Two entry mechanisms of HIV occur in both lymphocytes and macrophages incubated with purified virus suspensions: (a) direct fusion of the viral envelope with the cell membrane and (b) receptor-mediated endocytosis via clathrin-coated pits and vesicles. Both mechanisms are shown in detail in a time-interval series of electron micrographs. The two lipid bilayers of the viral envelope and of the cellular membrane usually fuse seamlessly within 1-3 min at 37 degrees C, but occasionally membrane ruptures occur, leading to rapid cytopathic effects, i.e., vacuolization and cytolysis only a few minutes later. In the course of virus-cell fusion, gp 120 is integrated into the cell membrane; subsequent syncytia formation was observed after 1 h of incubation. The core disintegrates and releases the viral ribonucleoprotein through the opening at the fusion site into the cytoplasm.
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Mol Biol Cell
January 2025
Institute for Biochemistry & Research Center for Emerging Infections and Zoonoses (RIZ), University of Veterinary Medicine Hannover, Hannover, Germany.
Tetraspanins (Tspans) are transmembrane proteins that coordinate life cycle steps of viruses from distinct families. Here, we identify the human Tspan10 and Tspan15, both members of the TspanC8 subfamily, as replication factors for alphavirus Venezuelan equine encephalitis virus (VEEV) in astrocytoma cells. Pharmacological inhibition and siRNA-mediated silencing of TspanC8 interactor a disintegrin and metalloproteinase 10 (ADAM10) reduced VEEV infection.
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State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
The evolution of SARS-CoV-2 pathogenicity has been a major focus of attention. However, the determinants of pathogenicity are still unclear. Various hypotheses have attempted to elucidate the mechanisms underlying the evolution of viral pathogenicity, but a definitive conclusion has yet to be reached.
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January 2025
Department of Fundamental Veterinary Medicine, College of Veterinary Medicine, Shandong Agricultural University, 61 Daizong Street, Tai'an, 271018, Shandong, China.
Porcine reproductive and respiratory syndrome virus (PRRSV) is one of the most harmful pathogens in the swine industry. Our previous studies demonstrated that the small extracellular domain (ECL2) of CLDN4 effectively blocks PRRSV infection. In this study, we explored the in vivo administration of swine ECL2 (sECL2) and found that it blocked HP-PRRSV infection and alleviated histopathological changes in organs.
View Article and Find Full Text PDFPLoS Pathog
January 2025
Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
We have demonstrated that the cellular protein M-Sec promotes the transmission of human T-cell leukemia virus type 1 (HTLV-1) in vitro and in vivo. Here, we show how HTLV-1 utilizes M-Sec for its efficient transmission. HTLV-1-infected CD4+ T cells expressed M-Sec at a higher level than uninfected CD4+ T cells.
View Article and Find Full Text PDFJ Med Virol
February 2025
Department of Microbiology, School of Basic Medicine, Air Force Military Medical University, Xi'an, China.
Virus budding is a critical step in the replication cycle of enveloped viruses, closely linked to viral spread, disease progression, and clinical outcomes. The budding of many enveloped RNA viruses is facilitated by the hijacking of the host endosomal sorting complex required for transport (ESCRT) proteins through viral late domains. These late domains are essential for progeny virus production and are highly conserved, making the interaction between late domains and host ESCRT proteins a potential target for the development of antiviral therapeutics.
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