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    Immune responses to viruses

    Via cytotoxic cells When a virus infects a person (host), it invades the cells of its host in order to survive and replicate. Once inside, the cells of the immune system cannot ‘see’ the virus and therefore do not know that the host cell is infected. To overcome this, cells employ a system that allows them to show other cells what is inside them – they use molecules called

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    Kerry Laing, Fred Hutchinson Cancer Research Centre, Seattle, USA

    Via cytotoxic cells

    When a virus infects a person (host), it invades the cells of its host in order to survive and replicate. Once inside, the cells of the immune system cannot ‘see’ the virus and therefore do not know that the host cell is infected. To overcome this, cells employ a system that allows them to show other cells what is inside them – they use molecules called class I major histocompatibility complex proteins (or MHC class I, for short) to display pieces of protein from inside the cell upon the cell surface. If the cell is infected with a virus, these pieces of peptide will include fragments of proteins made by the virus.

    A special cell of the immune system called a T cell circulates looking for infections. One type of T cell is called a cytotoxic T cell because it kills cells that are infected with viruses with toxic mediators. Cytotoxic T cells have specialised proteins on their surface that help them to recognise virally-infected cells. These proteins are called T cell receptors (TCRs). Each cytotoxic T cell has a TCR that can specifically recognise a particular antigenic peptide bound to an MHC molecule. If the T cell receptor detects a peptide from a virus, it warns its T cell of an infection. The T cell releases cytotoxic factors to kill the infected cell and, therefore, prevent survival of the invading virus (Figure 1).

    Viruses are highly adaptable, and have developed ways to avoid detection by T cells.  Some viruses stop MHC molecules from getting to the cell surface to display viral peptides. If this happens, the T cell doesn’t know there’s a virus inside the infected cell.

    However, another immune cell specialises in killing cells that have a reduced number of MHC class I molecules on their surface – this cell is a natural killer cell or NK cell for short.  When the NK cell finds a cell displaying fewer than normal MHC molecules it releases toxic substances, in a similar way to cytotoxic T cells, which kill the virally-infected cell.

    Cytotoxic cells are armed with preformed mediators. Cytotoxic factors are stored inside compartments called granules, in both cytotoxic T cells and NK cells, until contact with an infected cell triggers their release. One of these mediators is perforin, a protein that can make pores in cell membranes; these pores allow entry of other factors into a target cell to facilitate destruction of the cell. Enzymes called granzymes are also stored in, and released from, the granules. Granzymes enter target cells through the holes made by perforin.

    Once inside the target cell, they initiate a process known as programmed cell death or apoptosis, causing the target cell to die. Another released cytotoxic factor is granulysin, which directly attacks the outer membrane of the target cell, destroying it by lysis. Cytotoxic cells also newly synthesise and release other proteins, called cytokines, after making contact with infected cells.  Cytokines include interferon-g and tumour necrosis factor-a, and transfer a signal from the T cell to the infected, or other neighbouring cells, to enhance the killing mechanisms.

    Via interferons

    Virally infected cells produce and release small proteins called interferons, which play a role in immune protection against viruses. Interferons prevent replication of viruses, by directly interfering with their ability to replicate within an infected cell. They also act as signalling molecules that allow infected cells to warn nearby cells of a viral presence – this signal makes neighbouring cells increase the numbers of MHC class I molecules upon their surfaces, so that T cells surveying the area can identify and eliminate the viral infection as described above.

    Via antibodies

    Viruses can also be removed from the body by antibodies before they get the chance to infect a cell. Antibodies are proteins that specifically recognise invading pathogens and bind (stick) to them. This binding serves many purposes in the eradication of the virus:

    Firstly, the antibodies neutralise the virus, meaning that it is no longer capable of infecting the host cell.

    Secondly, many antibodies can work together, causing virus particles to stick together in a process called agglutination. Agglutinated viruses make an easier target for immune cells than single viral particles.

    A third mechanism used by antibodies to eradicate viruses, is the activation of phagocytes. A virus-bound antibody binds to receptors, called Fc receptors, on the surface of phagocytic cells and triggers a mechanism known as phagocytosis, by which the cell engulfs and destroys the virus.

    Finally, antibodies can also activate the complement system, which opsonises and promotes phagocytosis of viruses. Complement can also damage the envelope (phospholipid bilayer) that is present on some types of virus

    Source : www.immunology.org

    Viruses and interferon: a fight for supremacy

    The action of interferons (IFNs) on virus-infected cells and surrounding tissues elicits an antiviral state that is characterized by the expression and antiviral activity of IFN-stimulated genes. In turn, viruses encode mechanisms to counteract the host response and support efficient viral replication, thereby minimizing the therapeutic antiviral power of IFNs. In this review, we discuss the interplay between the IFN system and four medically important and challenging viruses — influenza, hepatitis C, herpes simplex and vaccinia — to highlight the diversity of viral strategies. Understanding the complex network of cellular antiviral processes and virus–host interactions should aid in identifying new and common targets for the therapeutic intervention of virus infection. This effort must take advantage of the recent developments in functional genomics, bioinformatics and other emerging technologies.

