Recombination in the hemagglutinin gene of the 1918 "Spanish flu"

When gene sequences from the influenza virus that caused the 1918 pandemic were first compared with those of related viruses, they yielded few clues about its origins and virulence. Our reanalysis indicates that the hemagglutinin gene, a key virulence determinant, originated by recombination. The "globular domain" of the 1918 hemagglutinin protein was encoded by a part of a gene derived from a swine-lineage influenza, whereas the "stalk" was encoded by parts derived from a human-lineage influenza. Phylogenetic analyses showed that this recombination, which probably changed the virulence of the virus, occurred at the start of, or immediately before, the pandemic and thus may have triggered it.     

Characterization of the reconstructed 1918 Spanish influenza pandemic virus

The pandemic influenza virus of 1918-1919 killed an estimated 20 to 50 million people worldwide. With the recent availability of the complete 1918 influenza virus coding sequence, we used reverse genetics to generate an influenza virus bearing all eight gene segments of the pandemic virus to study the properties associated with its extraordinary virulence. In stark contrast to contemporary human influenza H1N1 viruses, the 1918 pandemic virus had the ability to replicate in the absence of trypsin, caused death in mice and embryonated chicken eggs, and displayed a high-growth phenotype in human bronchial epithelial cells. Moreover, the coordinated expression of the 1918 virus genes most certainly confers the unique high-virulence phenotype observed with this pandemic virus.     

A two-amino acid change in the hemagglutinin of the 1918 influenza virus abolishes transmission

The 1918 influenza pandemic was a catastrophic series of virus outbreaks that spread across the globe. Here, we show that only a modest change in the 1918 influenza hemagglutinin receptor binding site alters the transmissibility of this pandemic virus. Two amino acid mutations that cause a switch in receptor binding preference from the human alpha-2,6 to the avian alpha-2,3 sialic acid resulted in a virus incapable of respiratory droplet transmission between ferrets but that maintained its lethality and replication efficiency in the upper respiratory tract. Furthermore, poor transmission of a 1918 virus with dual alpha-2,6 and alpha-2,3 specificity suggests that a predominant human alpha-2,6 sialic acid binding preference is essential for optimal transmission of this pandemic virus. These findings confirm an essential role of hemagglutinin receptor specificity for the transmission of influenza viruses among mammals.     

Selective stimulation of one of the mechanisms for genetic recombination of bacteriophage S13

In certain recombination-deficient (Rec(-)) bacterial strains genetic recombination of bacteriophage S13 is reduced, but the existence of some residual recombination has suggested that there is a secondary mechanism of phage recombination that is still functioning. In these Rec(-)strains it is found that there is no stimulation of recombination by irradiation of the parental phage with ultraviolet light, in contrast to the large increase found when irradiated phage particles infect a Rec(+) host. This selective stimulation of phage recombination in the Rec(+) but not in the Rec(-) strains supports the view that the phage uses at least two mechanisms of genetic recombination.     

Virus of the 1918 influenza pandemic era: new evidence about its antigenic character

In serums of unusually isolated Pacific islanders whose only exposure to influenza occurred during the era of the 1918 pandemic the residual neutralizing antibody was greatest to the PR/8 and BH strains of human type A influenza virus, significantly lower to swine influenza virus, and absent to equine or later human type A virus strains. The pandemic virus was thus antigenically closer to human type A strains isolated during the middle 1930's than to other known influenza virus types.     

Structure of the uncleaved human H1 hemagglutinin from the extinct 1918 influenza virus

The 1918 "Spanish" influenza pandemic represents the largest recorded outbreak of any infectious disease. The crystal structure of the uncleaved precursor of the major surface antigen of the extinct 1918 virus was determined at 3.0 angstrom resolution after reassembly of the hemagglutinin gene from viral RNA fragments preserved in 1918 formalin-fixed lung tissues. A narrow avian-like receptor-binding site, two previously unobserved histidine patches, and a less exposed surface loop at the cleavage site that activates viral membrane fusion reveal structural features primarily found in avian viruses, which may have contributed to the extraordinarily high infectivity and mortality rates observed during 1918.     

