What is the pathophysiology of viral pneumonia?

Updated: Mar 24, 2021
  • Author: Zab Mosenifar, MD, FACP, FCCP; Chief Editor: John J Oppenheimer, MD  more...
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A full understanding of the pathophysiology and pathogenesis of viral diseases does not presently exist.

After contamination, most respiratory viruses tend to multiply in the epithelium of the upper airway and secondarily infect the lung by means of airway secretions or hematogenous spread. Severe pneumonias may result in extensive consolidation of the lungs with varying degrees of hemorrhage, with some patients developing bloody pleural effusions and diffuse alveolar damage. [10]

The mechanism of damage to tissues depends on the virus involved. Some viruses are mainly cytopathic, directly affecting the pneumocytes or the bronchial cells. With others, overexuberant inflammation from the immune response is the mainstay of the pathogenic process.

Immune responses can be categorized according to patterns of cytokine production. Type 1 cytokines promote cell-mediated immunity, while type 2 cytokines mediate allergic responses. Children infected with respiratory syncytial virus (RSV) who develop acute bronchiolitis, rather than mild upper respiratory infection symptoms, have impaired type 1 immunity or augmented type 2 immunity. [11]

In addition to humoral responses, cell-mediated immunity appears to be important for recovery from certain respiratory viral infections. [12] Impaired type 1 response may explain why immunocompromised patients have more severe viral pneumonias.

Respiratory viruses damage the respiratory tract and stimulate the host to release multiple humoral factors, including histamine, leukotriene C4, and virus-specific IgE in RSV infection and bradykinin, interleukin (IL)–1, IL-6, and IL-8 in rhinovirus infections. RSV infections can also alter bacterial colonization patterns, increase bacterial adherence to respiratory epithelium, reduce mucociliary clearance, and alter bacterial phagocytosis by host cells.

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