Phylogeny of Greya (Lepidoptera: Prodoxidae), based on nucleotide sequence variation in mitochondrial cytochrome oxidase I and II: congruence with morphological data

The phylogeny of Greya Busck (Lepidoptera: Prodoxidae) was inferred from nucleotide sequence variation across a 765-bp region in the cytochrome oxidase I and II genes of the mitochondrial genome. Most parsimonious relationships of 25 haplotypes from 16 Greya species and two outgroup genera (Tetragma and Prodoxus) showed substantial congruence with the species relationships indicated by morphological variation. Differences between mitochondrial and morphological trees were found primarily in the positions of two species, G. variabilis and G. pectinifera, and in the branching order of the three major species groups in the genus. Conflicts between the data sets were examined by comparing levels of homoplasy in characters supporting alternative hypotheses. The phylogeny of Greya species suggests that host-plant association at the family level and larval feeding mode are conservative characters. Transition/transversion ratios estimated by reconstruction of nucleotide substitutions on the phylogeny had a range of 2.0-9.3, when different subsets of the phylogeny were used. The decline of this ratio with the increase in maximum sequence divergence among taxa indicates that transitions are masked by transversions along deeper internodes or long branches of the phylogeny. Among transitions, substitutions of A-->G and T-->C outnumbered their reciprocal substitutions by 2-6 times, presumably because of the approximately 4:1 (77%) A+T-bias in nucleotide base composition. Of all transversions, 73%-80% were A<-->T substitutions, 85% of which occurred at third positions of codons; these estimates did not decrease with an increase in maximum sequence divergence of taxa included in the analysis. The high frequency of A<-->T substitutions is either a reflection or an explanation of the 92% A+T bias at third codon positions.      

Immune Evasion by Helicobacter pylori: Gastric Spiral Bacteria Lack Surface Immunoglobulin Deposition and Reactivity with Homologous Antibodies

Background. Helicobacter pylori infection persists in the presence of potent serum and gastric mucosal anti-body responses against bacterial antigens. The aim of this article is to report on a study determine whether there is antibody deposition on H. pylori in vivo in the stomach of infected patients and whether gastric and cultured forms of H. pylori differ in their antibody reactivity.
Materials and Methods. Serum, gastric biopsies, and antral brushings were obtained from 10 patients having endoscopy. H. pylori was cultured from gastric biopsies. Bacterial samples were stained directly for immunoglobulin deposition and indirectly using rabbit antiurease serum or patient serum. Samples were examined by immunofluorescence microscopy and flow cytometry.
Results. Although spiral bacteria could be identified easily by acridine orange staining and antiurease staining of gastric brushings from H. pylori infected patients, gastric bacteria did not have detectable IgG or IgA present, and only one of five samples could be stained for IgG and IgA indirectly using patient serum. In contrast, cultured bacteria could be stained readily with homologous serum for IgG and IgA in the majority of cases. Low pH inhibited immunoglobulin reactivity with cultured H. pylori.
Conclusions. Gastric H. pylori may evade humoral defense owing to poor deposition of immunoglobulin in the gastric environment or failure to express surface antigens that are present on cultured forms of H. pylori.     

Mechanism of immune transfer by RNA extracts

Summary Immune RNA (I-RNA) was extracted from lymphoid organs of BALB/c mice immunized with AKR lymphoid cells. Incubation of normal BALB/c spleen cells with this I-RNA (but not with normal RNA) resulted in leukocyte migration inhibition reactions (LMIR) against AKR extracts but not against purified protein derivative or BALB/c sarcoma extracts. This transfer was abolished by pretreating I-RNA with RNAse but not with pronase. The active fraction of I-RNA was retained by and could be eluted from Poly-U Sepharose columns. Normal cells pretreated with I-RNA also reacted in the presence of an anti-idiotypic anti-serum of anti-(BALB/c anti-AKR) specificity. Pretreatment of cells with anti-idiotypic serum plus complement did not inhibit the subsequent transfer of LMIR with I-RNA. Idiotypic receptors were expressed on I-RNA treated cells less than one hour after I-RNA treatment. Using an I-RNA of double specificity, the results suggested that I-RNA entered into and acted on the cells through a nonspecific mechanism. Finally, I-RNA could induce BALB/c anti-AKR idiotypic markers in C57B1/6 cells, genetically committed for different idiotypes, while RNA extracted from C57131/6 immune cells could not induce in BALB/ c cells their own genetically acquired idiotypes. This series of data would prove that I-RNA acting as a mRNA is able to induce in normal noncommitted cells the de novo synthesis of antigen receptors similar or identical to those present in the surface of in vivo immunized lymphoid cells of the same strain.