Mice that lack a gene for a key component of the immune system are more susceptible to colitis and develop altered gut flora. Furthermore, when these knockout mice were housed with mice with a functional copy of the gene, both groups were susceptible to colitis, suggesting that gut microbial composition of the knockout mice spreads to the wild-type, and that both genes and microbes are involved in this autoimmune disease.
The influenza virus is typically skilled at evading immune surveillance, but scientists have identified ten lab-made antibodies that effectively neutralize all group 1 influenza viruses tested, including H5N1 “bird flu” and the H1N1 “Spanish flu.” The antibodies bind an obscure but highly conserved region of the viruses. Once bound, they cannot change their shape to fuse with the membrane of a target cell, thus preventing infection.
J. Sui et al., “Structural and functional bases for broad-spectrum neutralization of avian and human influenza A viruses,” Nat Struct Mol Biol, 16:265-73, 2009.3. Gut safety
Toll-like receptors (TLRs) normally recognize microbes and activate the immune system to eliminate them, yet commensal microbes in the gut somehow manage to avoid this inflammatory immune response. It turns out a prominent commensal gut bacterium, Bacteroides fragilis, uses a TLR pathway to actually promote immune tolerance: the microbe activates TLR2 on CD4 T helper cells which initiates a pathway to suppress immunity and establish host-microbial symbiosis in mice.
J.L. Round et al., “The Toll-like receptor 2 pathway establishes colonization by a commensal of the human microbiota,” Science, 332:974-7, 2011.4. A century of immunity
Nearly 90 years after the outbreak of the 1918 Spanish flu, survivors of the pandemic still carry functional antibodies against the virus in their blood, demonstrating the longevity of immunological memory in humans. What’s more, these antibodies are able to protect mice from lethal infection with the reconstructed 1918 virus.
X. Yu et al., “Neutralizing antibodies derived from the B cells of 1918 influenza pandemic survivors,” Nature, 455:532-6, 2008.5. Death to Salmonella
For the first time, scientists have identified a mechanism by which autophagosomes recognize Salmonella for degradation: ubiquitin marks the bacteria as waste, and once marked, the microbe binds two proteins, LC3 and optineurin. Finally, the phosphorylation of optineruin acts as a trigger to activate autophagy, in which the Salmonella cell is digested in a lysosome.
P. Wild et al., “Phosphorylation of the autophagy receptor optineurin restricts Salmonella growth,” Science, 333:228-33, 2011.6. Snoring parasites
In the ancient protozoan parasite Giardia lamblia, small nucleolar RNAs (snoRNAs) in the nucleus produce even smaller microRNAs that localize to the cytoplasm, where they appear to mediate translation. The finding demonstrates that microRNA pathways are evolutionarily conserved in early eukaryotes, and that snoRNAs are a potential new source for microRNAs.
A.A. Saraiya et al., “snoRNA, a novel precursor of microRNA in Giardia lamblia,” PLoS Pathog, 4:e1000224, 2008.7. HIV-2’s secret weapon
Macrophages are resistant to HIV-1 infection but not HIV-2 infection. This difference can be attributed to a protein, SAMHD1, which inhibits HIV infection by interfering with viral DNA synthesis. In HIV-1 infections, SAMHD1 is present in macrophages and effective in blocking viral replication, but in HIV-2 infected cells, the protein is bound by a viral HIV-2 protein, Vpx, and marked for degradation.
K. Hrecka et al., “Vpx relieves inhibition of HIV-1 infection of macrophages mediated by the SAMHD1 protein,” Nature, 474:658-61, 2011.The F1000 Top 7 is a snapshot of the highest ranked articles from a 30-day period on Faculty of 1000 Microbiology, as calculated on July 22, 2011. Faculty Members evaluate and rate the most important papers in their field. To see the latest rankings, search the database, and read daily evaluations, visit http://f1000.com.