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Immunity Against Viruses


Viruses are small particles which infect living cells; this makes them obligate intracellular parasites. They have no reproductive mechanisms of their own so instead must use host cells to replicate. There are two main threats for a virus; the host’s immunity and the death of the host. Both of which will typically prevent the virus from propagating.

Many viruses are able to survive within the host for a long time without causing disease to the primary host. However when this virus is transferred to a secondary host, it is possible for a lethal disease to arise as a result. (An example is the transmission of the rabies virus to man). Vaccinating against the harmful effects of a virus therefore works best in the secondary host where the virus is not well adapted.

Structure of a Virus

Particles of a virus are known as virions. Virions encapsulate the nucleic acid core, which is surrounded by a layer of lipoprotein (or protein); this is known as the capsid. The degree of complexity of a virus can differ greatly. Viruses can contain either RNA or DNA and they can be either single stranded or double stranded, any combination of these still allows the virus (once in the host cell) to replicate.

Viral Pathogenicity

The virion is able to bind to a wide range of molecules to mediate attachment and internalisation by a host cell (by endocytosis). Once inside the cell, the capsid of the virion breaks down releasing the viral nucleic acid into the cytoplasm of the host cell. Once inside the cytoplasm, the viral nucleic acid is able to replicate and at the same time, it is also able to inhibit the production of DNA/RNA (thus protein synthesis) of the host cell.

Possible outcomes for a cell infected by a virus:

  • Lytic Infection – Host cell is destroyed, this is caused by virulent viruses
  • Persistent Infection – Host cell is not lysed, but virions are released slowly, over a longer period
  • Latent Infection – Occurs when there is a delay between the infection by the virus and the onset of symptoms
  • Transformation – Some viruses are able to transform a normal cell into a tumour cell



Time Scale

The immune response to a viral infection is typically as follows:

  • 1 hour after infection – Interferon (and other cytokine/interleukin) activity is stimulated
  • 3 hours after infection – NK cells are stimulated
  • 6-9 hours after infection – T-cell mediated killing is initiated
  • 7-9+ hours after infection – Antibody mediated anti-viral activities begin

Immune Responses to Viruses

Innate Immune Responses


An interferon (IFN) is an important anti-viral factor produced early (hours) in response to a viral infection. It is produced by cells in response to various infectious agents and bacterial endotoxins. Interferons mechanism of action is to interfere with the growth of viruses (and other intracellular organisms). Interferons are released locally protecting neighbouring cells from the virus, giving them anti-viral resistance.

Types of Interferon:

  • Type I interferons – Provide anti-viral resistance, stimulate NK activity against viral cells and promote NK secretion of IFNγ:
    • IFNβ and IFNα
    • Type II interferons – Provide anti-viral resistance, are used immunologically as a cytokine and can activate macrophages. They are secreted from normal tissue cells as well as T and NK cells. They prevent viral growth by the induction of nitric oxide secretion and stimulating IFN secretion:
      • IFNγ

Interferons give anti-viral resistance to cells by binding to viral receptors (not specific to each virus), preventing the translation of viral RNA; however normal host cell translation is not inhibited.

NK (Natural killer) Cells

NK cells are also part of the innate immune response, they origin from the same progenitor cell as T and B lymphocytes, but they differ as they are able to ‘kill’ virus-infected cells without the need for pre-sensitisation or Class I MHC expression. IFNα greatly enhances NK activity; this in turn stimulates the secretion of IFNγ which makes host cells more resistant to viral infection. This occurs a few hours after initial infection which is a little longer than the time taken for initial interferon anti-viral activity.

NK cells can only be activated by infected, damaged or malignant cells (not by healthy cells). Viruses use this for protection – they attempt to hide in host cells by blocking their MHC class I expression. This stops cytotoxic T cells responding to the infected host cell. However, the body recognises this and NK cells are activated by the reduced MHC expression from the host cell, the NK cell then destroys the infected host cell.

Acquired Immune Responses

Cytotoxic T-Cells (Tc)

Cytotoxic T-cells are considered more important for controlling viral infections than complement or antibodies. Cytotoxic T-cells destroy virus infected cells in a similar manner to rejected graft cells.

Shortly after a host cell is infected with a virus, virion proteins in association with MHC class I are expressed on the surface of the infected cells (although as above, some may prevent this in an attempt to prevent detection). The cytotoxic T-cells then recognise the cell as foreign and so are destroyed by the antigen-specific Tc.

Note how this differs from NK cells, requiring the expression of foreign proteins associated with MHC for the virus to be detected, whereas the NK cells do not require this.

It is possible for cytotoxic T-cells to destroy host cells without their dependence on MHC class I, but this only occurs when they are sufficiently activated by cytokines.


Antibodies can either lyse certain viruses/viral infected cells through the complement system (Membrane attack complex), or in combination with the appropriate leukocyte – they are able to destroy viral infected cells through antibody-dependent cell-mediated cytotoxicity (ADCC). They may also prevent the adhesion of viruses to host cells as well as agglutinating virus particles/infected cells together to make phagocytosis more efficient.

Antibodies recognise proteins on free virions as well as the proteins expressed in association with MHC on infected host cells. The antibodies recognise small protein sequences (epitopes) and bind to these.

In some cases it is possible for the binding of an antibody and the activation of complement may enable the spread of a virus by enabling infection by endocytosis by attachment to the Fc portion of the antibodies and C3 receptors. (E.g. African swine fever)

Evasion of Immunity

The evolution of viruses has made them very adept at evading these immune responses. Any attempts to remove the virus infection can take a long time; prolonged immune responses however can lead to detrimental pathological changes to the host causing damage or infection of neighbouring cells.

Methods of Evasion

  • Interfering with interferons – The virus can inhibit the production of IFNγ in infected cells by production of IL-10 analogues or synthesise soluble IFN receptors
  • Survive phagocytosis – By surviving phagocytosis, viruses are able to continue to proliferate (e.g. Foot and mouth)
  • Inhibit apoptosis – The inhibition of MHC class I expression prevents the viral infected cell from being destroyed
  • Evade antibody responses – By altering the proteins expressed by the virus, the virus is able to continually evade antibodies. This can occur by; mutation of certain viral sequences allowing antigenic variation to arise (such as the influenza virus), antigenic drift due to recombination of viral DNA/RNA, the replacement of antigenic viral proteins or poor expression of antigenic proteins
  • Inducing immunosuppression – This can occur when the virus infects B or T cells, the infection spreads to the thymus and tolerance to the virus is induced. The virus is then able to destroy antigen presenting cells and modulate the balance of T-Helper cells
  • Evading T-cell responses – The virus infects cells lacking in expression of MHC class I and inhibits any further production of MHC. This prevents the expression of viral protein on the surface.
  • Stress – Stress can lower the immune efficiency and cause the induction of latent infections.

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