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A virus-infected cell releases viral particles that can infect nearby cells. However, the infected cell can protect neighboring cells against a potential infection of the virus by releasing interferons. In response to interferon, cells produce large amounts of an enzyme known as protein kinase R (PKR).
The precise role of double-stranded (ds)RNA is still widely investigated as a central player in the Interferon System. Groups have found that positive-strand RNA viruses and dsRNA viruses produced significant amounts of dsRNA, but the precise methods mammalian cells leverage to distinguish between self vs. non-self dsRNA have yet to be uncovered.
Interferon regulatory factors contain a conserved N-terminal region of about 120 amino acids, which folds into a structure that binds specifically to the IRF-element (IRF-E) motifs, which is located upstream of the interferon genes. [2] Some viruses have evolved defense mechanisms that regulate and interfere with IRF functions to escape the ...
An interferon-stimulated gene (ISG) is a gene that can be expressed in response to stimulation by interferon. [ 1 ] [ 2 ] Interferons bind to receptors on the surface of a cell, initiating protein signaling pathways within the cell.
Viral interference is considered the most common outcome of coinfection, or the simultaneous infection of a host by two or more distinct viruses. [5] The primary form of viral interference is known as superinfection exclusion, in which the initial infection stimulates a resistance to subsequent infection by related viruses.
The type-I interferons (IFN) are cytokines which play essential roles in inflammation, immunoregulation, tumor cells recognition, and T-cell responses. In the human genome, a cluster of thirteen functional IFN genes is located at the 9p21.3 cytoband over approximately 400 kb including coding genes for IFNα (IFNA1, IFNA2, IFNA4, IFNA5, IFNA6, IFNA7, IFNA8, IFNA10, IFNA13, IFNA14, IFNA16 ...
Adenovirus, herpes simplex virus, HSV-1 and HSV-2, as well as the negative-stranded RNA virus, vesicular stomatitis virus (VSV), have been shown to be able to activate a STING-dependent innate immune response. [14] STING deficiency in mice led to lethal susceptibility to HSV-1 infection due to the lack of a successful type I interferon response ...
Interferon gamma (IFNG or IFN-γ) is a dimerized soluble cytokine that is the only member of the type II class of interferons. [5] The existence of this interferon, which early in its history was known as immune interferon, was described by E. F. Wheelock as a product of human leukocytes stimulated with phytohemagglutinin, and by others as a product of antigen-stimulated lymphocytes. [6]