Format for the Research Introduction includes Biology and Epidemiology Pathogenesis- the disease pattern Clinical/laboratory diagnosis Prevention/control References National Library of Medicine (NLM) Methods Authors(Last name First Name Initial). Article title. Abbreviated Journal Title. Year Month Date; Volume Number(Issue Number):Inclusive Pages. Example: Meneton P, Jeunemaitre X, de Wardener HE, MacGregor GA. Links between dietary salt intake, renal salt handling, blood pressure, and cardiovascular diseases. Physiol Rev. 2005 Apr;85(2):679-715. No Author given • When there is no author, begin the citation with the title of the article. Do not use anonymous. • Title. Article title. Journal Title. Date of Publication. Vol. (issue): page numbers. Place of Publication. Example: Drug-resistance tuberculosis among the foreign-born in Canada. Can Commun Dis Rep. 2005 Feb 15;31(4):46-52. English, French. Online Journal from a database • The general format for a reference to a database/retrieval system on the Internet, including punctuation: o For a single database: Title [Type of Medium]. Place of Publication: Publisher; Date of Publication [modified Date of Update/Revision; Date of Citation]. Available from: URL. Example: Database of Human Disease Causing Gene Homologues in Dictyostelium Discoideum [Internet]. San Diego (CA): San Diego Supercomputer Center; 2003 [modified 2003 Mar 30; cited 2007 Feb 2]. Available from: http://dictyworldbench.sdsc.edu/HDGDD/. When you cite in the body of the paper Preexisting human antibodies neutralize recently emerged H7N9 influenza strains Introduction Influenza A viruses evade the human immune system by changing the antigenic regions of their surface glycoproteins using two mechanisms: antigenic drift (point mutations) and antigenic shift (gene segment reassortments) (1). Antigenic variation is further increased by divergent evolution, as influenza virus strains recirculate continually among different host reservoirs, especially humans and avian species. The HA glycoprotein is the main target of neutralizing antibodies and is composed of an immunodominant globular head domain and a stalk domain (2). HA subtypes are classified into two groups based on their antigenic properties: amino acid sequences and structural features (3). Group 2 influenza A viruses include the H3 subtype, which further contains the seasonal H3N2 human strains, and the H7 subtype, which contains highly pathogenic avian influenza A viruses (4). Previously, infections with H7 viruses, through exposure to poultry, generally resulted in uncomplicated influenza illness and/or mild conjunctivitis (demonstrated for H7N3), with only one fatal case observed during an outbreak in The Netherlands (H7N7) (5, 6). However in 2013, a novel influenza A virus (H7N9), the product of genetic reassortment of various avian strains, emerged in China. This virus, associated with a high frequency of fatal human disease, appeared to have a wide dispersion and the potential for human-to-human transmission (7–12). Although the virus received the most publicity in 2013 (a year with 153 cases), the H7N9 virus shows a seasonal pattern, with most infections occurring during the winter season. The incidence of infection continues to increase, with nearly twice as many new H7N9 infections (301 cases) reported in 2014, totaling 454 cases, according to the World Health Organization, as of July 2014. These cases occurred in 12 provinces of China, with imported cases in Malaysia and Taiwan. The incidence of H7N9 infection combined with its abilities to bind to human receptor orthologs and to develop resistance to neuraminidase inhibitors without fitness loss has raised concerns about the pandemic potential of the H7N9 virus (13–15). With H7 strains currently posing a threat to human health, it is important to determine whether there is cross-protection generated from group 2 influenza virus vaccinations. Over several years, we have generated human antibodies from plasmablasts of volunteers vaccinated with the seasonal influenza virus vaccine (refs. 16, 17, and our unpublished data). Because plasmablasts are activated during an ongoing immune response, this allows us to determine whether prior vaccination, especially with H3N2 strains, induced cross-reactive antibodies that neutralize H7 strains. Given the lack of a vaccine against novel H7 viruses, the isolation and characterization of monoclonal antibodies with neutralizing activity can direct vaccine design and also provide a therapeutic resource. References 1. Shaw ML Palese P. Orthomyxoviruses. In: Knipe DM, Howley PM, eds. Fields Virology. 6th ed. Philadelphia, Pennsylvania, USA: Lippincott Williams and Wilkins; 2013:1151–1185. 2. Kaur K, Sullivan M, Wilson PC. Targeting B cell responses in universal influenza vaccine design. Trends Immunol. 2011;32(11):524–531. 3. Air GM. Sequence relationships among the hemagglutinin genes of 12 subtypes of influenza A virus. Proc Natl Acad Sci U S A. 1981;78(12):7639–7643. 4. Medina RA, Garcia-Sastre A. Influenza A viruses: new research developments. Nat Rev Microbiol. 2011;9(8):590–603. 5. Hirst M, et al. Novel avian influenza H7N3 strain outbreak, British Columbia. Emerg Infect Dis. 2004;10(12):2192–2195. 6. Fouchier RA, et al. Avian influenza A virus (H7N7) associated with human conjunctivitis and a fatal case of acute respiratory distress syndrome. Proc Natl Acad Sci U S A. 2004;101(5):1356–1361. 7. Gao R, et al. Human infection with a novel avian-origin influenza A (H7N9) virus. N Engl J Med. 2013;368(20):1888–1897. 8. Belser JA, et al. Pathogenesis transmission of avian influenza A (H7N9) virus in ferrets mice. Nature. 2013;501(7468):556–559. 9. Watanabe T, et al. Characterization of H7N9 influenza A viruses isolated from humans. Nature. 2013;501(7468):551–555. 10. Morens DM, Taubenberger JK, Fauci AS. H7N9 avian influenza A virus and the perpetual challenge of potential human pandemicity. MBio. 2013;4(4):1–14.