Viral Pathogenesis

Published on 18/02/2015 by admin

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Last modified 18/02/2015

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Chapter 19

Viral Pathogenesis

Factors Affecting Viral Virulence

Host range

Routes of viral entry into host cells

Tissue specificity (tropism)

1. Local infection without spread (e.g., rhinovirus, other common cold viruses)

2. Viremic spread from viral point of entry (e.g., measles, mumps, and chickenpox viruses) results in diseases with longer incubation periods.

3. Neuronal spread (e.g., rabies virus, HSV)

Support of viral replication by host cells

II Viral Cytopathogenesis

Pathogenic mechanisms

1. Major viral mechanisms for disrupting the structure and functioning of infected cells are summarized in Table 19-1.

TABLE 19-1

Viral Cytopathogenesis

Mechanism Representative Viruses
Inhibition of cellular protein synthesis Polioviruses, HSV, togaviruses
Inhibition of cellular DNA synthesis; degradation of DNA Herpesviruses
Alteration of cell membranes
 Glycoprotein insertion All enveloped viruses
 Syncytia (giant cell) formation HSV, varicella-zoster virus, paramyxoviruses, HIV
 Permeability changes Togaviruses, herpesviruses
Disruption of cytoskeleton Naked capsid viruses, HSV
Formation of inclusion bodies
 Negri bodies (cytoplasmic) Rabies
 Basophilic (owl’s eye) nuclear bodies Cytomegalovirus
 Cowdry type A nuclear bodies HSV
 Nuclear basophilic bodies Adenoviruses
 Acidophilic perinuclear bodies Reoviruses
Toxicity of virion components Adenovirus fibers
Immunosuppression HIV, cytomegalovirus, measles virus, influenza virus

HIV, human immunodeficiency virus; HSV, herpes simplex virus.

2. Appearance of characteristic inclusion bodies in infected cells facilitates laboratory diagnosis of infection by some viruses (e.g., rabies, HSV, and cytomegalovirus).

Types of infections