To wells containing 2610 5 MN purified as described above, 50 ml of an asynchronous parasite culture at 0.5 % parasitemia and 4 % hematocrit were added. Wells were then supplemented with test or control antibodies (Ab) and the total volume adjusted to 100 ml with culture medium. After 48 h and 72 h, 50 ml of culture medium were added to each well and after 96 h the ADCI assay was stopped and the final parasitemia was determined by light microscopy on Giemsa-stained smears by counting $50,000 red blood cells. For each Ab tested, duplicate wells included the following controls 1) non-specific monocytic inhibition, both MN+parasite, and MN+N-IgG+parasites and 2) direct inhibition by control or test IgG, both N-IgG+parasites, and test Abs+parasites. PIAG and N-IgG were used at a final concentration of 1 mg/ml as positive and negative controls respectively. Immunopurified tests Abs were used at 15 mg/ml. The Specific Growth inhibitory Index (SGI) which considers the parasite growth inhibition due to the effect of test Abs cooperating with MN was calculated as follows: SGI = 1006[12(% parasitemia with MN and test Abs/% parasitemia test Abs)/(% parasitemia with MN and N-IgG/% parasitemia N-IgG)]. Figure S1 CD spectra of the peptides 45 (S1A) and 12 (S1B) Found at: doi:10.1371/journal.pone.0000645.s001 (12.32 MB TIF) Figure S2 ELISA inhibition assay using anti-human peptide specific antibodies. Binding of peptide specific antibodies to peptides 76 (S2A) and 9 (S2B) absorbed on ELISA plates was inhibited by incubating specific antibodies (1-2 mg/ml) with peptides 14, 76 and 81 (S2A) and peptides 8 and 9 (S2B), respectively (see Material and Methods). Peptides 14, 76 and 79 share NNM or MNN as sequence similarity while peptides 8 and 9 do not exhibit any apparent sequence similarity. Table S3 Structural feature and cellular location prediction of the proteins containing the peptides whose specific antibodies were tested in ADCI (Table 1) . Found at: doi:10.1371/journal.pone.0000645.s005 (0.05 MB DOC) FluGenome: a web tool for genotyping influenza A virus Influenza A viruses are hosted by numerous avian and mammalian species, which have shaped their evolution into distinct lineages worldwide. The viral genome consists of eight RNA segments that are frequently exchanged between different viruses via a process known as genetic reassortment. A complete genotype nomenclature is essential to describe gene segment reassortment. Specialized bioinformatic tools to analyze reassortment are not available, which hampers progress in understanding its role in host range, virulence and transmissibility of influenza viruses. To meet this need, we have developed a nomenclature to name influenza A genotypes and implemented a web server, FluGenome (http://www.flugenome.org/), for the assignment of lineages and genotypes. FluGenome provides functions for the user to interrogate the database in different modalities and get detailed reports on lineages and genotypes. These features make FluGenome unique in its ability to automatically detect genotype differences attributable to reassortment events in influenza A virus evolution. Infections with influenza A viruses continue to be a public health problem, causing seasonal epidemics and sporadic but devastating pandemics. Each year in the US, influenza epidemics cause more than 200 000 hospitalizations and result in over 30 000 influenza-related deaths (1) . Influenza pandemics are infrequent but they can result in high mortality. It is estimated that $20-100 million people were killed worldwide by the 1918-1919 influenza pandemic (2) (3) (4) . The current level of pandemic alert is at the highest level, phase 3, since the most recent pandemic of 1968 (5) .