November 18, 2006
H5N1 Flu Strains Mutate For Easier Human Spread

Yoshiro Kawaoka and colleagues at University of Wisconsin in Madisonj have found that some strains of H5N1 bird influenza have mutations that increase their ability to bind to human cells.

Two mutations in the viral hemagglutinin surface protein independently enable H5N1 influenza A virus to bind to human receptors, researchers report in Nature this week.

That's not good news. Avian influenza is highly lethal for infected humans.

Two mutations found in human patients increase binding of the virus to human cells.

Whereas viruses from chickens and ducks could only recognize avian receptors, some viruses from human patients could recognize both human and avian cell receptors. "Once we identified the differences between the isolates, we narrowed down the specific changes that make avian H5N1 recognize the 2,6 receptors," Kawaoka explained. The changes were just two mutations, at positions 182 and 192 on the hemagglutinin sequence.

Half the 250 people known to have been infected by H5N1 have died. If the virus mutates into a form that is transmitted easily between humans while still retaining much of its current lethality you would be well advised to buy a lot of supplies and avoid contact with other humans for several months while a vaccine gets developed.

A highly lethal H5N1 would probably become less lethal with time since less sick people will get around more and spread the disease more widely. So you are also better off avoiding the disease in the early months in hopes that if eventually exposed you'll get a less lethal version.

It is also possible that antibodies taken from infected people who recover could be extracted and used as treatment for those who get it later. So, again, don't be the first one on your block to get a pandemic influenza virus.

In a few years the risk from H5N1 or any other influenza strain will go down due to development of faster means to scale up and produce vaccines. Also, better drugs will be found for suppressing the excess inflammation response by which more deadly influenza strains probably kill.

Share |      Randall Parker, 2006 November 18 01:05 PM  Dangers Natural Bio

Doug said at November 25, 2006 6:23 PM:


John J. Cannell, M.D., and co-authors including Reinhold Vieth and Michael Holick have won acceptance by the journal Epidemiology and Infection (Cambridge University Press) of an article, "Epidemic influenza and vitamin D." The article is a review of the literature on vitamin D3 and respiratory illnesses, presenting evidence that the annual variation in frequency of influenza, influenza-like illness, and other infectious respiratory illnesses is due to changes in the innate and acquired immune systems resulting from seasonal variation in the intensity of the UVB radiation that reaches the earth from the sun, and consequent variation in vitamin D3 production in the skin and in the serum concentration of 25-hydroxy-vitamin-D3.

I've provided URLs for John Cannell's web site and the article's web page, and I've pasted in the abstract of the article. (I've also redacted Cannell's email address, below, in order to make it more difficult for web crawlers to collect it for spamming.)

Forthcoming article PDF (177 KB)
Epidemiology and Infection
Copyright © 2006 Cambridge University Press

Review Article

Epidemic influenza and vitamin D

J. J. CANNELL a1c1, R. VIETH a2, J. C. UMHAU a3, M. F. HOLICK a4, W. B. GRANT a5, S. MADRONICH a6, C. F. GARLAND a7 and E. GIOVANNUCCI a8
a1 Atascadero State Hospital, 10333 El Camino Real, Atascadero, CA, USA
a2 Mount Sinai Hospital, Pathology and Laboratory Medicine, Department of Medicine, Toronto, Ontario, Canada
a3 Laboratory of Clinical and Translational Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD
a4 Departments of Medicine and Physiology, Boston University School of Medicine, Boston, MA, USA
a5 SUNARC, San Francisco, CA, USA
a6 Atmospheric Chemistry Division, National Center for Atmospheric Research, Boulder, CO, USA
a7 Department of Family and Preventive Medicine, University of California San Diego, La Jolla, CA, USA
a8 Departments of Nutrition and Epidemiology, Harvard School of Public Health, Boston, MA, USA


In 1981, R. Edgar Hope-Simpson proposed that a ‘seasonal stimulus’ intimately associated with solar radiation explained the remarkable seasonality of epidemic influenza. Solar radiation triggers robust seasonal vitamin D production in the skin; vitamin D deficiency is common in the winter, and activated vitamin D, 1,25(OH)2D, a steroid hormone, has profound effects on human immunity. 1,25(OH)2D acts as an immune system modulator, preventing excessive expression of inflammatory cytokines and increasing the ‘oxidative burst’ potential of macrophages. Perhaps most importantly, it dramatically stimulates the expression of potent anti-microbial peptides, which exist in neutrophils, monocytes, natural killer cells, and in epithelial cells lining the respiratory tract where they play a major role in protecting the lung from infection. Volunteers inoculated with live attenuated influenza virus are more likely to develop fever and serological evidence of an immune response in the winter. Vitamin D deficiency predisposes children to respiratory infections. Ultraviolet radiation (either from artificial sources or from sunlight) reduces the incidence of viral respiratory infections, as does cod liver oil (which contains vitamin D). An interventional study showed that vitamin D reduces the incidence of respiratory infections in children. We conclude that vitamin D, or lack of it, may be Hope-Simpson's ‘seasonal stimulus’.

(Accepted August 5 2006)

c1 Atascadero State Hospital, 10333 El Camino Real, Atascadero, CA 93422, USA. (Email: jcannell[put an 'at' sign here]

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