The poultry farming industry encounters considerable obstacles stemming from viral diseases, resulting in elevated mortality rates and substantial economic losses. Current research highlights the significant involvement of long non-coding RNAs (lncRNAs) in the interactions between hosts and pathogens by enhancing antiviral responses at different levels, such as the activation of pathogen recognition receptors, as well as through epigenetic, transcriptional, and post-transcriptional modifications. Specific long non-coding RNAs (lncRNAs), including ERL lncRNA, linc-GALMD3, and loc107051710, have been recognized as significant contributors to the antiviral immune response to multiple avian viral pathogens. Understanding the mechanisms by which long non-coding RNAs (lncRNAs) act offers valuable insights into prospective diagnostic and therapeutic approaches aimed at improving disease resistance in poultry. Differentially expressed lncRNAs may also be utilized as biomarkers for both prognosis and diagnosis of avian viral diseases. This review delves into the various roles of long non-coding RNAs (lncRNAs) in the context of viral diseases in chickens, such as avian leukosis, Marek’s disease, infectious bursal disease, avian influenza, infectious bronchitis, and Newcastle disease. It highlights the pivotal role of lncRNAs in the complex dynamics between the host and viral pathogens, particularly their interactions with specific viral proteins. Understanding these interactions may provide valuable insights into the spatial and temporal regulation of lncRNAs, aid in the identification of potential drug targets, and reveal the expression patterns of lncRNA and coding gene transcripts in response to different viral infections in avian species.

Background: The cohesin complex is essential for proper chromosome structure and gene expression. Defects in cohesin subunits and regulators cause changes in cohesin complex dynamics and thereby alter three-dimensional genome organization. However, the molecular mechanisms that drive cohesin localization and function remain poorly understood. Results: In this study, we observe that loss of WIZ causes changes to cohesin localization that are distinct from loss of the known WIZ binding partner G9a. Whereas loss of WIZ uniformly increases cohesin levels on chromatin at known binding sites and leads to new, ectopic cohesin binding sites, loss of G9a does not. Ectopic cohesin binding on chromatin after the loss of WIZ occurs at regions that are enriched for activating histone modifications and transcription factors motifs. Furthermore, loss of WIZ causes changes in cohesin localization that are distinct from those observed by loss of WAPL, the canonical cohesin unloading factor. Conclusions: The evidence presented here suggests that WIZ can function independently from its previously identified role with G9a and GLP in heterochromatin formation. Furthermore, while WIZ limits the levels and localization pattern of cohesin across the genome, it appears to function independently of WAPL-mediated cohesin unloading.

The present study was carried out to analyze the complete genome sequences of infectious bursal disease virus (IBDV) isolates obtained from field outbreaks in the southern regions of India. Bursal tissue samples were collected and screened by RT-PCR, targeting the VP2 gene. Positive samples were subjected to serological identification via AGID. Following this, eight samples (BGE14, BGE15, MDI14, THI14, EDE14, RPM14, VCN14, and NKL14) were subjected to virus isolation in 9 to 11-day-old embryonated chicken eggs, and their complete genomes were sequenced. Analysis of the VP2 hypervariable region (HVR) revealed that all eight isolates had five unique and highly conserved amino acids (A222, I242, Q249, I256, and S299). However, all the isolates reveal a substitution of Isoleucine by Valine at residue 294 (I294V). Furthermore, analysis of segment B from all Indian IBDV sequences revealed that the triplet amino acid pattern was NEG (residues 145–147) and the amino acid at position 242 was consistently D across all isolates. These findings suggest that segment B of the isolates in this study resembled that of vaccine strains and non-vvIBDV strains. Additionally, the presence of the signature D242 in all Indian isolates, characteristic of non-vvIBDV strains, implies a potential attenuation. Moreover, in the phylogenetic analysis of VP2-HVR, all isolates clustered with very virulent reference strains, while segment B clustered with classical attenuated strains. Notably, the phylogenetic analysis of VP2-HVR and VP1 of these viruses demonstrated genetic variances, suggesting evolutionary changes in segment B across all eight Indian isolates, likely indicative of natural genome reassortment resulting in these specific outbreaks in the flocks.

Poultry farming faces significant challenges due to viral diseases, which lead to high mortality and economic losses. Long noncoding RNAs (lncRNAs) have emerged as crucial regulators in the host immune response to viral infections. This review explores the multifaceted roles of lncRNAs in chicken viral diseases, including avian leukosis, Marek’s disease, infectious bursal disease, avian influenza, infectious bronchitis, and Newcastle disease. LncRNAs influence gene expression at various levels, such as chromatin remodeling, transcriptional regulation, and post-transcriptional modifications. They interact with viral and host genes, modulating immune responses and viral replication processes. Specific lncRNAs, such as ERL lncRNA, linc-GALMD3, and loc107051710, have been identified as key players in the pathogenesis and immune response to these viral infections. Understanding the mechanisms of lncRNA action provides insights into potential diagnostic and therapeutic strategies to enhance disease resistance in poultry. This review highlights the importance of lncRNAs in the complex interplay between host and virus, paving the way for future research and applications in poultry health management.