To the Editor —Occasionally, scientific discoveries sink into oblivion, and later investigators find difficulties in explaining forgotten connections. McCullers and Rehg [1] discuss the role that platelet-activating factor receptor (PAFr) plays in the lethal synergism between influenza virus and Streptococcus pneumoniae PAFr is an important factor in the attachment and invasion of cells by virulent pneumococcal strains. Different effects—that is, acid, inflammatory cytokines, and viral neuraminidase (NA)—are enhanced by the up-regulation of PAFr. Moreover, the authors discuss the cleavage of terminal sialic acid moieties by influenza NA-exposing cryptic receptors. In all of those ways, pneumococcus adheres and invades. NA is, indeed, a key influenza-virus pathogenic factor, as the new NA inhibitors show However, pneumococci also produce NA. Thirty years ago, several reports were published that describe the pathogenic role that NA plays in pneumococcal infections [2–5]. The NAs of influenza virus and of pneumococcus are likely to be synergistic, although pneumococcal NA is more powerful because of its stronger activity and broader substrate spectrum [6]
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Hans E. Müller (2003) studied this question.
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