innate immunity
Cellular Response to InfectionPeople with HIV-1 Demonstrate Type 1 Interferon Refractoriness Associated with Upregulated USP18People living with HIV-1 (PLWH) have elevated constitutive expression of type 1 interferons (IFN). However, it is unclear whether this affects downstream innate immune responses.
Cellular Response to InfectionThe Polybasic Cleavage Site in SARS-CoV-2 Spike Modulates Viral Sensitivity to Type I Interferon and IFITM2The furin cleavage site in the spike protein is a distinguishing feature of SARS-CoV-2 and has been proposed to be a determinant for the higher transmissibility between individuals, compared to SARS-CoV-1. One explanation for this is that it permits more efficient activation of fusion at or near the cell surface rather than requiring processing in the endosome of the target cell.
Cellular Response to InfectionReduced Nucleoprotein Availability Impairs Negative-Sense RNA Virus Replication and Promotes Host RecognitionNegative-sense RNA viruses comprise some of the most important known human pathogens, including influenza A virus, measles virus, and Ebola virus. These viruses possess RNA genomes that are unreadable to the host, as they require specific viral RNA-dependent RNA polymerases in conjunction with other viral proteins, such as nucleoprotein, to be replicated and transcribed.
Pathogenesis and ImmunityNonsegmented Negative-Sense RNA Viruses Utilize N6-Methyladenosine (m6A) as a Common Strategy To Evade Host Innate ImmunityThe nonsegmented negative-sense (NNS) RNA viruses share many common replication and gene expression strategies. There are no vaccines or antiviral drugs for many of these viruses.
Virus-Cell InteractionsIdentification of the Interferon-Inducible GTPase GBP1 as a Major Restriction Factor for Hepatitis E VirusAlthough HEV represents a worldwide public health problem with 20 million infections and 44,000 deaths per year, there are still no specific antivirals available and many aspects of the viral life cycle are not well understood. Here, we identify guanylate binding protein 1 (GBP1) as a restriction factor affecting the life cycle of HEV.
Virus-Cell InteractionsDDIT3 Targets Innate Immunity via the DDIT3-OTUD1-MAVS Pathway To Promote Bovine Viral Diarrhea Virus ReplicationExtensive studies have demonstrated roles of DDIT3 in apoptosis and autophagy during viral infection. However, the role of DDIT3 in innate immunity remains largely unknown.
Pathogenesis and ImmunityProtein Tyrosine Phosphatase SHP2 Suppresses Host Innate Immunity against Influenza A Virus by Regulating EGFR-Mediated SignalingViral immune evasion is the most important strategy whereby viruses evolve for their survival. This work shows that influenza A virus (IAV) suppressed the antiviral innate immunity through downregulation of IFNs and ISGs by activating EGFR/ERK signaling.
Virus-Cell InteractionsInducible Guanylate-Binding Protein 7 Facilitates Influenza A Virus Replication by Suppressing Innate Immunity via NF-κB and JAK-STAT Signaling PathwaysSo far, few studies have mentioned the distinct function of guanylate-binding protein 7 (GBP7) on virus infection. Here, we reported that GBP7 expression was significantly upregulated in the lungs of mice, human PBMCs, and A549 cells during IAV infection.
Virus-Cell InteractionsClassical Swine Fever Virus Npro Antagonizes IRF3 To Prevent Interferon-Independent TLR3- and RIG-I-Mediated ApoptosisResponsible for severe hemorrhagic disease in domestic pigs and wild boar, classical swine fever is recognized by the World Organisation for Animal Health (OIE) and European Union as a notifiable disease of economic importance. Persistent infection, immunotolerance, and early dissemination of the virus at local sites of infection have been linked to the antagonism of type I IFN induction by Npro.
Pathogenesis and Immunity | SpotlightC Protein Is Essential for Canine Distemper Virus Virulence and Pathogenicity in FerretsThe measles (MeV) and canine distemper (CDV) viruses express accessory proteins that regulate the host’s immune response and enhance replication. The MeV C protein is critical in preventing the generation of excess immunostimulatory double-stranded RNA.