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Pastimes : SARS - what next? -- Ignore unavailable to you. Want to Upgrade?

To: Ilaine who wrote (751)	9/26/2003 5:23:34 PM
From: Henry Niman	Read Replies (1) \| Respond to of 1070

I agree with the critical comments. Here is the original paper which did not find significance in the broad group, but had borderline significance in a very subjective subgroup: Association of HLA Class I with Severe Acute Respiratory Syndrome Coronavirus Infection Marie Lin , Hsiang-Kuang Tseng , Jean A Trejaut , Hui-Lin Lee , Jun-Hun Loo , Chen-Chung Chu , Pei-Jan Chen , Ying-Wen Su , Ken Hong Lim , Zen-Uong Tsai , Ruey-Yi Lin , Ruey-Shiung Lin and Chun-Hsiung Huang BMC Medical Genetics 2003 4:9 (published 12 September 2003) Abstract (provisional) Background The human leukocyte antigen (HLA) system is widely used as a strategy in the search for the etiology of infectious diseases and autoimmune disorders. During the Taiwan epidemic of severe acute respiratory syndrome (SARS), many health care workers were infected. In an effort to establish a screening program for high risk personal, the distribution of HLA class I and II alleles in case and control groups was examined for the presence of an association to a genetic susceptibly or resistance to SARS coronavirus infection. Methods HLA-class I and II allele typing by PCR-SSOP was performed on 37 cases of probable SARS, 28 fever patients excluded later as probable SARS, and 101 non-infected health care workers who were exposed or possibly exposed to SARS coronavirus. An additional control set of 190 normal healthy unrelated Taiwanese was also used in the analysis. Results Woolf and Haldane Odds ratio (OR) and corrected P-value (Pc) obtained from two tails Fisher exact test were used to show susceptibility of HLA class I or class II alleles with coronavirus infection. At first, when analyzing infected SARS patients and high risk health care workers groups, HLA-B4601 (OR=2.08, P=0.04, Pc= n.s.) and HLA-B5401 (OR=5.44, P=0.02, Pc=n.s.) appeared as the most probable elements that may be favoring SARS coronavirus infection. After selecting only a "severe cases" patient group from the infected "probable SARS" patient group and comparing them with the high risk health care workers group, the severity of SARS was shown to be significantly associated with HLA-B4601 (P=0.0008 or Pc=0.0279). Conclusions Densely populated regions with genetically related southern Asian populations appear to be more affected by the spreading of SARS infection. Up until recently, no probable SARS patients were reported among Taiwan indigenous peoples who are genetically distinct from the Taiwanese general population, have no HLA-B4601 and have high frequency of HLA-B1301. While increase of HLA-B4601 allele frequency was observed in the "Probable SARS infected" patient group, a further significant increase of the allele was seen in the "Severe cases" patient group. These results appeared to indicate association of HLA-B*4601 with the severity of SARS infection in Asian populations. Independent studies are needed to test these results.

To: Ilaine who wrote (751)	9/26/2003 5:41:40 PM
From: Henry Niman	Read Replies (2) \| Respond to of 1070

The number of "severe" cases was very small, and the numbers in Taiwan are very controversial (WHO doubled the number of reported deaths because many died if SARS but were cremated before samples could be tested and were therefore classified as non-SARS). However, a quick analysis of some of the high profile cases suggests that the HLA associations are far from absolute. I doubt that Carlos Urbani was HLA-B46 (French WHO worker). Same for Pekka Aro (Finnish International Labor official). Age and underlying disease are the major risks factors for fatal SARS but Urbani and Aro were relatively young (46 and 53) and Aro happened to sit next to a Beijing official who had flown on the ill fated China Air flight 112 on March 15.

To: Ilaine who wrote (751)	9/27/2003 6:26:59 AM
From: Maurice Winn	Read Replies (2) \| Respond to of 1070

CB, a major urban myth these days is intended to be anti-racist, but is actually just absurd. It's the idea that we are all just the same. It's not true. Genetics is the basis for most of our lives. While environmental influences are significant in people [which is why we have big brains capable of learning lots of stuff about our surroundings], we are essentially DNA beings with billions of years of gene selection by biological warfare and through the slings and arrows of death by misadventure shaping our DNA into a record of all that has gone before in a probablistic way. We are all part of a very slow-running quantum computer, which tries all forms, creating all possible genetic states through mutation and combinations. Nearly all mutations, [99.999999999% at a guess], fail to make the grade and die in the attempt, either immediately or from later generations. It is a horrifically cruel way to design DNA for sentient, fearful and pain-suffering creatures. If engineers built aircraft, buildings or car brakes by randomly making all possible types, and just keeping those which didn't crash and kill, there would be uproar and lawsuits galore. But that's how nature does DNA engineering. One or two space shuttle crashes and there's uproar. Imagine if 99.99999999% of space shuttles were destroyed in action. It's a hell of a way for an omniscient, omnipotent and loving being to run a railroad. It looks more like a cruel joke to me. Anyway, during the sars epidemic, I'd noticed that Chinese Asians were the only people who seemed to die from sars, other than a few people such as Dr Urbani, our champion bug buster. Having been involved with lymphoma and statistics and genes and stuff a bit over the last few years, I've learned that we are each genetically and statistically unique, and environmentally unique. Nevertheless, there are broad categories of sameness, with exceptions to each category. So, everyone with a particular DNA might die from some effect. Except for the one who doesn't. For example, everyone with a genetic vulnerability to malaria, AIDS, sars or smallpox will get really ill or die. Unless they don't, which might be due to: 1....sickle cells against malaria 2....the genes which confer immunity to AIDS virus [as shown up in some African prostitutes who didn't get sick] 3....genetic immunity to sars 4....vaccination against smallpox We are not all the same. We are all different. Whether it's the <human leucocype antigen (HLA)-B46 gene are more likely to fall victim to SARS, while people with the HLA-B13 gene are relatively immune to the SARS virus.> factor, or something else, I wouldn't have a clue. But not everyone dies. Not everyone gets very sick, despite no immune system prior challenges by the sars bug. It's an individual business. As Henry says, being old is a major risk factor. I don't know why that is. Being Chinese without the HLA-B13 gene, is perhaps a good safety factor. Maybe being European gives a turbo boost to protection. Humans inadvertently wage germ warfare on each other. Those with the right genes survive and those who are genetically distant and susceptible to a disease die. So Europeans invaded the North American aborigines and the killer Euro bugs did most of the work [I guess]. The aborigines appear not to have had diseases to pass back to defeat the invaders. Their spears and stuff weren't a match for muskets, smallpox [or noocular bombs]. Anyway, that's my theory which seems to fit what's happening. It's subject to change without notice during any subsequent sars attacks and I'm not giving my usual double your money back guarantee. Mqurice PS: I also plead guilty to being ignorant about biological stuff, but with sars on the rampage I'm somewhat curious and my theory seems like a good story. I like it anyway. I will not be testing my theory voluntarily - I will avoid sars like the plague.