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Varicella zoster virus (VZV) is a human-specific herpesvirus that establishes latency in peripheral neurons. The only transcripts detected in infected human trigeminal ganglia (TG) obtained shortly after death correspond to the VZV latency-associated transcript (VLT) and associated VLT-ORF63 splice variants. In vitro studies showed that VLT-ORF63 is translated into a protein (pVLT-ORF63) that induces VZV transcription. The mechanisms that lead to this restricted gene expression and the transition to lytic replication remain unknown, partly due to the difficulty of working with human neurons. In this study, we addressed whether the neuroblastoma-derived cell line SH-SY5Y could serve as a model to investigate the mechanisms that lead to repression of VZV gene expression followed by reactivation. VZV productively infected differentiated SH-SY5Y (dSH-SY5Y) whereas incubation with acyclovir (ACV) inhibited virus replication and induced a progressive repression of the virus. Upon removal of ACV there was production of viral particles in a subset of cells, while others contained non-replicating VZV genomes and VLT-containing transcripts for at least 20 days post-infection (dpi). Exogenous expression of VLT-ORF63 induced productive infection, suggesting that the non-replicating and repressed genomes remained functional. Interestingly, histone deposition was undetectable at VZV genomes in quiescently infected dSH-SY5Y cells, pointing to a potential novel mechanism leading to VZV repression in this neuronal setting. Author summary: Varicella zoster virus (VZV) establishes latent infection exclusively in human neurons. This phase of infection is characterized by restricted viral gene expression, lack of detectable protein and no infectious viral particles. Upon reactivation, infectious viruses spread to new cells, causing disease. How VZV gene expression is repressed and regulated during latency is not well understood, partly due to the difficulty of obtaining large amounts of human neurons. Here, we established differentiated neuron-like SH-SY5Y cells as a model to study quiescent VZV infection in the presence of acyclovir, an inhibitor of VZV replication. Acyclovir incubation for six days led to very low VZV gene expression, no detectable viral protein and lack of infectious viral particles. Some of the cells contained viable VZV genomes for up to thirty days post-infection. We hypothesised that, similar to other herpesviruses, histones and their modifications would be present in VZV genomes during quiescent infection. However, we could not detect evidence of histone deposition in the majority of the VZV genomes, suggesting that they lacked chromatinization. These results point to other mechanisms restricting VZV gene expression while allowing genome persistence. [ABSTRACT FROM AUTHOR]

Background: Marek's disease (MD) is a pathology affecting chickens caused by Marek's disease virus (MDV), an acute transforming alphaherpesvirus of the genus Mardivirus. MD is characterized by paralysis, immune suppression, and the rapid formation of T-cell (primarily CD4+) lymphomas. Over the last 50 years, losses due to MDV infection have been controlled worldwide through vaccination; however, these live-attenuated vaccines are non-sterilizing and potentially contributed to the virulence evolution of MDV field strains. Mutations common to field strains that can overcome vaccine protection were identified in the C-terminal proline-rich repeats of the oncoprotein Meq (Marek's EcoRI-Q-encoded protein). These mutations in meq have been found to be distinct to their region of origin, with high virulence strains obtained in Europe differing from those having evolved in the US. The present work reports on meq mutations identified in MDV field strains in Nigeria, arising at farms employing different vaccination practices. Materials and Methods: DNA was isolated from FTA cards obtained at 12 farms affected by increased MD in the Plateau State, Nigeria. These sequences included partial whole genomes as well as targeted sequences of the meq oncogenes from these strains. Several of the meq genes were cloned for expression and their localization ability to interact with the chicken NF-IL3 protein, a putative Meq dimerization partner, were assessed. Results: Sequence analysis of the meq genes from these Nigerian field strains revealed an RB1B-like lineage co-circulating with a European Polen5-like lineage, as well as recombinants harboring a combination of these mutations. In a number of these isolates, Meq mutations accumulated in both N-terminal and C-terminal domains. Discussion: Our data, suggest a direct effect of the vaccine strategy on the selection of Meq mutations. Moreover, we posit the evolution of the next higher level of virulence MDVs, a very virulent plus plus pathotype (vv++). [ABSTRACT FROM AUTHOR]

Background: The porcine cytomegalovirus, a porcine roseolovirus (PCMV/PRV), is widely distributed in pig populations. It has been shown that PCMV/PRV was transmitted by pig xenotransplants to non‐human primates, and significantly reduced the survival time of the recipient. PCMV/PRV was also transmitted during the first transplantation of a pig heart into a human patient. PCMV/PRV establishes a lifelong persistent infection (latency) in the host, is difficult to detect in this stage, and consequential poses a threat to future clinical xenotransplantations. Therefore, sensitive and specific methods and goal‐oriented strategies how, when, and where to test should be used for screening donor pigs. Methods: In this study we compared experimentally the PCMV/PRV detection methods including PCR‐based (real‐time PCR, nested PCR) and immunological methods (Western blot assay, ELISA) recently published by Halecker et al. (Sci. Rep. 2022;12(1):21545) and Fischer et al. (Xenotransplantation 2023:e12803). We also compared the antigens used for antibody detection (a recombinant protein and synthetic peptides corresponding to a conserved region of the glycoprotein B, gB). Results: The published methods can be used for screening donor pigs, with the results being similar. The antigens used for the detection of PCMV/PRV‐specific antibodies are almost identical and give comparable results. Overall, the optimal diagnostic tests, the samples used for testing and the time of sampling play a crucial role in preventing the transmission of PCMV/PRV during xenotransplantation. Conclusion: Sensitive methods are available to screen donor pigs for PCMV/PRV, but a rational application of a combination of PCR‐based and immunological methods as well as rational detection strategies are important for the detection of the virus during latency. [ABSTRACT FROM AUTHOR]

The correction notice for the article "Evaluation of Tissue Tropism and Horizontal Transmission of a Duck Enteritis Virus Vectored Vaccine in One-Day-Old Chicken" in the journal Viruses includes the addition of author Benedikt B. Kaufer, updated author contributions, new affiliations, and corrected funding information. The authors affirm that the scientific conclusions remain unchanged, and the correction was approved by the Academic Editor. The original publication has been updated to reflect these changes. [Extracted from the article]

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