apoptosis
- Virus-Cell InteractionsHuman Parainfluenza Virus Type 2 V Protein Modulates Iron Homeostasis
hPIV-2 V protein interferes with interaction between FTH1 and NCOA4 and inhibits NCOA4-mediated ferritin degradation, leading to the inhibition of iron release to the cytoplasm. This iron homeostasis modulation allows infected cells to avoid apoptotic cell death, resulting in effective growth of hPIV-2.
- Virus-Cell InteractionsType I Interferon Acts as a Major Barrier to the Establishment of Persistent Infectious Bursal Disease Virus Infections
Members of the Birnaviridae family, including infectious bursal disease virus (IBDV), exhibit a dual behavior, causing acute infections that are often followed by the establishment of lifelong persistent asymptomatic infections. Indeed, persistently infected specimens might act as efficient virus reservoirs, potentially contributing to virus dissemination.
- Virus-Cell InteractionsClassical Swine Fever Virus Npro Antagonizes IRF3 To Prevent Interferon-Independent TLR3- and RIG-I-Mediated Apoptosis
Responsible 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.
- Genome Replication and Regulation of Viral Gene ExpressionSuberoyl Bis-Hydroxamic Acid Reactivates Kaposi’s Sarcoma-Associated Herpesvirus through Histone Acetylation and Induces Apoptosis in Lymphoma Cells
Kaposi’s sarcoma and primary effusion lymphoma cells are latently infected with Kaposi’s sarcoma-associated herpesvirus (KSHV), whereas KSHV replication is frequently observed in multicentric Castleman disease. Although KSHV replication can be induced by some chemical reagents (e.g., 12-O-tetradecanoylphorbol-13-acetate), the mechanism of KSHV replication is not fully understood.
- Virus-Cell InteractionsA Gammacoronavirus, Avian Infectious Bronchitis Virus, and an Alphacoronavirus, Porcine Epidemic Diarrhea Virus, Exploit a Cell Survival Strategy by Upregulating cFOS To Promote Virus Replication
The ongoing pandemic of coronavirus disease 2019 (COVID-19), caused by a newly emerged zoonotic coronavirus (severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2]), highlights the importance of coronaviruses as human and animal pathogens and our knowledge gaps in understanding the cellular mechanisms, especially the mechanisms shared among human and animal coronaviruses, exploited by coronaviruses for optimal replication and...
- Cellular Response to InfectionTelomere and ATM Dynamics in CD4 T-Cell Depletion in Active and Virus-Suppressed HIV Infections
The hallmark of HIV infection is a gradual depletion of CD4 T cells, with a progressive decline of host immunity. How CD4 T cells are depleted in individuals with active and virus-suppressed HIV infection remains unclear. In this study, we employed a cellular model of HIV infection to characterize the mechanisms underlying CD4 T-cell destruction by analyzing the chromosome end (telomere) DNA damage response (DDR) and cellular apoptosis...
- Pathogenesis and Immunity | SpotlightSelective Interferon Responses of Intestinal Epithelial Cells Minimize Tumor Necrosis Factor Alpha Cytotoxicity
Enteric viral infections are a major cause of gastroenteritis worldwide and have the potential to trigger or exacerbate intestinal inflammatory diseases. Prior studies have identified specialized innate immune responses that are active in the intestinal epithelium following viral infection, but our understanding of the benefits of such an epithelium-specific response is incomplete. Here, we show that the intestinal epithelial antiviral...
- Virus-Cell InteractionsAntiapoptotic Clone 11-Derived Peptides Induce In Vitro Death of CD4+ T Cells Susceptible to HIV-1 Infection
Although antiretroviral treatment efficiently blocks HIV multiplication, it cannot eliminate cells already carrying integrated proviruses. In the search for an HIV cure, the identification of new potential targets to selectively eliminate infected cells is of the outmost importance. We show here that peptides derived from antiapoptotic clone 11 (AAC-11), whose expression levels correlated with susceptibility to HIV-1 infection of CD4...
- Transformation and OncogenesisPolyomavirus Small T Antigen Induces Apoptosis in Mammalian Cells through the UNC5B Pathway in a PP2A-Dependent Manner
UNC5B, PP2A, and netrin-1 are deregulated in a variety of cancers. UNC5B and PP2A are regarded as tumor suppressors, as they promote apoptosis and are deleted or mutated in many cancers. In contrast, netrin-1 promotes survival by inhibiting dependence receptors, including UNC5B, and is upregulated in many cancers. Here, we show that UNC5B-mediated apoptosis can occur independently of p53 but in a PP2A-dependent manner. A substantial...
- Transformation and OncogenesisBeta Human Papillomavirus 8E6 Attenuates LATS Phosphorylation after Failed Cytokinesis
β-HPVs contribute to cSCC development in immunocompromised populations. However, it is unclear if these common cutaneous viruses are tumorigenic in the general population. Thus, a more thorough investigation of β-HPV biology is warranted. If β-HPV infections do promote cSCCs, they are hypothesized to destabilize the cellular genome. In vitro data support this idea by demonstrating the ability of the β-HPV E6 protein to disrupt...