Research Notes

HIV Hitches a Ride The statistics are grim: More than 34 million people worldwide affected with HIV/AIDS, and 800,000- 900,000 cases in the United States with a steady rate of 40,000 new HIV infections each year. Fueled by such statistics, HIV research continues with scientists at the National Institute of Allergy and Infectious Diseases (NIAID) recently discovering a mechanism providing insight into the pathogenesis of the virus in which HIV may hitch a ride from select cells to target cells. Researchers report that B cells, the antibody-producing cells of the immune system, can likely deliver HIV to immune system T cells, those essential for a vigorous immune response (S. Moir et al., "B cells of HIV-1-infected patients bind virions through CD21-complement interactions and transmit infectious virus to activated T cells," Journal of Experimental Medicine, 192:637-45, Sept. 5, 2000). HIV devastates the body's ability to fight off infection by destroying a key class of these T cells. According to Susan Moir, of the Laboratory of Immunoregulation, NIAID, "Our present focus is to establish the genetic relationship between the virus we found on the B cells and the other viruses that are circulating in the body. We are finding that they are related, thus proving that the virus on the B cells does indeed contribute to systemic production of virus." Moir says that NIAID is also investigating the dysfunction of B cells with regard to a docking point for HIV, a molecule called CD21 that is on the B cell's surface. CD21 normally binds complement, a protein that marks invading microbes for destruction, with B cells being signaled to produce antibody. "We are describing how B cells suffer from being constantly 'tickled' by the interaction between HIV and CD21," which may be the cause of the uncontrolled production of multiple antibodies that is seen in HIV patients. --Kate Devine Shedding Light on the Subject The ability to harvest and use light is the lifeblood of countless organisms. Yet scientists know little about how evolution initially gave rise to photosynthesis in the first light harvester, bacteria. A recent paper makes some headway toward sorting out the evolutionary phylogeny of photosynthesis genes (J. Xiong et al., "Molecular evidence for the early evolution of photosynthesis," Science, 289:1724-30, Sept. 8, 2000). To the surprise of many biologists, the results suggest that the exceedingly common purple bacteria, and not as was commonly believed, the much less common green nonsulfurous bacteria, were the first to use photosynthesis. Investigators PCR-amplified and cloned all the photosynthesis genes they could get their hands on from each of the five known branches of photosynthetic bacteria. "A lot of classic microbiology had been done with those different branches," explains senior author Carl Bauer, a biologist at Indiana University in Bloomington. "But nobody actually went in and actually fished out all the genes." Biologists know that cyanobacteria (also known as blue-green algae) mastered photosynthesis relatively recently in evolutionary terms--about 2.5 billion years ago. Plants became photosynthesizers by acquiring cyanobacteria, which gave rise to plants' light-absorbing chloroplasts. By comparing bacterial sequences, researchers built evolutionary trees showing that chlorophyll a and b, found in the photosystems of cyanobacteria and plants, evolved after bacteriochlorophyll, which is found in other bacteria. The results contradict previous conclusions that were based on the commonplace method of 16S ribosomal RNA. Researchers had believed that the simpler structures of chlorophyll a and b implied earlier origins (the Granick hypothesis) but it seems as if evolution saw fit to pare down the system rather than make it more complex. Additional DNA sequences and more sophisticated sequence-analyzing programs will likely further elucidate the evolutionary origin of photosynthesis among purple bacteria, though Bauer suggests his group's general framework is likely correct. --Eugene Russo Colonization, Not Invasion The genetics of Salmonella typhimurium infection are not as well-known as scientists previously thought, according to a recent paper (R.A. Murray et al., "Invasion genes are not required for Salmonella enterica serovar typhimurium to breach the intestinal epithelium: Evidence that Salmonella pathogenicity island 1 has alternative functions during infection," Infection and Immunity, 68:5050-5, September 2000). Researchers at Harvard Medical School found that a cluster of genes thought to be responsible for intestinal wall invasion actually code for proteins that help the bacteria colonize the intestinal cavity. At least in this species of Salmonella, the bacteria might be able to colonize the intestine by attracting and then killing immune cells, hypothesizes senior author Catherine Lee, an associate professor of microbiology at Harvard. Lee's graduate student, lead author Rose Ann Murray, found the unexpected colonization in mutant bacteria missing all the genes thought to be required for pathogenicity. Lee remembers Rose Ann saying, "'Oh, I want to try this one,'" and her response was, "'Oh, whatever. You know, if you must. I'll humor you.'" Lee adds, "And it turned out to be so, so interesting." Salmonella typhimurium causes typhoid fever, a major problem in countries with poor sanitation systems; other types of harmful but less deadly Salmonella are a problem worldwide. Researchers now will have to investigate the commonality of this colonization phenomenon across Salmonella species. According to Lee, future studies in other mouse models, and especially in well-characterized calf models, should elucidate the cellular pathway that leads to colonization, findings that could lead to novel treatment modalities. --Eugene Russo Meanwhile, Back at the Ranch As research continues on the feline genome (M.E. Watanabe, "Feline Genome Research Advances," The Scientist, 14[15]:16, July 24, 2000), considered closest to the human genome excepting primates, others are focusing on genomes of other mammals such as cattle. Researchers at the University of Illinois, Urbana-Champaign recently announced the most detailed map to date of cattle genes (Band et al., "An ordered comparative map of the cattle and human genomics," Genome Research, 10:1359-68, September 2000). A first comparison map of cattle and human genomes shows that many genes, and even whole chromosomes, are configured in the same way in the two species. Scientists will be able to use the human map to locate genes controlling similar traits in the cow. According to Harris Lewin, director of the W.M. Keck Center for Comparative and Functional Genomics at the University of Illinois and lead researcher, "Understanding the genome of cattle will permit us to understand the evolution and development of the ruminant digestive system, as well as other distinctive features of the species, including a very low incidence of spontaneous tumors. An important reason for mapping the cattle genome is to understand the molecular genetic basis for superior milk yield and resistance to infectious diseases, for example. Breeding for resistance to infectious diseases will reduce dependence on antibiotics in feed, a major concern for human health and food safety." Lewin indicates that the center now plans to complete the comparative map of the cattle and human genomes by targeted mapping of about 1,000 more genes. "We are beginning experiments with microarrays in order to help us identify genes for resistance to specific diseases as well as those that control reproduction and are rate limiting in metabolism. Eventually, we would like to participate in sequencing the whole genome." --Kate Devine

Research Notes

HIV Hitches a Ride

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