Virus Genes最新文献

Koala retrovirus (KoRV) causes multiple disease phenotypes in koalas, including carcinogenesis. The study aimed to assess oncogene expression in spleen tissues from ten deceased koalas coinfected with different subtypes and peripheral blood mononuclear cells (PBMCs) from two subclinically coinfected koalas with KoRV-A and KoRV-B. Initially, KoRV subtyping involved amplifying endogenous KoRV-A, and exogenous KoRV-B, -C specific env gene fragments, followed by sequencing. Using quantitative real-time polymerase chain reaction (RT-qPCR), we examined five oncogenes (BCL2, BAX, BCL2L1, BCL3, and MYC) in spleen and PBMCs from dead and alive koalas coinfected with multiple KoRV subtypes, respectively. Significant (p < 0.05) increases in BCL2 and BAX oncogene expression were observed in deceased koalas that were coinfected with multiple KoRV subtypes compared with healthy koalas. Thus, this study highlights a potential link between KoRV subtype infections, oncogene expression, and koala diseases.

PB1-like phages belong to Pbunavirus and are widespread in various environments. This group of phages is a promising candidate for treating human or animal infectious diseases caused by antibiotic-resistant P. aeruginosa. The lipopolysaccharide (LPS) has been identified as the receptor of different PB1-like phages, while little is known about the receptor-binding proteins (RBPs) of these phages. We constructed the tail fiber protein (gp50) of a PB1-like phage, PHW2, and its C- or N-terminus truncation variants to identify its role during the phage infection. The anti-gp50_(453-964) antibody showed a similar effect to the antibody against gp50 in blocking the phage infection. The protein competition and cell binding assays showed that the gp50_(1-451) doesn't exhibit an effect on the adsorption of the host cells. These results indicated that the C-terminus of gp50 is the essential region that mediates phage PHW2 adsorption and infection.

In the year 2022, the outbreak of monkeypox virus (MPXV) occurred in the various countries of Africa, particularly Central and West Africa, North America, South America, Europe, and other countries. Without any delay it spread across more than 100 countries infecting around 116,015 people causing around 255 deaths. Monkeypox is a major public health issue, and it is important to search for new therapeutic approaches. This review article is a review of molecular docking studies to identify possible protein inhibition approaches against Monkeypox virus. The exploration on the molecular architecture of the main viral proteins and their relationships with the host cell, emphasizing how these interactions are important in the viral cycle. By gathering data from multiple molecular docking studies, the evaluation of how effective different structural elements are in disrupting these protein interactions is conducted. The results of the analysis reveal how narrowed the focus of molecular interventions is, which holds the promise for the development of antiviral therapies for Monkeypox (Mpox). Not only does this review update the current understanding of the pathophysiology of Monkeypox, but it also provides a basis for more research to deal with this new viral threat. It will be important for the design of inhibitors that can block the replication and dissemination of MPXV to understand the mechanisms of action of the viral proteins and their interactions with the host cell.

This study investigates the effects of pseudorabies virus (PRV) infection on the antiviral immune signaling pathway and type I interferon factors in mouse trigeminal ganglion (TG) cells. The experiment involved inoculating TG primary cells with PRV and intranasally infecting mice. The results indicated that PRV infection of mouse TG primary cells led to alterations in the gene and protein expression of TLR3, TRIF, TBK1, and IRF3, while inhibiting the expression of IκBα protein in the later stages of infection. Additionally, the phosphorylation of IRF3 and IκBα was induced both in vivo and in vitro. Following PRV infection, the expression of IFN-α was up-regulated in the supernatant, whereas its expression was down-regulated in the cell lysates and mouse TG. To further investigate the role of TLR3 in the IRF3 signaling pathway and type I interferon factors, siRNA was employed to interfere with TLR3 expression in TG cells. Western blot analysis was conducted to assess the expression of TLR3 signaling pathway-related proteins and the secretion of IFN-α following the interference. The findings demonstrated that siTLR3 effectively reduced TLR3 protein expression in TG cells and concurrently modulated the secretion of type I interferon factors via the TLR3-TRIF-TBK1-IRF3 signaling axis. Furthermore, PRV infection was shown to induce TLR3 expression in both mouse TG primary cells and mouse TG, thereby activating the TLR3-TRIF-TBK1-IRF3 signaling axis to regulate the antiviral immune response in TG cells, while simultaneously inhibiting IFN-α expression within TG cells and TG through the TLR3 signaling pathway. These experimental results elucidate the antiviral immune mechanism associated with the TLR3 signaling pathway following PRV infection of mouse TG cells, offering new insights into the immune evasion strategies employed by PRV.

Plant viruses use the plasmodesmata and vascular systems to spread systemically in a plant, which may influence the translocation of exogenous transgene products in genetically modified (GM) plants. Transgrafting is a technique that involves the use of GM plants as grafting partners for non-GM plants, and yields non-GM edible harvests from transgrafted crops; thus, there is potential for its distribution as a non-GM product. However, when growing in agricultural fields, transgrafts are exposed to biotic stresses, such as plant virus infections. In this study, we investigated the influence of a plant virus infection on translocation of transgene products between GM and non-GM parts of transgrafts. We generated homo- and hetero-transgrafts of green fluorescent protein (GFP)-expressing GM tomatoes and GM Nicotiana benthamiana rootstocks with non-GM tomato scions and infected them with cucumber mosaic virus (CMV), a major plant virus, and analyzed the translocation of GFP protein in transgrafts. The results showed that CMV infection did not promote GFP transfer from GM rootstock to non-GM scions.

