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Chapter 19 : Immunity to Viruses

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Abstract:

Although biologically and genetically simple by comparison to other organisms, viruses nonetheless have potent means to evade the immune response, indicating that their genetic constitution is sufficient for them to be adept at confounding and frustrating both innate and acquired immunity. The antiviral antibodies directed to antigens on the viral surface, referred to as envelope or capsid antigens, are the most effective in controlling and clearing viral infections, although antibodies to other viral components, such as enzymes involved in replication or proteins found in the core of the virus particle, also are present in the host and may be beneficial. With enveloped viruses, the membrane of the virus fuses with the host-cell membrane and the viral capsid enters the cell, where it is degraded by intracellular proteolytic enzymes, releasing the viral genome into the host-cell cytoplasm. Disruption of the mitotic spindle apparatus in cells infected with some types of viruses produces crescent-shaped bodies in their cytoplasm. Many viruses have developed mechanisms to modulate the host’s defense system. Poxviruses also encode soluble receptors for interferon (IFN)- γ, tumor necrosis factor (TNF)- α and -β, and interleukin-10 (IL-10), enabling them to prevent these cytokines from binding to their receptors on natural killer (NK) cells and cytotoxic T lymphocytes (CTLs) involved in controlling the virus. Although viruses are generally cytopathic, some viral infections lead to chronic production of virus, dormancy, or in some cases, oncogenesis.

Citation: Barker E. 2004. Immunity to Viruses, p 453-468. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch19

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Figures

Image of Figure 19.1
Figure 19.1

Interferon can control viral infections by binding to receptors on cells infected with the virus or on neighboring uninfected cells and prevent further spread of the virus. The binding of interferon to its receptor inhibits synthesis of viral protein by induction of DAI (double-stranded RNA-activated inhibitor of translation; also called RNA-dependent protein kinase, or PKR). Upon interaction with its receptors, interferon can increase the expression of MHC class I molecules, which enhances the destruction of infected cells by CTLs and prevents uninfected cells from being killed by NK cells. Upon interaction with specific receptors on NK cells, interferon can increase their capacity to kill virus-infected cells that have decreased MHC class I molecules on their surface and/or are coated with antiviral antibodies.

Citation: Barker E. 2004. Immunity to Viruses, p 453-468. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch19
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Image of Figure 19.2
Figure 19.2

NK cells can control viral infections in several ways. (i) MHC class I molecules on the surface of the infected cells are downmodulated by the virus to evade killing by CTLs. This reduction in the expression of MHC class I triggers the NK cells to kill the infected cells though their ability to induce apoptosis. (ii) NK cells, through their Fc receptors, recognize the infected cells coated with antiviral antibodies and destroy them via perforin/granzymes or Fas-Fas-L interactions through the mechanism of ADCC. (iii) NK cells produce increased amounts of IFN-γ following exposure to IL-12 (produced by antigenpresenting cells during antiviral immune responses). IFN-γ can then bind to receptors and control or prevent the production of virus.

Citation: Barker E. 2004. Immunity to Viruses, p 453-468. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch19
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Image of Figure 19.3
Figure 19.3

Antibody-dependent control of viruses. Antibodies directed to viral epitopes can control HIV infection in several ways. The antibodies (blue) can prevent a viral ligand (green) from binding to the host-cell receptor (red) and entering the host cell. If a virus succeeds in infecting a cell, the antibody (blue) can recognize viral antigens (green) on the membrane of the infected cell. This can lead to lysis of the infected cell through the activation of complement (red) or by ADCC by activating NK cells expressing Fc receptors (purple), which in turn can induce the infected cell to undergo programmed cell death (apoptosis).

Citation: Barker E. 2004. Immunity to Viruses, p 453-468. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch19
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Image of Figure 19.4
Figure 19.4

Stages of the response of CTLs to viruses. During an acute viral infection, the antiviral CTL response generally occurs in four phases: an induction phase, an AICD phase, a silencing phase, and a memory phase. During the induction phase, CTL precursors that can recognize specific antigens expressed by the virus develop into effector cells that replicate and are capable of responding to infected cells expressing the viral antigens and of destroying them. This leads to a decline in virus levels in the host. This stage is followed by the AICD stage, in which the CTL responding to another encounter with the viral antigen is programmed to die. This stage is marked by a plateau in the number of CTLs. The silencing phase is marked by a decrease in the number of CTLs. Despite this loss of a large number of virusspecific CTLs, some of these cells not only remain viable but also continue to be stable in the final phase of CTL responses, the memory phase. These memory cells are in a resting state but still have the ability to recognize specific viral antigens and to become reactivated when the host encounters the virus again.

