Re article in May 28 Observer:
Michael Worobey et al provide new explanations for the age distribution of mortality during the 1918 influenza pandemic. However, other factors also affected the pattern of influenza-related deaths.
Exposure to one influenza virus might affect the probability of infection by another virus years later, but it might not have the same effect on the risk of dying. Influenza mortality isn’t all about the immune response to the virus; underlying risk conditions are also important. In 1918, a 28-year-old woman who was pregnant had a much higher risk of dying than one who was not. Moreover, experimental influenza in pre-pubertal mice has a much lower mortality than it has in post-pubertal mice, and this has nothing to do with previous exposure to the influenza virus.
Worobey et al suggest that antibiotics and vaccines against pneumonia-causing bacteria might reduce pandemic mortality, but this is unlikely to happen. In outbreaks of seasonal influenza and in pandemics, only about one-third of fatal cases have had documented bacterial superinfection.
Worobey et al say that new influenza vaccines that mimic the lifetime protection afforded by initial childhood exposure to influenza might dramatically reduce mortality due to seasonal and pandemic influenza. Such vaccines might eventually be developed, but it is unlikely they will become globally available in the foreseeable future; a global influenza pandemic is much more likely. In the 2009 pandemic, the U.S. was better prepared than most countries to use vaccines, yet vaccination affected only 2-4 per cent of all pandemic cases, hospitalizations and deaths.
Effective reduction of pandemic mortality will probably require the use of drugs like statins, ACE inhibitors, and angiotensin receptor blockers that modify the host response to infection. Unfortunately, influenza scientists and health officials who support their work have shown almost no interest in undertaking research to show whether this approach would work.
David Fedson