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on of 14-3-3 regulated host signaling pathways not previously associated with W, suggesting new avenues of research. The co-crystal structure of the NiV W14-3-3 complex, as only the second structure of a 14-3-3 mode III interactor, provides further insight into this less well understood 14-3-3 binding motif. Copyright © 2020 American Society for Microbiology.The human cytomegalovirus (HCMV) UL50 gene encodes a transmembrane protein, pUL50, which acts as a core component of the nuclear egress complex (NEC) for nucleocapsids. Recently, pUL50 has been shown to have NEC-independent activities; downregulation of IRE1 to repress the unfolded protein response and degradation of UBE1L to inhibit the protein ISG15 modification pathway. Here, we demonstrate that a 26-kDa N-terminal truncated isoform of pUL50 (UL50-p26) is expressed from an internal methionine at amino acid position 199, and regulates the activity of pUL50 to induce loss of valosin-containing protein (VCP/p97). UL50(M199V) mutant virus expressing pUL50(M199V) but not UL50-p26 showed delayed growth at low multiplicity of infection. There was also delayed accumulation of viral immediate-early (IE) 2 protein in the mutant virus, and this correlated with reduced expression of VCP/p97, which promotes IE2 expression. Infection with mutant virus did not significantly alter ISGylation levels. In transient expressio complex (NEC), which facilitates capsid transport from the nucleus to the cytoplasm. Here, we demonstrate that pUL50 induces loss of valosin-containing protein (VCP/p97), which promotes the expression of viral major immediate-early gene products, in a manner dependent on its membrane targeting, but a small isoform of pUL50 is expressed to negatively regulate this pUL50 activity. This study reports a new NEC-independent function of pUL50 and highlights the fine regulation of pUL50 activity by a smaller isoform for efficient viral growth. Copyright © 2020 American Society for Microbiology.It is widely held that clinical isolates of human cytomegalovirus (HCMV) are highly cell-associated, and mutations affecting the UL128-131 and RL13 loci that arise in culture lead to the appearance of a cell-free spread phenotype. The BAC-clone Merlin (ME), expresses abundant UL128-131, is RL13-impaired and produces low infectivity virions in fibroblasts, whereas TB40/e (TB) and TR are low in UL128-131, RL13-intact and produce virions of much higher infectivity. Despite these differences, quantification of spread by flow cytometry revealed remarkably similar spread efficiencies in fibroblasts. In epithelial cells, ME spread more efficiently, consistent with robust UL128-131 expression. TPA PKC activator Strikingly, ME spread far better than TB or TR in the presence of neutralizing antibodies on both cell types, indicating that ME is not simply deficient at cell-free spread, but is particularly efficient at cell-to-cell spread, whereas TB and TR cell-to-cell spread is poor. Sonically disrupted ME-infected cells contained scant esult of poor cell-free spread, or are indicative of particularly efficient cell-to-cell spread mechanisms. By measuring the kinetics of spread at early time points, we were able to show that HCMV strains can be highly specialized to either cell-free or cell-to-cell mechanisms, and this was not strictly linked the efficiency of cell-free spread. Our results provide a conceptual approach to evaluating intervention strategies for their ability to limit cell-free or cell-to-cell spread as independent processes. Copyright © 2020 American Society for Microbiology.Porcine circovirus type 2 (PCV2) is an important swine pathogen that causes significant economic losses to the pig industry. PCV2 interacts with host cellular factors to regulate its replication. High-mobility group box 1 protein (HMGB1), a major non-histone protein in the nuclei, was recently discovered to participate in viral infections. Here, we demonstrate that nuclear HMGB1 negatively regulated PCV2 replication as shown by over-expression of HMGB1 or blockage of its nucleocytoplasmic translocation with ethyl pyruvate. The B box domain was essential in restricting PCV2 replication. Nuclear HMGB1 restricted PCV2 replication by sequestering the viral genome via binding to the Ori region. However, PCV2 infection could induce translocation of HMGB1 from cell nuclei to the cytoplasmic compartment. Elevation of reactive oxygen species (ROS) induced by PCV2 infection was closely associated with cytosolic translocation of nuclear HMGB1. Treatment of PCV2-infected cells with ethyl pyruvate or N-acetylcysteine downs. This study also provides insight into justification and pharmacological basis of antioxidants as an adjunct therapy in PCV2 infection, or possibly other diseases caused by the viruses that deploy the ROS-HMGB1 interaction favoring their replication. Copyright © 2020 American Society for Microbiology.Respiratory syncytial virus (RSV) is the most important cause of lower respiratory tract infection in infants and young children. The vaccine-enhanced disease (VED) has greatly hindered the development of RSV vaccine. Currently, there is no licensed vaccines for RSV. In this study, mice immunized with hepatitis B virus core particles containing a conserved region of the G protein (HBc-tG) combined with interleukin-35 (IL-35) elicited Th1-biased response, high frequency of regulatory T (Treg) cells and increased IL-10, TGF-β and IL-35 production. Importantly, immunization of HBc-tG together with IL-35 protected mice against RSV infection without vaccine-enhanced immunopathology. To explore the mechanism of how IL-35 reduces lung inflammation at gene expression level, transcription profiles were obtained from lung tissues of immunized mice after RSV infection by Illumina sequencing technique and further analyzed by a system biology method. In total, 2644 differentially expressed genes (DEGs) were identified. Twct of IL-35 on host response and immunopathology following RSV infection in vaccinated mice. Our results indicated that HBc-tG together with IL-35 elicited balanced immune response and protected mice against RSV infection without vaccine-enhanced immunopathology. Applying a system biology method, we identified Il10 was the key regulator in reducing the excessive lung inflammation. Our study provides new insight into the function of IL-35 and its regulatory mechanism of VED at a network level. Copyright © 2020 American Society for Microbiology.TPA PKC activator