of individuals. The prevalence and viral-DNA quantification have been taken into account for prognosis of vertebrate herpesvirus infections (46,47). However, real-time PCR did not specify whether viral DNA corresponded to infective viruses (enveloped virus particles), which are necessary to initiate the viral infection in host cells (48).…”

Establishment of six homozygous MHC-B haplotype populations associated with susceptibility to Marek’s disease in Chinese specific pathogen-free BWEL chickens

“…In contrast, greater resistance to the same MDV strains was associated with lower mortality and lower virus replication capacity. Islam et al (2006) investigated MDV viral loads in peripheral blood lymphocytes of infected chickens, with the same MDV infection, virus copy numbers in chickens that died were higher than in those that resisted, while chickens without MD symptoms possessed the lowest virus loads. In this study, viral loads in feather pulp were examined using the duplex real-time fluorescence PCR with both meq and ovo genes (Baigent et al, 2005).…”