Herpesvirus 2, Gallid

  • 文章类型: Case Reports
    本研究调查了在意大利因嗜好而饲养的后院Cochin鸡的经典马立克氏病(MD)的爆发。检查的鸡显示腿部痉挛瘫痪,尸检时,与显微A和B型MD病变相匹配的周围神经和神经丛的扩大和变色。检测到的Gallidα疱疹病毒2(GaHV‑2)株的meq基因的分子分析,显示出低毒力的典型标记,并且该菌株与在意大利后院鸡中传播的菌株共享整个meq基因序列。此外,在受影响的鸡中定义了主要组织相容性复合体(MHC)的单倍型B19,表明这些鸟类具有对MD的高度易感性的遗传特征,允许在感染明显低致病性GaHV-2菌株后出现经典的神经临床形式。生活观赏纯种鸡的贸易经常发生在嗜好农民和生物安全实践之间,例如检疫期,应应用于避免引入受感染的动物。兽医应提高对这一问题的认识,并促进使用针对MD的疫苗。
    The present study investigates an outbreak of classical Marek\'s disease (MD) in backyard Cochin chickens reared for hobby in Italy. Examined chickens showed spastic paralysis of the legs and at necropsy, enlargement and discoloration of the peripheral nerves and plexuses that matched microscopic A‑ and B‑ type MD lesions. Molecular analysis of the meq gene of the detected Gallid alphaherpesvirus 2 (GaHV‑2) strain, showed typical markers of low virulence and the strain shared the entire meq gene sequence with strains circulating in Italian backyard chickens. Furthermore, the haplotype B19 of the major histocompatibility complex (MHC) was defined in the affected chickens, showing that the birds possessed a genetic profile of high susceptibility to MD, allowing the appearance of a classical nervous clinical form after infection with an apparently low pathogenicity GaHV‑2 strain. Trade of live ornamental purebred chickens occurs frequently between hobby farmers and biosecurity practices, such as quarantine periods, should be applied to avoid the introduction of infected animals. Veterinarians should raise awareness of this issue and promote the use of vaccines against MD.
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  • 文章类型: Journal Article
    Both reticuloendotheliosis and Marek\'s disease are neoplastic diseases of chickens caused by reticuloendotheliosis virus (REV) and Marek\'s disease virus (MDV), respectively. The infection of REV or MDV may lead to clinical tumors and also result in immunosuppression and easily allow secondary infection by other pathogens. Here, we investigated a breeder flock of three-yellow chickens in southern China that had been vaccinated with CVI988/Rispens at hatching and had experienced depression, weakness, reduction in weight gain, and an increased death rate after 120 d of age. The morbidity and mortality were 20% and 10%, respectively, at 140 d of age when this infection was diagnosed. The necropsy of the birds revealed significant tumor-like lesions in the heart, liver, spleen, and ceca. Peripheral blood lymphocytes and tumor-like tissues were sampled for PCR detection and for histopathological observation, for virus isolation and the subsequent immunofluorescent assay on the cell cultures and for gene sequencing of the isolated viruses. A REV isolate GX18NNR1 and a MDV isolate GX18NNM5 were both recovered from the sampled bird. Further phylogenetic analysis based on the env gene of REV and the meq gene of MDV demonstrated that GX18NNR1 was closely related to the reference REV strain MD-2, which was isolated from a contaminated commercial turkey herpesvirus vaccine. In addition, the GX18NNM5 was found to belong to the Chinese very virulent MDV strains\' cluster. The coinfection of REV and MDV may contribute to tumor outbreaks with high morbidity and mortality in three-yellow chicken flocks.
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  • 文章类型: Case Reports
    BACKGROUND: Marek\'s disease virus (MDV) resides in the genus Mardivirus in the family Herpesviridae. MDV is a highly contagious virus that can cause neurological lesions, lymphocytic proliferation, immune suppression, and death in avian species, including Galliformes (chickens, quails, partridges, and pheasants), Strigiformes (owls), Anseriformes (ducks, geese, and swans), and Falconiformes (kestrels).
    METHODS: In 2015, two red-crowned cranes died in Nanjing (Jiangsu, China). It was determined that the birds were infected with Marek\'s disease virus by histopathological examination, polymerase chain reaction (PCR), gene sequencing and sequence analysis of tissue samples from two cranes. Gross lesions included diffuse nodules in the skin, muscle, liver, spleen, kidney, gizzard and heart, along with liver enlargement and gizzard mucosa hemorrhage. Histopathological assay showed that infiltrative lymphocytes and mitotic figures existed in liver and heart. The presence of MDV was confirmed by PCR. The sequence analysis of the Meq gene showed 100% identity with Md5, while the VP22 gene showed the highest homology with CVI988. Furthermore, the phylogenetic analysis of the VP22 and Meq genes suggested that the MDV (from cranes) belongs to MDV serotype 1.
    CONCLUSIONS: We describe the first molecular detection of Marek\'s disease in red-crowned cranes based on the findings previously described. To our knowledge, this is also the first molecular identification of Marek\'s disease virus in the order Gruiformes and represents detection of a novel MDV strain.
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  • DOI:
    文章类型: Journal Article
    Herpesviruses evolved from an ancestral viral genome that contained five blocks of genes which provide the members of this family of viruses with structural and enzymatic properties. These genes allow the herpesviruses to infect a host by entering into the nuclei of the cells, the site of replication and transcription of the viral DNA. The viral mRNAs are released into the cell cytoplasm where synthesis of enzymatic and structural proteins occurs. The latter proteins are responsible for the formation of the infectious virions. Herpesviruses that were able to adapt to different hosts during the evolution of the species (speciation) had acquired additional genes from transposons or retrotransposons that allowed them to successfully maintain their hold in the specific vertebrate host. The present overview deals with molecular differences between Marek\'s disease virus type 1 (MDV-1) and herpes simplex virus type 1 (HSV-1) and the specialized genes that differentiate MDV-1 from HSV-1, the promoters of the viral genes that control gene expression and the nuclear localization signals. Dynamic changes in the viral genomes that may occur during viral DNA replication and recombination and their effects on virus pathogenicity and genome evolution will be discussed.
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