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    Steps in Viral Pathogenesis-Lecture Three

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    The document outlines the key steps in viral pathogenesis: 1. Entry and primary replication occurs when a virus attaches and enters host cells, usually at the site of entry. Some viruses only produce disease locally while others spread systemically. 2. Viral spread and cell tropism involves viruses traveling from the initial site of entry, often via blood or lymphatics, and targeting specific host cell types through receptor binding. 3. Cell injury and clinical illness result from destruction of infected cells and physiological changes caused by tissue damage, leading to disease development. The host may recover through immune responses and clearance of the virus.

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    Steps in Viral Pathogenesis-Lecture Three

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    IM CT
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    The document outlines the key steps in viral pathogenesis: 1. Entry and primary replication occurs when a virus attaches and enters host cells, usually at the site of entry. Some viruses only produce disease locally while others spread systemically. 2. Viral spread and cell tropism involves viruses traveling from the initial site of entry, often via blood or lymphatics, and targeting specific host cell types through receptor binding. 3. Cell injury and clinical illness result from destruction of infected cells and physiological changes caused by tissue damage, leading to disease development. The host may recover through immune responses and clearance of the virus.

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    The document outlines the key steps in viral pathogenesis: 1. Entry and primary replication occurs when a virus attaches and enters host cells, usually at the site of entry. Some viruses only produce disease locally while others spread systemically. 2. Viral spread and cell tropism involves viruses traveling from the initial site of entry, often via blood or lymphatics, and targeting specific host cell types through receptor binding. 3. Cell injury and clinical illness result from destruction of infected cells and physiological changes caused by tissue damage, leading to disease development. The host may recover through immune responses and clearance of the virus.

    Copyright:

    © All Rights Reserved
    Download as DOC, PDF, TXT or read online from Scribd
    Download as doc, pdf, or txt
    124 views3 pages

    Steps in Viral Pathogenesis-Lecture Three

    Uploaded by

    IM CT
    The document outlines the key steps in viral pathogenesis: 1. Entry and primary replication occurs when a virus attaches and enters host cells, usually at the site of entry. Some viruses only produce disease locally while others spread systemically. 2. Viral spread and cell tropism involves viruses traveling from the initial site of entry, often via blood or lymphatics, and targeting specific host cell types through receptor binding. 3. Cell injury and clinical illness result from destruction of infected cells and physiological changes caused by tissue damage, leading to disease development. The host may recover through immune responses and clearance of the virus.

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    of 3

    Clinical Virology / Lecture No. Three / Dr. B. A.

    Al-
    Haidary

    Steps in Viral Pathogenesis:

     Entry & Primary Replication: In order for host infection to occur, a


    virus must first attach to and enter the cells of one body surfaces. Virus
    usually replicate at the primary site of entry . Some produce disease at the
    portal of entry & have no necessity for further systemic spread. They
    spread locally over the epithelial surfaces, but there is no invasion of
    underlying tissues or spread to distant sites.

     Viral Spread & Cell Tropism: Many viruses produce dz. at sites
    distant from their point of entry. After primary replication at the site of
    entry , viruses then spread within the host. Mechanism of spread vary but
    the most common route is via blood stream or lymphatics. Viremia
    occurs in two form either the virus free in plasma or associated with a
    particular cells. Some viruses even multiply within these cells. The
    viremic phase is short in many viral infections.
    The tendency to exhibit organ and cell specificities. Such
    tissue & cell tropism by a given virus reflects the presence of specific
    cell surface receptors for that virus. These receptors are of normal cell's
    constituents with high affinity for a particular virus.
    Factors affecting cell tropism & gene expression are:
    1. Enhancer regions 2. Proteolytic enzymes. 3.Viral Genes.

     Cell injury & Clinical Illness: Destruction of virally infected cells


    & physiological alteration produced in the host by the tissue injury are
    partially responsible for dz. development Inapparent infection by viruses
    are very common.

     Recovery from Infection: The host either succumbs or recovers


    from viral infection. Recovery mechanisms involve Humoral & cell-
    mediated immunity, Interferon & other Cytokines and other host defense
    mechanisms. In acute infections, recovery is associated with viral
    clearance. However, there are times when the host remains persistently
    infected with the virus.

     Virus Shedding: The last stage in pathogenesis is the shedding of


    infectious virus into environment. This is necessary step to maintain a
    viral infection in the populations of hosts. Shedding usually occurs from
    the body surfaces involved in viral entry.

    1
    Clinical Virology / Lecture No. Three / Dr. B. A. Al-
    Haidary
    Host Immune Response:
    Both humoral & cellular immune response involved in control
    of viral infection.
    Virus-encoded proteins serve as targets for the immune
    response. Cytotoxic T lymphocytes play the major role in lysis of virally
    infected cell in addition to NK cells. Humoral immunity protects the host
    against reinfection by the same virus. Viral neutralizing Ab blocks the
    initiation of viral infection. Secretory IgA Ab is important in protecting
    against by viruses at the mucosal surfaces.
    Moreover some non-specific host defense mechanisms may be
    elicited by viral infection. The most prominent among the "nonimmune"
    responses is the induction of Interferons.

    Interferon: It is a hormone like protein secreted by the virally infected


    cells in addition to other cells. It acts to protect other cells from viral
    infection by blocking the mechanism of viral replication. I t characterized
    by :
    1. Unlike antibody interferon is non-specific.
    2. It acts in very minute amounts.
    3. It appears and elevates before the antibody production.
    4. Interferon is classified into three subclasses:
    A- α- INF which secreted by leukocytes.
    B- β- INF which synthesized by fibroblast.
    C- γ- INF which produced mainly by lymphocytes.
    5. This cytokine enhances or activates NK .

    Viral Persistence: Chronic, Latent & Slow Virus Infections:


    Virus infections are usually self-limiting infection. Sometimes,
    however, the virus persists for long periods of times in the host. Long-
    term virus-host interaction may take several form:

    1. Chronic infections: Those are in which virus can be continuously


    detected; mild or no clinical symptoms may be evident. This persistence
    infection is age-dependent of the host when infected, such as rubella &
    CMV infections . Hepatitis-B virus frequently become persistently
    [chronic carriers]

    2. Latent infections: the infections in which the virus persists in an


    occult, or cryptic, form most of the time. There will be intermittent

    2
    Clinical Virology / Lecture No. Three / Dr. B. A. Al-
    Haidary

    flare-up of clinical dz; infectious virus can be recovered during flare-up.


    Herpes simplex viruses typically produe latent infections.

    3. Slow virus infections: The infection in which the virus has a prolonged
    incubation period, lasting months or years, during which virus
    continues to multiply. Clinical symptoms are usually not evident during
    the long incubation period. Spongiform encephalopathies are a group of
    chronic, progressive, fatal infections of the central nervous system
    caused by unconventional, transmissible agents. The best example of
    this slow virus infection is crappie in sheep, Kuru and Cretzfeldt-Jacob
    dz. occur in human with unknown mechanism for inducing these agent
    the human dz.

    4. Inapparent or Subclinical Infection: They are give no overt clinical


    sign of their presence at the host-parasite level.

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