What is the mechanism of viral injury?

Mechanisms of Viral Injury

1. Viral Tropism (Tissue and Cell Specificity)

  • Host receptors for viruses
    Viruses are coated with surface proteins that bind with high specificity to particular host cell surface proteins. Entry of many viruses into cells commences with binding to normal host cell receptors. For example, HIV glycoprotein gp120 binds to CD4 and CXCR4 and CCR5 on T cells and macrophages. Host proteases may be needed to enable binding of the virus to host cells; for instance, a host protease cleaves and activates the influenza virus hemagglutinin.

  • Specificity of transcription factors
    The ability of the virus to replicate inside particular cell types depends on the presence of lineage-specific transcription factors that recognize viral enhancer and promoter elements. For example, the JC virus, which causes leukoencephalopathy, replicates only in oligodendroglia in the CNS because the promoter and enhancer DNA sequences regulating viral gene expression are active in glial cells but not in neurons or endothelial cells.

  • Physical characteristics of tissues
    Host environment and temperature can contribute to tissue tropism. For example, enteroviruses replicate in the intestine in part because they can resist inactivation by acids, bile, and digestive enzymes. Rhinoviruses infect cells only within the upper respiratory tract because they replicate optimally at the lower temperatures characteristic of this site.

2. Mechanisms of Host Cell Damage

  • Direct cytopathic effects
    Viruses can kill cells by preventing synthesis of critical host macromolecules, by producing degradative enzymes and toxic proteins, or by inducing apoptosis. For example, poliovirus blocks synthesis of host proteins by inactivating cap-binding protein. HSV produces proteins that inhibit synthesis of cellular DNA and mRNA and other proteins that degrade host DNA. Viral replication also can trigger apoptosis of host cells by cell-intrinsic mechanisms such as perturbations of the endoplasmic reticulum during virus assembly, which can activate caspases that mediate apoptosis.

  • Anti-oral immune responses
    Viral proteins on the surface of host cells may be recognized by the immune system, and lymphocytes may attack virus-infected cells. Cytotoxic T lymphocytes (CTLs) are important for combating viral infections, but CTLs also can be responsible for tissue injury. Hepatitis B infection comes from CTL-mediated destruction of infected hepatocytes, a normal response that is attempting to clear the infection.

  • Transformation of infected cells
    Different oncogenic viruses (e.g., HPV, EBV) can stimulate cell growth and survival by a variety of mechanisms, including hijacking the control of cell cycle machinery, anti-apoptotic strategies, and insertional mutagenesis (in which the insertion of viral DNA into the host genome alters the expression of nearby host genes). Mechanisms of viral transformation.


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