The genus Spodoptera (Lepidoptera: Noctuidae) includes several major agricultural pests of crops of economic importance worldwide. Some of its species are widely distributed, while others are mainly found in Africa and Asia. Unfortunately, the use of insecticides and Bt transgenic crops is not environmentally suitable for beneficial insects and human health, as it contributes to the rapid selection of resistant insects. For this reason, viruses infecting Spodoptera spp. become promising biological control strategies, as they allow for targeted and specific pest management with significantly lower environmental impact. As part of an investigation to identify potential viral control agents for Spodoptera, we examined the diversity of rhabdoviruses associated with Spodoptera species through a meta-analysis of 1,457 public RNA-seq datasets. Our results revealed a tentative new Alphapaprhavirus associated with S. frugiperda and S. exigua, as well as two newly identified viruses not previously described and associated with S. litura and S. littoralis that likely represent a new genus within the subfamily Deltarhabdovirinae. Our results also revealed new Spodoptera frugiperda rhabdovirus (Betapaprhavirus frugiperda) sequences, including subclades associated with S. exigua and S. litura.

Mycobacterium, an opportunistic pathogen, is highly prone to causing infections in humans, and its resistance to antibiotics poses a significant challenge. Phage therapy has emerged as a highly promising alternative treatment. In this study, a bacteriophage infecting Mycobacterium smegmatis was isolated from soil, named MS619, and classified within the class Caudoviricetes. Phages have an icosahedral head (60 ± 2 nm in diameter) and a long, non-contractile tail with a size of 125 ± 2 nm. The genome of MS619 was found to be a double-stranded DNA composed of 48,955 bp, containing 76 open reading frames (ORFs), related to phage packaging, structure, lysin, regulation, and replication. The BLASTN results indicated that MS619 exhibits a high-sequence identity (93%) with Mycobacterium phage Georgie2, a known bacteriophage recorded in the NCBI GenBank database. A typical holin-lysin system was identified in the MS619 genome. The topology of holin was predicted to contain two transmembrane domains, which significantly contribute to antimicrobial activity. No antibiotic resistance- or virulence factor-related genes were detected in the phage. Moreover, the bacteriophage demonstrates biofilm growth inhibition capability. This study led to the isolation of MS619, a bacteriophage exhibiting potential antibacterial efficacy against Mycobacterium infections.

The key carcinogenic factor for nasopharyngeal cancer (NPC) is infection with the Epstein-Barr virus (EBV), significantly contributing to its occurrence and development. Insulin-like growth factor binding protein 2 (IGFBP2), known for its aberrant expression in various cancers, plays a pivotal role in oncogenic networks. Investigating IGFBP2's function and mechanism in EBV-associated NPC was the goal of the current study. The findings indicated that IGFBP2 expression was markedly higher in EBV-positive NPC cells compared to EBV-negative NPC cells, and EBV could up-regulate IGFBP2 expression by activating the TGF-β pathway through its encoded EBNA1. Furthermore, IGFBP2 influenced key carcinogenic processes, including proliferation, migration, epithelial-mesenchymal transition (EMT), and cell cycle progression in NPC cells. Notably, knockdown of IGFBP2 in the EBV-infected epithelial cell line C666-1 led to a reduction in the expression of EBV-encoded latent and lytic phase gene proteins, as well as a decrease in the copy number of the EBV genome. These results point to a reciprocal regulation link between EBV and IGFBP2, opening up a promising avenue for future clinical treatment and experimental research.

Pneumonia, characterized by infection-induced inflammation of the lungs, poses a significant health burden, particularly among children. ADP ribosylation factor 3 (ARF3) is a key regulatory protein implicated in various pathological processes; however, its role in pneumonia caused by influenza A virus (IAV) remains inadequately understood. In this study, we demonstrated that ARF3 expression was upregulated in a young mouse model of IAV-induced pneumonia. Knockdown of ARF3 effectively mitigated lung injury in this model. Furthermore, suppression of ARF3 expression alleviated pulmonary inflammation by reducing the levels of pro-inflammatory cytokines, including TNF-α, IL-6, and IL-1β. In vitro experiments further revealed that ARF3 downregulation inhibited replication of the H3N2 IAV strain. Notably, ARF3 knockdown also attenuated NLRP3 inflammasome activation, a key mediator of inflammatory responses. Collectively, these findings provide the first evidence that ARF3 knockdown suppresses both IAV replication and virus-induced pneumonia by modulating inflammasome activation, suggesting that ARF3 may serve as a potential therapeutic target for pneumonia intervention.

Potato virus S (PVS) is a widely distributed potato pathogen that typically causes mild or asymptomatic infections. Still, certain genotypes can cause up to 20% yield losses, especially when co-infected with other viruses. Aphids are the only currently recognized insect vectors of PVS; however, the mechanical transmission through plant contact is also known. The Colorado potato beetle (CPB) is a major potato pest. In this study, we report the partial PVS genome assembled from the RNA-seq data obtained from CPB field samples and the phylogenetic analysis of its triple gene block (TGB) nucleotide sequence with corresponding sequences, extracted from published PVS genomes and PVS genomes assembled from publicly available CPB RNA-Seq data. The CPB-derived PVS sequences clustered within the globally prevalent PVS^I phylogroup, indicating they are typical PVS strains rather than a highly divergent variant. These results demonstrate the wide presence of PVS genetic material in CPB. With the emerging PVS variants showing increased transmissibility and pathogenicity, PVS could be considered an underappreciated potato pathogen and thus further studies are needed to determine whether CPB may play a role in PVS transmission.