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There was a long and bitter battle behind the scenes in western Africa. The observation was (and remains true) that for people exposed to the Ebola virus one of three things happen: (1) they get full-blown Ebola and die – about half the time; (2) they get full-blown Ebola but survive (*) – the other half of the time; and (3) they do not get noticeable symptoms.

So one question is why does one live through the fever? Part has to do with not being under-nourished, pregnant, very young, very old or otherwise weakened by some other medical condition like AIDS. Although there is no cure or vaccine, how soon (and how effectively) treatment for Ebola is started helps. But it was suspected that since Ebola had been around for a long time and we humans (and primates in general) are not all dead perhaps some people have a genetic advantage.

The asterisk above is they survive but are weakened as far as possibly being more susceptible to other diseases or even a relapse of Ebola. What the extent of this weakening is should be tracked. It won’t be. Of interest is whether there is a genetic component there also.

If there is a genetic component, one model might be if you have two good copies of a gene you are resistent; one good copy and one defective copy and you get Ebola but survive; both defective and you die. It is also possible  that multiple genes can be involved. The point was that DNA should be sequenced as samples were collected. Alas, no guarantee that knowing which genes, if any, were involved would lead to an understanding of what proteins those genes produced or influenced.

A very important aspect of tai chi chuan in particular and most martial arts in general is breathing. My favorite treatment of the subject in Cai Songfang’s book Wujishi Breathing Exercises (in English) published by the fine folks at Plum Publications (www.plumub.com).

So there I was plowing through human genome databases looking for genetic indicators of asthma. One is officially named “hepatitis A virus cellular receptor 1”, but known as HAVCR1 to those in a hurry. This gene is located on chromosome 5 in region q33.2 (base pairs 156,979,480 to 157,069,527). Related pseudogenes have been identified on chromosomes 4, 12 and 19. This location is not far from the interesting TIMD4 gene (at q33.3). TIMD stands for T-cell immunoglobulin and mucin domain or T-cell membrane protein.

I quote

“HAVCR1 MAY play a role in T-helper cell development and the regulation of asthma and allergic diseases. Receptor for TIMD4 (By similarity). May play a role in kidney injury and repair.(Microbial infection) Acts as a receptor for hepatitis A virus (PubMed:9658108). Acts as a receptor for ebolavirus and marburg virus by binding exposed phosphatidyl-serine at the surface of virion membrane (PubMed:21536871). Acts as a receptor for Dengue virus by binding exposed phosphatidyl-serine at the surface of virion membrane (PubMed:23084921).”