Respiratory viral infections drive chemokine expression and exacerbate the asthmatic response

A number of investigations have linked respiratory vial infections and the intensity and subsequent exacerbation of asthma through host response mechanisms. For example, it is likely that the immune-inflammatory response to respiratory syncytial virus can cause a predisposition toward an intense inflammatory reaction associated with asthma, and adenovirus might cause exacerbation of the immune response associated with chronic obstructive pulmonary disease. In each of these situations, the host's immune response plays a critical mechanistic role through the production of certain cytokines and chemokines. Specific aspects of these augmented immune responses are determined by the biology of the virus, the genetic variability of the host, and the cytokine-chemokine phenotype of the involved tissue. For instance, the type 1/type 2 cytokine ratio in the airways during infection with rhinovirus determines how long the viral infection endures. By this same theory, it has been demonstrated that chemokine levels produced during respiratory syncytial virus infection determine host responses to later immune stimuli in the lung, with the potential to augment the asthmatic response. Further research in this area will clarify cytokines, chemokines, or cell targets, which will provide the basis for next-generation therapies.

Key words: Asthma, chemokine, exacerbation, pulmonary, respiratory virus, rhinovirus, influenza, respiratory syncytial virus, rhinovirus

Abbreviations used: BAL, Bronchoalveolar lavage, COPD, Chronic obstructive pulmonary disease, NLF, Nasal lavage fluid, OVA, Ovalbumin, RSV, Respiratory syncytial virus