Citation: Barker E. 2004. Immunity to Viruses, p 453-468. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch19
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Image of Figure 19.5
Figure 19.5

Schematic cross-section of a rhabdovirus particle. The virus is an enveloped virus with glycoproteins and matrix proteins embedded in the lipid bilayer. The viral capsid protein, together with the negative- sense single-stranded (ss) RNA, makes up the ribonucleocapsid core, which forms a helix structure. L and P are viral proteins that, when complexed together, form functional enzymes necessary for viral replication.

Citation: Barker E. 2004. Immunity to Viruses, p 453-468. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch19
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Image of Figure 19.6
Figure 19.6

Morphology of viruses. The structures of viruses of different families are separated into groups on the basis of whether they are enveloped or nonenveloped and whether their genome is RNA or DNA. ds, double-stranded; ss, single-stranded. Redrawn from J. A. Levy et al., , 3rd ed. (Prentice Hall, Englewood Cliffs, N.J., 1994), with permission.

Citation: Barker E. 2004. Immunity to Viruses, p 453-468. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch19
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Image of Figure 19.7
Figure 19.7

Different forms of viral DNA and RNA. Viral RNA can exist in either a linear single-stranded or double-stranded form. Viral DNA can exist as a single-stranded or double-stranded form in either a linear or circular form Double-stranded DNA may also exist in a linear form with covalently linked ends or have covalently linked terminal proteins

Citation: Barker E. 2004. Immunity to Viruses, p 453-468. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch19
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Image of Figure 19.8
Figure 19.8

Steps in infection of a cell by rhabdovirus. Virus attaches to its receptor on the host cell. Virus enters the cell by endocytosis of the cytoplasmic membrane. The viral envelope fuses with the endosome membrane, and the nucleocapsid enters the cytoplasm. Uncoating of the nucleocapsid occurs. The negative-sense viral RNA is transcribed into a positive-sense viral RNA. N, NS, M, G, and L are mRNAs encoding various viral protein components (see Fig. 19.5 for precise definitions). The positive-sense RNA serves as a template for the viral genome. The negative-sense RNA becomes incorporated into a new nucleocapsid. The nucleocapsid joins with the matrix protein at the host cell membrane. The virus buds from the cell.

Citation: Barker E. 2004. Immunity to Viruses, p 453-468. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch19
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References

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1. Grandvaux, N.,, B. R. tenOever,, M. J. Servant,, and J. Hiscott. 2002. The interferon antiviral response: from viral invasion to evasion. Curr. Opin. Infect. Dis. 15:259267.
2. Greber, U. F. 2002. Signalling in viral entry. Cell. Mol. Life Sci. 59:608626.
3. Jung, M. C.,, and G. R. Pape. 2002. Immunology of hepatitis B infection. Lancet Infect. Dis. 2:4350.
4. Klasse, P. J.,, and Q. J. Sattentau. 2002. Occupancy and mechanism in antibody-mediated neutralization of animal viruses. J. Gen. Virol. 83:20912108.
5. Klenerman, P.,, M. Lucas,, E. Barnes,, and G. Harcourt. 2002. Immunity to hepatitis C virus: stunned but not defeated. Microbes Infect. 4:5765.
6. Russell, J. H.,, and T. J. Ley. 2002. Lymphocyte-mediated cytotoxicity. Annu. Rev. Immunol. 20:323370.
7. Sieczkarski, S. B.,, and G. R. Whittaker. 2002. Dissecting virus entry via endocytosis. J. Gen. Virol. 83:15351545.
8. Taniguchi, T.,, and A. Takaoka. 2002. The interferon-alpha/beta system in antiviral responses: a multimodal machinery of gene regulation by the IRF family of transcription factors. Curr. Opin. Immunol. 14:111116.
9. Weiss, R. A. 2002. Virulence and pathogenesis. Trends Microbiol. 10:314317.
10. Zinkernagel, R. M. 2002. Anti-infection immunity and autoimmunity. Ann. N. Y. Acad. Sci. 958:36.

Tables

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Table 19.1

Some common diseases caused by viruses in humans

Citation: Barker E. 2004. Immunity to Viruses, p 453-468. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch19
Generic image for table
Table 19.2

Host-cell receptors for some human-pathogenic viruses

Citation: Barker E. 2004. Immunity to Viruses, p 453-468. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch19
Generic image for table
Table 19.3

Defense mechanisms used by viruses against immune responses

Citation: Barker E. 2004. Immunity to Viruses, p 453-468. In Pier G, Lyczak J, Wetzler L (ed), Immunology, Infection, and Immunity. ASM Press, Washington, DC. doi: 10.1128/9781555816148.ch19

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