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Efficient mutagenesis of Marek's disease virus-encoded microRNAs using a CRISPR/Cas9-based gene editing system

The virus-encoded microRNAs (miRNAs) have been demonstrated to have important regulatory roles in herpesvirus biology, including virus replication, latency, pathogenesis and/or tumorigenesis. As an emerging efficient tool for gene editing, the clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9 system has been successfully applied in manipulating the genomes of large DNA viruses.

ATM-mediated DNA double-strand break response facilitated oncolytic Newcastle disease virus replication and promoted syncytium formation in tumor cells

Deoxyribonucleic acid (DNA) damage response (DDR) is the fundamental cellular response for maintaining genomic integrity and suppressing tumorigenesis. The activation of ataxia telangiectasia-mutated (ATM) kinase is central to DNA double-strand break (DSB) for maintaining host-genome integrity in mammalian cells. Oncolytic Newcastle disease virus (NDV) can selectively replicate in tumor cells; however, its influence on the genome integrity of tumor cells is not well-elucidated. Here, we found that membrane fusion and NDV infection triggered DSBs in tumor cells.

Avian leukosis virus subgroup J induces B cell anergy mediated by Lyn inhibited BCR signal transduction

Immune tolerance induced by avian leukosis virus subgroup J (ALV-J) is a prerequisite for tumorigenesis. Although we had reported that B cell anergy induced by ALV-J was the main reason for immune tolerance, the molecular mechanism still remains unclear. Here, we found SU protein of ALV-J interacted with tyrosine kinase Lyn (a key protein in BCR signaling pathway) by confocal laser scanning microscopy and co-immunoprecipitation test, which suggested that Lyn might play an important role in B cell anergy induced by ALV-J.

CCCH-type zinc finger antiviral protein is specifically overexpressed in spleen in response to subgroup J avian leukosis virus infection in chicken

The CCCH-type zinc finger antiviral protein (ZAP), a host antiviral factor, plays an important role in innate defenses. Although the anti-viral mechanism of ZAP has been elucidated, however, the tissue specificity and the viral infection correlativity have not been fully understood. Here, we tested the dynamic distribution and localization of chicken ZAP (chZAP) before and after avian leukosis virus subgroup J (ALV-J) infection.

Interplay between CTHRC1 and the SU protein of avian leukosis virus subgroup J (ALV-J) facilitates viral replication

The lifecycle of avian leukosis virus subgroup J (ALV-J), a typical tumorigenic retrovirus, is highly dependent upon host cellular proteins. However, there have been few studies directed at uncovering the host proteins responsible for ALV-J replication, which could provide insights into new strategies for ALV-J prevention and control. Here, we used proteomics to identify the association of differential levels of collagen triple helix-repeat-containing 1 (CTHRC1) and with viral replication.

Avian influenza viruses at the wild-domestic bird interface in Egypt

Wild birds of the orders Anseriformes (mainly ducks, geese and swans) and Charadriiformes (mainly gulls, terns and waders) constitute the natural reservoir for low pathogenic avian influenza (LPAI) viruses. In Egypt, highly pathogenic avian influenza (HPAI) H5N1 and LPAI H9N2 viruses are endemic in domestic poultry, forming a threat to animal and human health and raising questions about the routes of introduction and mechanisms of persistence. Recently, HPAI H5N8 virus was also introduced into Egyptian domestic birds.

Multifunctional miR-155 pathway in avian oncogenic virus-induced neoplastic diseases

MicroRNAs (miRNAs) are small noncoding RNAs that fine-tune the responses of the cell by modulating the cell transcriptome and gene expression. MicroRNA 155 (miR-155) is a conserved multifunctional miRNA involved in multiple roles including the modulation of the immune responses. When deregulated, miR-155 can also contribute to cancer as has been demonstrated in several human malignancies such as diffuse large B cell lymphoma, chronic lymphocytic leukemia, as well as in Epstein–Barr virus (EBV)-induced B cell transformation.

Insights from the crystal structure of the chicken CREB3 bZIP suggest members of the CREB3 subfamily transcription factors may be activated in response to oxidative stress

cAMP response element binding Protein 3 (CREB3) is an endoplasmic reticulum (ER) membrane‐bound transcription factor, which belongs to the basic leucine zipper (bZIP) superfamily of eukaryotic transcription factors. CREB3 plays a role in the ER‐stress induced unfolded protein response (UPR) and is a multifunctional cellular factor implicated in a number of biological processes including cell proliferation and migration, tumor suppression, and immune‐related gene expression.

Sequential disruption of ALV host receptor genes reveals no sharing of receptors between ALV subgroups A, B, and J


Previously, we showed that targeted disruption of viral receptor genes in avian leukosis virus (ALV) subgroups using clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9))-based genome editing confers resistance to ALV subgroups B and J. Here, we used the same strategy to target the receptor expressed by ALV subgroup A (TVA) and generate chicken cells resistant to infection by this virus.


Targeted editing of the pp38 gene in Marek's disease virus-transformed cell lines using CRISPR/Cas9 system.

Marek's disease virus (MDV), a lymphotropic alpha-herpesvirus associated with T-cell lymphomas in chickens, is an excellent model for herpesvirus biology and virus-induced oncogenesis. Marek's disease (MD) is also one of the cancers against which a vaccine was first used. In the lymphomas and lymphoblastoid cell lines (LCLs) derived from them, MDV establishes latent infection with limited gene expression.


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