Abstract

Marek's disease (MD) is a contagious avian viral disease that is responsible for large economic losses to farmers. The disease is caused by Marek's disease virus (species Gallid alphaherpesvirus 2), which causes neurological lesions, immune suppression, and tumor proliferation of lymphoid cells that invade a large number of organs and tissues. Despite widespread vaccination, Marek's disease virus (MDV), has shown a continuous increase in its virulence and has acquired the ability to overcome immune responses induced by vaccines. In the present study, the oncogenic serotype MDV-1 was detected by real-time PCR in DNA samples extracted from organs developing tumor infiltrations. Identification of the pathotype based on a 132-bp tandem repeat and sequencing and phylogenetic analysis of the Meq gene and its encoded protein allowed classification of the isolated viruses as "very virulent", with two new and unique mutations in the Meq gene resulting in amino acid substitutions. Sequencing of pp38, vIl-8, UL1 and UL44 genes did not reveal any new mutations that were characteristic of the Tunisian isolates or correlated with virulence. These results raised concerns about the ability of HVT and CVI988 vaccines, which are currently used in Tunisia and other countries, to protect chickens against highly virulent virus strains.

Highlights

  • Marek’s disease (MD) is a highly contagious immunosuppressive disease that is characterized by paralysis and lymphoma development of T-cells in viscera and muscles [1]

  • It consists of several regions, namely, long unique (UL) and unique short (US) regions flanked by long terminal repeats (TRLs) and short terminal repeats (TRSs), long internal repeats (IRLs) and short internal repeats (IRSs)

  • To better understand the evolution of Tunisian isolates, we studied the pathotypes of Marek’s disease virus (MDV) strains circulating on farms based on the Meq, viral interleukin-8 (vIL-8), pp38, UL1 and UL44 genes

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Summary

Introduction

Marek’s disease (MD) is a highly contagious immunosuppressive disease that is characterized by paralysis and lymphoma development of T-cells in viscera and muscles [1]. The molecular basis for increased MDV virulence is currently unknown, but mutations in some regions of the viral genome, including the Meq (Marek’s disease virus EcoRI fragment Q), Handling Editor: Tim Skern. The MDV genome consists of a double-stranded linear DNA molecule of about 180 kbp It consists of several regions, namely, long unique (UL) and unique short (US) regions flanked by long terminal repeats (TRLs) and short terminal repeats (TRSs), long internal repeats (IRLs) and short internal repeats (IRSs). There are other genes, such as vIL-8, whose deletion or mutation may decrease tumor development and lead to attenuation of virulence [5, 12]. Another gene that is suspected to contribute to the virulence

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