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[Hepatic echinococcus granulosus: the clinicopathological examination associated with 12 cases].
Thus, immunosurveillance activities by columnar epithelial cells in the endocervix can cause endogenous HIV-1 reactivation, which may contribute to viral blips during ART or rebound following ART interruption. Copyright © 2020 American Society for Microbiology.Herpesvirus nucleocapsids leave the nucleus by a vesicle-mediated translocation coordinated by the viral nuclear egress complex (NEC). The NEC, composed of two conserved viral proteins, designated as pUL34 and pUL31 in the alphaherpesvirus pseudorabies virus (PrV) is required for efficient nuclear egress and sufficient for vesicle formation and scission from the inner nuclear membrane (INM). Structure-based mutagenesis identified a lysine at position 242 (K242) in pUL31 located in the most membrane distal part of the NEC as crucial for efficient nucleocapsid incorporation into budding vesicles. Replacing the lysine by alanine (K242A) resulted in accumulations of empty vesicles in the perinuclear space despite presence of excess nucleocapsids in the nucleus. However, it remained unclear, whether the defect in capsid incorporation was due to interference with a direct, electrostatic interaction between the capsid and the NEC or structural restrictions. Tofacitinib cell line To test this, we substituted K242 by several amino acids thanism of nucleocapsid incorporation remained unclear. In accordance with structure-based predictions, a basic amino acid could be pinpointed in the most membrane-distal domain of the NEC (pUL31-K242) indicating that capsid incorporation might depend on a direct electrostatic interaction. Our follow-up study here however shows that the positive charge is not relevant but that overall structure matters. Copyright © 2020 American Society for Microbiology.Given that the Ebola virus (EBOV) infects a wide array of organs and cells yet displays a relative lack of neurotropism, we asked whether a chimeric vesicular stomatitis virus (VSV) expressing the EBOV glycoprotein (GP) might selectively target brain tumors. The mucin-like domain (MLD) of the EBOV GP may enhance virus immune system evasion. Here we compare chimeric VSVs in which EBOV GP replaces the VSV glycoprotein, thereby reducing the neurotoxicity associated with wildtype VSV. A chimeric VSV expressing the full-length EBOV GP (VSV-EBOV) containing the MLD was substantially more effective and safer than a parallel construct with an EBOV GP lacking the MLD (VSV-EBOVΔMLD). One-step growth, RT-qPCR, and Western blot assessment showed VSV-EBOVΔMLD produced substantially more progeny faster than VSV-EBOV. Using immunodeficient SCID mice, we focused on targeting human brain tumors with these VSV-EBOVs. Similar to our previous report using an attenuated VSV-EBOV with no MLD that expressed GFP (VSV-EBOVΔMLD-GFP), ng brain tumors in immunodeficient mice when the MLD is expressed within the EBOV glycoprotein compared with EBOV lacking the mucin-like domain. Copyright © 2020 American Society for Microbiology.Influenza A viruses (IAV) are lytic viruses that have recently been found to activate necroptosis in many of the cell types they infect. Necroptotic cell death is potently immunogenic, and limits IAV spread by directly eliminating infected cells and by mobilizing both innate and adaptive immune responses. The benefits of necroptosis to the host, however, may sometimes be outweighed by the potentially deleterious hyperinflammatory consequences of activating this death modality in pulmonary and other tissues. Copyright © 2020 American Society for Microbiology.Kaposi sarcoma-associated herpesvirus (KSHV) is the causal agent for Kaposi sarcoma (KS), the most common malignancy in people living with HIV/AIDS. The oral cavity is a major route for KSHV infection and transmission. However, how KSHV breaches the oral epithelial barrier for spreading to the body is not clear. Here we show that exosomes purified from either the saliva of HIV-positive individuals or culture supernatants of HIV-1-infected T cell lines promote KSHV infectivity in immortalized and primary human oral epithelial cells. HIV-associated saliva exosomes contain the HIV trans-activation response (TAR) element, Tat, and Nef RNAs, but do not express Tat and Nef proteins. The TAR RNA in HIV-associated exosomes contributes to enhancing KSHV infectivity through the epidermal growth factor receptor (EGFR). An inhibitory aptamer to TAR RNA reduces KSHV infection facilitated by the synthetic TAR RNA in oral epithelial cells. Cetuximab, a monoclonal neutralizing antibody to EGFR, blocks HIV-associated exosome-al that HIV-associated exosomes are a risk factor for KSHV infection in the HIV-infected population. Copyright © 2020 Chen et al.Our understanding of how rotavirus (RV) subverts host innate immune signaling has greatly increased over the past decade. However, the relative contribution of each virus-encoded innate immune antagonist has not been fully studied in the context of RV infection in vivo Here, we present both in vitro and in vivo evidence that the host IFN-inducible 2'-5'-oligoadenylate synthetase (OAS) and ribonuclease L (RNase L) pathway effectively suppresses the replication of heterologous RV strains. VP3 from homologous RVs relies on its 2'-5'-phosphodiesterase (PDE) domain to counteract RNase L mediated antiviral signaling. Using a RV reverse genetics system, we show that compared to the parental strain, VP3 PDE mutant RVs replicated at a lower level in the small intestine and shed less in the feces of wild-type mice and such defects were rescued in Rnasel -/- suckling mice. Collectively, these findings highlight an important role of VP3 in promoting viral replication and pathogenesis in vivo in addition to its well characterized function as the viral RNA capping enzyme.ImportanceRotaviruses are significant human pathogens that result in diarrhea, dehydration, and deaths in many children around the world. Rotavirus vaccines have suboptimal efficacy in low to middle income countries, where the burden of the diseases is the most severe. With the ultimate goal to improve current vaccines, we aim to better understand how rotavirus interacts with the host innate immune system in the small intestine. Here, we demonstrate that the interferon-activated RNase L signaling blocks rotavirus replication in a strain-specific manner. In addition, virus encoded VP3 antagonizes RNase L activity both in vitro and in vivo These studies highlight an ever-evolving arms race between antiviral factors and viral pathogens and provide a new means of targeted attenuation for the next-generation rotavirus vaccine design. Copyright © 2020 American Society for Microbiology.
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