    Published: 01 September 2002

    Viruses and interferon: a fight for supremacy

    Michael G. Katze, Yupeng He & Michael Gale Jr

    volume 2, pages

    675–687 (2002)Cite this article

    22k Accesses 786 Citations 53 Altmetric Metrics details

    Key Points

    Interferons (IFNs) — the body's first line of antiviral defence — are cytokines that are secreted by host cells in response to virus infection. By inducing the expression of hundreds of IFN-stimulated genes, several of which have antiviral functions, IFNs block virus replication at many levels.

    The global antiviral state of the cell involves cross-talk between IFN signalling and pathways that regulate apoptosis, inflammation and cellular stress-response programmes.

    Viruses counteract the antiviral response by encoding mechanisms to control IFN signalling, block the actions of IFN-stimulated gene products and disrupt the various levels of cross-talk between IFNs and other cellular pathways. Studies of influenza virus, hepatitis C virus, herpes simplex virus and vaccinia virus highlight the importance of IFNs for the control of virus replication and pathogenesis.

    Studies of both host antiviral pathways and viral-counteracting strategies will greatly benefit from the recent development of functional-genomic technologies, such as microarrays, proteomics and DNA shuffling. Our 'virus compendium' — a multi-faceted, functional genomics effort focusing in the field of virus–host interactions — will be useful to assimilate these data.

    Abstract

    The action of interferons (IFNs) on virus-infected cells and surrounding tissues elicits an antiviral state that is characterized by the expression and antiviral activity of IFN-stimulated genes. In turn, viruses encode mechanisms to counteract the host response and support efficient viral replication, thereby minimizing the therapeutic antiviral power of IFNs. In this review, we discuss the interplay between the IFN system and four medically important and challenging viruses — influenza, hepatitis C, herpes simplex and vaccinia — to highlight the diversity of viral strategies. Understanding the complex network of cellular antiviral processes and virus–host interactions should aid in identifying new and common targets for the therapeutic intervention of virus infection. This effort must take advantage of the recent developments in functional genomics, bioinformatics and other emerging technologies.

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    Main

    Interferons (IFNs), although best known for their antiviral properties1,2, are potent regulators of cell growth3 and have immunomodulatory activity4. Indeed, an emerging theme is that these cytokines are important regulators of innate and adaptive immune responses. Furthermore, studies now highlight the importance of cross-talk between cellular regulatory pathways that control IFN signalling, apoptosis, inflammation and the stress response (Box 1). There are two main types of IFN, type I and type II. Type I or 'viral' IFNs include IFN-α, IFN-β, IFN-ω and IFN-τ; type II IFN is IFN-γ. Most types of cell can produce IFN-α and IFN-β, which are the best-characterized type I IFNs, whereas IFN-γ is produced only by certain cells of the immune system, including natural killer (NK) cells, CD4+ T helper 1 (TH1) cells and CD8+ cytotoxic T cells. There are 14 different IFN-α genes, but only one IFN-β and one IFN-γ gene. IFNs mediate their effects through interactions with type-specific receptors, which are different and non-redundant for the type I and type II IFNs5. IFNα/β-receptor-knockout mice (as well as IFN-γ-receptor knockouts) cannot mount effective antiviral responses6,7. The IFN receptors do not have enzymatic activity, but they set in motion a complex signalling pathway that ultimately results in the transcription of hundreds of IFN-stimulated genes (ISGs) (Fig. 1 and Box 2). It is now clear that although IFN levels markedly increase in response to virus infection, the sequence of events, types of IFN that are produced and ISGs that are targeted have an important effect on the outcome.

    Figure 1: Overview of the IFN pathway and viral-counteracting strategies.

    Type I interferons (IFNs) are a group of antiviral cytokines that are induced during viral infection by viral-replication products, such as double-stranded (ds)RNA. IFNs exert their biological functions by binding to specific cell-surface receptors. In turn, this triggers the intracellular IFN signalling pathway — mainly the JAK–STAT pathway (see Box 2 figure) — which eventually induces the expression of a large number of IFN-stimulated genes (ISGs). The ISGs, the workhorses of the IFN response, set up an antiviral, antiproliferative and immunoregulatory state in the host cells. However, most, if not all, viruses have evolved a broad spectrum of strategies to block and interfere with the IFN pathway. Common viral strategies include a | blocking of IFN induction/expression b | intercepting receptor binding of IFNs through viral decoy IFN receptors c | perturbation of the intracellular IFN signalling pathway and d | directly downregulating the level of expression of ISGs. ADAR, RNA-specific adenosine deaminase; IRF, IFN-regulatory factor; JAK, Janus kinase; Mx, myxovirus-resistance proteins; OAS, oligoadenylate synthetase; PKR, protein kinase; STAT, signal transducer and activator of transcription.

    Source : www.nature.com

    How do interferons protect against viral infection in healthy cells?

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    How do interferons protect against viral infection in healthy cells?

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    How do interferons protect against viral infection in healthy cells?

    Viruses:

    Viruses are parasites that consist of a genome of RNA or DNA that is enclosed in a protein shell called a capsid. Many important human diseases like AIDS and Ebola are caused by viruses.

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    What Are Cytokines? - Definition, Types & Function

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    Chapter 9 / Lesson 10

    113K

    Cytokines are a group of immune system proteins that affect the actions of other cells. Explore the definition, understand the function of cytokines, and learn about the various types: chemokines, interferons, interleukins, lymphokines, and tumor necrosis factor.

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