H5N1's penchant for infecting type II rather than type I pneumocytes is due to the receptor preference found in avian viruses as opposed to human viruses, (including the 1918 ressortants used in the study), which primarily attack type I cells in the lung.
H5N1's attack on type II pneumocytes was sustained, from the point of initial infection through the 7 days of the study, as seen in figure 2. Examination of lung tissue showed widespread, prolonged replication of viruses and associated tissue destruction. "The fact that the infection of type II pneumocytes was so protracted directly contributed to the damage we saw," notes Baskin.
Another aspect of lung function debilitated by H5N1 involves the loss of surfactants, produced by type II pneumocytes and responsible for pliability of lung tissue. Without such surfactants, breathing becomes impossible.
The final act
A further critical finding of the study is that H5N1, having swamped the innate immune response, turns its attention next to the body's adaptive response, specifically, dendritic cells whose job it is to phagocytize protein components from the virus and present these to T cells, either locally or at the lymph nodes that drain the lungs. Normally, through this process, specific antibodies are then produced to combat the viral infection. Tissue sampling for the H5N1 found a notable absence of these dendritic cells, suggesting they were destroyed during the infection proce
|Contact: Joe Caspermeyer|
Arizona State University