In March 2007 a two-year-old boy in Chicago contracted the smallpox virus from his father, a soldier who had recently been vaccinated prior to a tour of duty in Iraq. Only an all-out response from a Who's Who of U.S. infectious disease experts saved the boy, who had become a victim, it appears, because of an immune defect associated with eczema.
Why does this matter to you? Or to me? I read this article in Science (sorry about the paywall) at the time and the story just leaped off the page at me. It's scary. If you have eczema, you basically shouldn't get vaccinated for smallpox because the risk of dying is too high. And the effects aren't pretty.
(You may notice that I never post images of this stuff. That's my policy. I have eczema, and it grosses me out enough on my own body that I don't need to see it on anyone else's. I eat dinner after writing these posts.)
In the year following that nasty discovery, the NIH founded a research group called the Atopic Dermatitis and Vaccinia Network (ADVN) to look into why vaccinia virus can cause such an extreme reaction. Vaccinia is closely related to variola, the agent of smallpox, and used as the vaccine. In most people, it's benign. An ADVN group at the La Jolla Institute for Allergy and Immunology found that levels of "natural killer" cells, a class of white blood cells, are low in a strain of mice used as models for atopic dermatitis, and which develop "eczema vaccinatum," the same condition the Chicago boy nearly died from. In normal people, the theory is, natural killer cells somehow keep the virus in check.
Science is complicated-- this is one paper, and it's a mouse model, but you can imagine that these results might point the way to studies that could find similar results in humans, and possibly therapies to boost natural killer cells to prevent deadly reactions to vaccine. (The ADVN must have published reams of papers, and right now I have no idea what their most significant findings were. Will have to find out.)
The ADVN has now morphed into the ADRN, the Atopic Dermatitis Research Network, the group that in July received $31.5 million from the NIH to conduct extensive research over five years into why patients with eczema are susceptible to deadly microbial infections. In the NIH's original request for proposals for this funding, they define four research areas; the first two are eczema vaccinatum and staph infections. The second two are vaccine reactions and infections from other organisms. The constraint was that applicants had to pick one of the first two areas, plus one to three of the remaining three. The successful consortium, led by Donald Leung at National Jewish Health in Denver, appears to have picked staph infections as their primary focus, according to their press release.
I wrote to Leung and he informed me that the group has not yet determined a protocol for its experiments, but will have done so by the end of the year. I can't wait to find out the details. It is an undertaking of huge scope-- ten academic centers involved. Staphylococcus, and MRSA, is surely a worthy enemy to vanquish. Imagine bringing up a child with eczema knowing that because of what they discovered on this project, you didn't have to worry about runaway staph infections. Life might not be all smooth sailing, but the fear factor would be a lot lower.
Initially, I called the NIH media department, asking whether they made the details of grant applications public. They do not, and the officer directed me to contact the scientists directly. "I'm an eczema sufferer myself," he told me. "I understand why you want to know."
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