Theoretical evidence for a c60 "window" mechanism

On the basis of semiempirical and high-level ab initio calculations, theoretical evidence is presented of a "window" mechanism operable on the surface of C(60) and other fullerenes. Through this mechanism, large holes may be formed in fullerenes excited to their triplet state, openings through which atoms and small molecules can pass. This work provides a theoretical foundation for experiments that have prepared endohedral noble gas compounds of C(60) under thermal excitation. A method is proposed that could increase the efficiency of the process of noble gas insertion into C(60) and provide a more general means to create endohedral fullerene compounds.     

减数分裂重组的分子遗传机制研究进展及在作物育种中的应用

减数分裂是真核生物有性生殖产生染色体数目减半的单倍体配子所必需的生命过程。重组是减数分裂的核心事件之一,既增加了同源染色体间遗传信息的交换,又保证了其在减数分裂后期Ⅰ的正确分离。因此,减数分裂重组不仅增加了后代遗传多样性,还是作物遗传育种的基础。通过提高重组频率或改变其分布可以加速农作物育种进程,而降低或抑制重组可以固定杂种优势。近年来对植物减数分裂重组的分子遗传机制的研究取得了很大进展,包括重组的遗传和表观遗传调控机制,重组的遗传操控技术、固定杂交优势和染色体工程等方面。本文针对以上方面进行了全面的总结,这些内容不仅方便了读者对减数分裂重组的理论认知,还拓展了通过调控减数分裂重组操控生物育种的思路。     

Word learning in a domestic dog: evidence for "fast mapping"

During speech acquisition, children form quick and rough hypotheses about the meaning of a new word after only a single exposure-a process dubbed "fast mapping." Here we provide evidence that a border collie, Rico, is able to fast map. Rico knew the labels of over 200 different items. He inferred the names of novel items by exclusion learning and correctly retrieved those items right away as well as 4 weeks after the initial exposure. Fast mapping thus appears to be mediated by general learning and memory mechanisms also found in other animals and not by a language acquisition device that is special to humans.     

A genetic map and recombination parameters of the human malaria parasite Plasmodium falciparum

Genetic investigations of malaria require a genome-wide, high-resolution linkage map of Plasmodium falciparum. A genetic cross was used to construct such a map from 901 markers that fall into 14 inferred linkage groups corresponding to the 14 nuclear chromosomes. Meiotic crossover activity in the genome proved high (17 kilobases per centimorgan) and notably uniform over chromosome length. Gene conversion events and spontaneous microsatellite length changes were evident in the inheritance data. The markers, map, and recombination parameters are facilitating genome sequence assembly, localization of determinants for such traits as virulence and drug resistance, and genetic studies of parasite field populations.     

Amino Acid transport: evidence for genetic control of two types in human kidney

In the report "Amino acid transport: evidence for genetic control of two types in human kidney" by C. R. Scriver and O. H. Wilson (17 Mar., p. 1428), the first sentence in the abstract should read "A mutation affecting renal transport of proline, hydroxyproline, and glycine occurs in man."     

Partial reversion in yeast: genetic evidence for a new type of bifunctional protein

Two kinds of phenotypic expression in purine biosynthesis result from recessive mutation to adel2 in baker's yeast. The mutants are adenine-specific, blocked in the conversion of inosine 5'-phosphate to adenylosuccinic acid; their response to inhibition of pathway activity by adenine is considerably reduced. Allelic partial reversions can restore prototrophy without correcting the regulatory defect imparted by the primary mutation. The separation of the two properties of the locus by allelic mutation supports the hypothesis that the locus specifies a protein of two independent functions, enzymatic and regulatory.     

Amino acid transport: evidence for genetic control of two types in human kidney

A mutation affecting renal transport of proline, hydroxyproline, and glycerine occurs in man. In the presumed homozygote there is still significant residual transport of these compounds; however, this remaining function is saturated at normal concentrations of substrate in the plasma and is not inhibited by L-proline in the expected way. The presumed heterozygote has partial loss of a transport system common to the three substrates, which becomes saturated at high concentrations of substrate and is inhibited by L-proline. Two different types of transport systems are proposed: a common system and systems with lower capacity and greater specificity. The two types of transport appear to be controlled by separate genes.