PopCulture
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- Jan 11, 2011
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Like Tiger Blood.
The CCR5 mutation is helpful against HIV because HIV uses it as a coreceptor. It doesn't play a similar role in influenza and might actually correlate with a worse prognosis for viruses other than HIV.
I think that is still under debate by the medical community.
CCR5 is supposed to be a result of small pox killing off the majority of people in Europe that did not have the gene. But then again, some people in the medical community think that its a result of the bubonic plague, and not small pox.
How else do you explain why certain demographic groups have higher fatality rates to the flu then others? When the swine flu broke out in Mexico there were several deaths. When the swine flu hit the USA, there were a lot fewer deaths then what Mexico had.
I think that is still under debate by the medical community.
CCR5 is supposed to be a result of small pox killing off the majority of people in Europe that did not have the gene. But then again, some people in the medical community think that its a result of the bubonic plague, and not small pox.
If CCR5 is the result of small pox, then that is at least 2 viruses
How else do you explain why certain demographic groups have higher fatality rates to the flu then others? When the swine flu broke out in Mexico there were several deaths. When the swine flu hit the USA, there were a lot fewer deaths then what Mexico had.
the delta 32 might indeed explain some of it, but opposite of the way you're suggesting.
http://www.cdc.gov/eid/content/16/10/1621.htm
The frequency of CCR5Δ32 heterozygosity among white populations has been reported to range from 10% to 15% (12,13); we found CCR5Δ32 heterozygosity at a higher than expected frequency (55.5%) among white patients with critical illness caused by pandemic (H1N1) 2009. Although deficiency of the receptor protects against acquisition of HIV, evidence is accumulating to suggest it plays a role in severity of illness caused by flavivirus infections (7,8). In animal models of influenza, CCR5 plays a role in directing CD8+ T cells to the site of infection, and its absence is associated with increased mortality rates (9,10);
But, how do you explain why the Mexican population (where the CCR5 gene is diluted from the Spanish breeding with native Mexicans) had such a negative response to H1N1?
I don't have an explanation. I'm not sure if anyone really does.Yes, I saw that same report a few months ago.
But, how do you explain why the Mexican population (where the CCR5 gene is diluted from the Spanish breeding with native Mexicans) had such a negative response to H1N1?
Yes, CCR5 is almost certainly a factor in flu resistance. The delta32 allele seems to cause increased severity of infection in humans. This is a fact in mouse models and supported by correlative evidence in humans, and in theory by what we know of its function.Even though the science has not been confirmed, I think CCR5 can be a factor in flu resistance.
As I've already said in this thread; there is far, far more to it than simply the genetics of the inhabitants. Socioeconomic conditions, common co-morbidities, access to medical care, quality of medical care (supportive), etc. played a large factor.
Everything you listed is a factor, but I think genetics plays a deciding factor in how people respond to infection.
Take a look at Africa, and their rate of HIV infection.
Native Americans, and how they responded to whooping cough and small pox.
Strangely, blacks did not share the same weaknesses to whooping cough and small pox like what the native Americans did. On islands like cuba where the native islanders died off due to European diseases, black were imported from Africa to harvest sugar cane, and the blacks did not die off like what the native islanders did.
With a flat base line, all things equal, genetics and previous exposure plays the deciding factor.
Vitamin C to the max. Who knows if it really works, but I had that and a few airborne pills and I stayed in bed.
You think there is a flat base line, all things equal, between the United States .. and impoverished Africa?
Your singling out 1 sentence of a whole paragraph that discusses how different races handle virus exposure.
If genetics does not play a major part in viral resistance, in the 1500s - 1800s, why did small pox kill millions of native Americans, but blacks imported straight from Africa did not die off at the same rate?
During outbreaks of the Black Death in 1348 and 1666, it was noted time and time again that the plague seemed to hit some families harder then others. The plague would skip 1 household, and then kill everyone in the next house - insinuating that certain families had a natural resistance. This natural resistance could only have been through genetics.
I never said that genetics do not play a major part in resistance. Of course they do, but you're implying that genetics are the deciding factor, which I would heavily disagree with.