DNA fingerprinting has confirmed a Biblical allusion to leprosy, and tothe Ice Age rise of cystic fibrosis.From a human bone carbon-dated to 600 A.D., microbiologists at theUniversity College London extracted DNA infected withMycobacterium leprae, the pathogen of leprosy. Their report is in thecurrent issue of Lancet.The metatarsal bone came from a grave in the Jordan Valley, where theNew Testament recounts that Jesus cleansed a leper named Naaman theSyrian in A.D. 26 (Luke 4. 27). The burial site which yielded the DNA-bearing sample is on the grounds of the ancient Monastery of St. Johnthe Baptist, south of Jericho.The monastery was the scene of a massacre of Christians by Persians in614 A.D., well within the 50-year standard error of the carbon dating.Leprosy In Scripture And In VitroMicrobiologist John Stanford and surgeon/archeologist MarkSpigelman co-signed the letter to Lancet describing their technique ofextracting DNA, from the bones' desiccated marrow, which left"morphologically identifiable lesions specific to M. leprae." PCRamplification of insertion sequence template primers encoded thebacterium's antigens, and other ancient mycobacterial proteins.Like its look-alike TB pathogen, M. tuberculosis, the leprosy bacteriumhas a thick wall that protects the DNA after death. Stanford toldBioWorld Today that he and Spigelman hope to extend theirpaleobacteriological exploration to ancient remains of softer-shelledmicroorganisms, "if any of these survive the rotting process that sets inafter death."As soon as a body dies, Stanford explained, "gut bacteria spray outeverywhere, and quickly break down body tissues. Local DNAsesleave very few base pairs surviving.""Amplification of genetic material from ancient bacteria, andsequencing the results, could have important medical implications," theLancet letter suggests, such as determining the pre-existence ofantibiotic resistance. He is curious to retrieve bubonic plaguepathogens from ancient clay pits, for example.Spigelman told BioWorld Today that he and Raul Cano of CaliforniaPolytechnic State University "are conducting a joint project on theorigins of syphilis _ did Europe export it to America, or vice versa?_ hoping finally to clear Columbus' name."Cystic Fibrosis In The Last Ice AgeThirty-one researchers from 19 centers in 13 countries of Europe andthe U.S. joined forces to produce a separate study reported in the Juneissue of Nature Genetics. Their paper, "The origin of the major cysticfibrosis mutation (DF508) in European populations," is based onsurveying DF508 chromosomes in 15 European regions. It concludesthat CF made its appearance on the European continent somewherebetween at least 52,000, and at most 173,000, years ago.This is well before the time, 40,000 years ago, when morphologicallymodern Europeans spread over the continent during the Old Stone Age.The number of gene mutations that can cause cystic fibrosis is up to400, and still counting. The key gene mutilated by these aberrantsequences is called CFTR, the Cystic Fibrosis TransmembraneConductance Regulator. One mutation alone accounts for 70 percent ofall CF chromosomes worldwide. It is a three-base-pair deletion atcodon 508 of the CFTR's DNA.This DF508 mutant gene permits molecular geneticists to diagnosepotential CF infants prenatally, as well as parental carriers. It has alsoenabled them to track back the existence of the disease in Europe for atleast 52,000 years, long before the end of the last ice age, and 10 timesas long ago as previously estimated.In Northern Europe and North America, the study found, DF508frequency runs from 70 to 90 percent, but is less than 50 percent in theMediterranean region. They could not account for this discrepancy.Their analytic tool was the mutational pattern changing down themillennia in an array of microsatellites _ dinucleotide repeatsequences _ in the intronic region of the CFTR gene. They observed54 haplotype variants evolving from one ancestral pattern in 1,738chromosomes analyzed.Two percent of the Caucasian population harbors one of the 400-plusCF genes, the report notes, and asks why fully 1.4 percent of these _70 percent _ should be the DF508 mutant. Its principal author, XavierEstivill of Barcelona, Spain's Duran y Reynals Hospital, speculates thatthis preponderance must indicate "a carrier advantage at the individual,gamete or gene level." If not for such a selective survival benefit, hereasoned, the processes of evolution would have lowered the frequencyof this recessive lethal allele in far less than 52,000 years. n

-- David N. Leff Science Editor

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