Deletion of the thymidine kinase gene attenuates Caprine alphaherpesvirus 1 in goats

Noll, Jéssica Caroline Gomes; Joshi, Lok R.; Nascimento, Gabriela Mansano do; Fernandes, Manuel; Sharma, Bimala; Flores, Eduardo Furtado; Diel, Diego G.

doi:10.1016/j.vetmic.2019.07.022

Cited by 3 publications

(2 citation statements)

References 32 publications

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“…Despite the widespread adoption of gene deletion vaccines and regional eradication initiatives utilizing DIVA ( Wang et al, 2014 ), PRV persists as an endemic disease in most Chinese provinces, primarily due to insufficient mandatory vaccination campaigns, inadequate awareness, and biosecurity measures ( Sun et al, 2016 ). Currently, no safe and effective vaccines have been produced for feline herpesvirus, bovine herpesvirus, or caprine herpesvirus ( Gomes Noll et al, 2019 ; Kim et al, 2024 ). Only some feasible solutions are still under development ( Jiao et al, 2024 ).…”

Section: Discussionmentioning

confidence: 99%

Advances in the immunoescape mechanisms exploited by alphaherpesviruses

Wang,

Ma,

Wang

et al. 2024

Front. Microbiol.

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Alphaherpesviruses, categorized as viruses with linear DNA composed of two complementary strands, can potentially to induce diseases in both humans and animals as pathogens. Mature viral particles comprise of a core, capsid, tegument, and envelope. While herpesvirus infection can elicit robust immune and inflammatory reactions in the host, its persistence stems from its prolonged interaction with the host, fostering a diverse array of immunoescape mechanisms. In recent years, significant advancements have been achieved in comprehending the immunoescape tactics employed by alphaherpesviruses, including pseudorabies virus (PRV), herpes simplex virus (HSV), varicella-zoster virus (VZV), feline herpesvirus (FeHV), equine herpesvirus (EHV), and caprine herpesvirus type I (CpHV-1). Researchers have unveiled the intricate adaptive mechanisms existing between viruses and their natural hosts. This review endeavors to illuminate the research advancements concerning the immunoescape mechanisms of alphaherpesviruses by delineating the pertinent proteins and genes involved in virus immunity. It aims to furnish valuable insights for further research on related mechanisms and vaccine development, ultimately contributing to virus control and containment efforts.

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Section: Discussionmentioning

confidence: 99%

Advances in the immunoescape mechanisms exploited by alphaherpesviruses

Wang,

Ma,

Wang

et al. 2024

Front. Microbiol.

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“…In addition, tk deletion often attenuates alpha herpesviruses infection in susceptible animals, although it has limited effects on viral growth in host cells in vitro. This indicates that tk supplies dNTP substrates essential for the viral DNA polymerase and plays a crucial role in alpha herpesvirus infection (3,8,18). In general, the tk gene and/or gE/gI genes have been deleted to develop PRV vaccines (2).…”

Section: Discussionmentioning

confidence: 99%

Tk-deleted pseudorabies virus retains high pathogenicity in rats

Zhang

Ruan

Sang

et al. 2021

Journal of Veterinary Research

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Introduction The pseudorabies virus (PRV) gene encoding thymidine kinase (tk) is an important virulence-associated factor. Attenuation of PRV in susceptible animals is a frequent result of tk deletion. The aim of the study was to assess the pathogenicity of tk-deleted PRV in rats. Material and Methods Sprague Dawley rats were infected with the tk-deleted PRV strain SuHV-1 ΔTK:247via intranasal or intramuscular inoculation. PRV loads in ten tissues from dead and euthanised rats were determined using real-time PCR. Results Infection with SuHV-1 ΔTK:247 could cause death in rats. The 50% lethal dose (LD50) of SuHV-1 ΔTK:247 via intranasal inoculation was 103.16 TCID50 in rats. Intramuscular inoculation required a higher dose of SuHV-1 ΔTK:247 (105.0 TCID50). A high SuHV-1 ΔTK:247 titre was observed in the trigeminal ganglia or spinal cord of dead rats. Conclusion The results of this study show that rats are highly susceptible to PRV infection, and tk deletion did not completely diminish the pathogenicity of PRV in rats.

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Deletion of the Viral Thymidine Kinase in a Meq-Deleted Recombinant Marek’s Disease Virus Reduces Lymphoid Atrophy but Is Less Protective

et al. 2021

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Marek’s disease (MD) is a ubiquitous disease of domesticated chickens and its etiologic agent is the Gallid alphaherpesvirus 2 (GaHV-2), also known as Marek’s disease virus (MDV). MD is currently controlled by vaccination using live attenuated strains of MDV (e.g., CVI988/Rispens), non-pathogenic serotypes of MDV (GaHV-3), or non-pathogenic strains of the related Melagrid alphaherpesvirus 1 (MeHV-1). One attractive strategy for the production of new vaccine strains is a recombinant MDV attenuated by the deletion of the major viral oncogene meq. However, meq-deleted variants of MDV cause atrophy of the bursa and thymus in maternal antibody-negative chickens, and the resulting immunosuppression makes them unsuitable. Herein we detail our attempt to mitigate the lymphoid atrophy caused by meq-deleted MDV by further attenuation of the virus through ablation of the viral thymidine kinase (tk) gene. We demonstrate that ablation of the viral tk from the meq-deleted virus rMd5B40/Δmeq resulted in a virus attenuated for replication in vitro and which spared chickens from atrophy of the lymphoid organs in vivo. When the rMd5B40/Δmeq/Δtk/GFP was used as a vaccine it was protective against challenge with the vv+MDV strain 686, but the protection was less than that provided by the CVI988/Rispens vaccine.

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Deletion of the thymidine kinase gene attenuates Caprine alphaherpesvirus 1 in goats

Cited by 3 publications

References 32 publications

Advances in the immunoescape mechanisms exploited by alphaherpesviruses

Advances in the immunoescape mechanisms exploited by alphaherpesviruses

Tk-deleted pseudorabies virus retains high pathogenicity in rats

Deletion of the Viral Thymidine Kinase in a Meq-Deleted Recombinant Marek’s Disease Virus Reduces Lymphoid Atrophy but Is Less Protective

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