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Salmonella enterica subspecies I, serovar Typhimurium ( S. typhimurium ), is a leading cause of human gastroenteritis, and is used as a mouse model of human typhoid fever 1 . The incidence of non-typhoid salmonellosis is increasing worldwide 2 , 3 , 4 , causing millions of infections and many deaths in the human population each year. Here we sequenced the 4,857-kilobase (kb) chromosome and 94-kb virulence plasmid of S. typhimurium strain LT2. The distribution of close homologues of S. typhimurium LT2 genes in eight related enterobacteria was determined using previously completed genomes of three related bacteria, sample sequencing of both S. enterica serovar Paratyphi A ( S. paratyphi A) and Klebsiella pneumoniae , and hybridization of three unsequenced genomes to a microarray of S. typhimurium LT2 genes. Lateral transfer of genes is frequent, with 11% of the S. typhimurium LT2 genes missing from S. enterica serovar Typhi ( S. typhi ), and 29% missing from Escherichia coli K12. The 352 gene homologues of S. typhimurium LT2 confined to subspecies I of S. enterica —containing most mammalian and bird pathogens 5 —are useful for studies of epidemiology, host specificity and pathogenesis. Most of these homologues were previously unknown, and 50 may be exported to the periplasm or outer membrane, rendering them accessible as therapeutic or vaccine targets.

Salmonella enterica serovars often have a broad host range, and some cause both gastrointestinal and systemic disease. But the serovars Paratyphi A and Typhi are restricted to humans and cause only systemic disease. It has been estimated that Typhi arose in the last few thousand years. The sequence and microarray analysis of the Paratyphi A genome indicates that it is similar to the Typhi genome but suggests that it has a more recent evolutionary origin. Both genomes have independently accumulated many pseudogenes among their ∼4,400 protein coding sequences: 173 in Paratyphi A and ∼210 in Typhi. The recent convergence of these two similar genomes on a similar phenotype is subtly reflected in their genotypes: only 30 genes are degraded in both serovars. Nevertheless, these 30 genes include three known to be important in gastroenteritis, which does not occur in these serovars, and four for Salmonella -translocated effectors, which are normally secreted into host cells to subvert host functions. Loss of function also occurs by mutation in different genes in the same pathway ( e.g. , in chemotaxis and in the production of fimbriae).

Life insurance companies share data with each other and use it to deny health insurance as well. If life insurers did not do this, opposition would decrease. You also say insurance companies would preserve confidentiality. In regard to homosexuals, their record is poor. There are also cases now in court in which insurance companies tried to deny insurance to all homosexuals, whether ill or healthy, by redlining certain professions and neighborhoods.

In your June 16 editorial, you omitted key reasons why many (not just \"homosexual groups,\" as the editorial said) oppose life insurance companies' use of socalled AIDS screening tests.

It's a shame The Tribune seems more concerned about irrational fears and hysteria of the uninformed than about medical science and human rights.

Raymond Coffey's Nov. 14 column was, to borrow his words, so \"goofy, loony, nutty, ridiculous\" that it made \"no sense.\" His argument against distribution of clean needle.