Influenza (Flu)
Types
Avian (A/H5N1 subtype) Canine Equine Swine (A/H1N1 subtype)
Vaccines
2009 pandemic (Pandemrix) ACAM-FLU-A Fluzone Influvac Live attenuated (FluMist) Optaflu
Treatment
Amantadine Arbidol Laninamivir Oseltamivir Peramivir Rimantadine Vitamin D Zanamivir
Pandemics
2009 Swine 1968–1969 Hong Kong 1918
Outbreaks
2008 West Bengal 2007 Bernard Matthews H5N1 2007 Australian equine 2006 H5N1 India 1976 swine flu
See also
Flu season Influenza evolution Influenza research Influenza-like illness
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To comply with Wikipedia's lead section guidelines, the introduction of this article may need to be rewritten. Please discuss this issue on the talk page and read the layout guide to make sure the section will be inclusive of all essential details. (April 2010)

The virus causing influenza is one of the best known pathogens found in various species. In particular, the virus is found in birds as well as mammals including horses, pigs, and humans.^[1] The phylogeny, or the evolutionary history of a particular species, is an important component when analyzing the evolution of influenza. Phylogenetic trees are graphical models of the relationships between various species. They can be used to trace the virus back to particular species and show how organisms that look so different may be so closely related.^[1]

Mechanisms of evolution[link]

Two common mechanisms by which viruses evolve are reassortment and genetic drift.^[2]

Reassortment[link]

Reassortment allows new viruses to evolve under both natural conditions and in artificial cultures.^[2] In fact, the 1957 evolution of the H2N2 virus is thought to be a result of reassortment.^[2] In this case, human H1N1 strains and avian influenza A genes were mixed.^[2] Infecting tissue cultures can demonstrate how pathogenic qualities can evolve for a particular species even though the reassorted virus may be nonpathogenic for another species.^[2] A prime example of evolution under natural conditions is the reassortment of two avian influenza strains that were discovered in dead seals back in 1979.^[2]

Drift[link]

New viruses can also emerge by drift. Drift can refer to genetic drift or antigenic drift.^[2] Mutation and selection for the most advantageous variation of the virus takes place during this form of evolution.^[2] Antigenic mutants can evolve quickly due to the high mutation rate in viruses. Influenza antigenic drift happens when two influenza viruses infect on cell. When new ones come out they have a segment from the others genome that could let some but not enough antibodies to bind. Also the receptor could not bind to antibodies.^[2] This evolution occurs under the pressure of antibodies or immune system responses.^[2]

Transmission[link]

Species and barriers[link]

The transmission, or how the influenza virus is passed from one species to another, varies. There are barriers that prevent the flow of the virus between some species ranging from high to low transmission. For example, there is no direct pathway between humans and birds.^[2] Pigs however, serve as an open pathway. There is a limited barrier for them to spread the virus.^[2] Therefore, pigs act as a donator of the virus relatively easily.

Geographic differences[link]

Phylogenetic maps are a graphical representation of the geographic relationships among species. They indicate that the human influenza virus is minimally impacted by geographic differences.^[1] However, both swine and avian influenza does appear to be geographically dependent.^[1] All three groups (avian, swine, and human) show chronological differences. The human influenza virus is retained in humans only, meaning it does not spread to other species.^[1] Some lineages and sublineages of the virus emerge and may be more prevalent in certain locations. For instance, many human influenza outbreaks begin in Southeast Asia.^[2]

Phylogenetic analysis[link]

Phylogenetic analysis can help determine past viruses and their patterns as well as determining a common ancestor of the virus. Past studies reveal that an avian virus spread to pigs and then to humans approximately 100 years ago.^[2] This resulted in human lineages further evolving and becoming more prominent and stable.^[2]

Analysis can also feature relationships between species. The 1918 Spanish influenza virus demonstrates this. Even though the hemagglutinin (HA) gene was closer in relation to avian strains than mammalian ones, it was, in fact, mammalian.^[3] The gene may have been adapting in humans even prior to 1918.^[3] Breaking down the phylogenetic history of the influenza virus shows that there is a common ancestor that reaches back before the 1918 outbreak that links the current human virus to the swine virus.^[4] The ancestor was derived from an avian host.^[2]

Future impact[link]

Looking at the past phylogenetic relationships of the influenza virus can help lead to information regarding treatment resistance, selecting vaccine strains, and future influenza strains.

In current years, there has been a huge increase in the amount of resistance to certain drugs, including the antiviral compound adamantine.^[5] In fact, its resistance has recently climbed from 2 percent to nearly 90 percent.^[5] These records of built up resistance infer that drugs, such as adamantine, will not be useful against the influenza virus in the future.

Various lineages may continue their presence and reassort indicating the importance of a complete-genome approach to determine new influenza strains and future epidemics.^[6][7] In terms of vaccine strain selection, antigenic clades evolve by reassortment, not by antigenic drift.^[6] This was shown in the 2003-2004 influenza outbreak.^[6]

Phylogenetic trees can help determine what codons in the HA gene of the influenza A virus have changed in past outbreaks.^[8] The more mutations there are in a virus strain, the more likely that strain is to be a generator of a new lineage in future influenza seasons.^[8]

References[link]

1. ^ ^{a b c d e} Liu, S; Kang, J; Chen, J; Tai, D; Jiang, W; Hou, G; Chen, J; Li, J et al. (2009). Field, Dawn. ed. "Panorama phylogenetic diversity and distribution of type A influenza virus". PLoS ONE 4 (3): 1–20. DOI:10.1371/journal.pone.0005022. http://www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0005022. 
2. ^ ^{a b c d e f g h i j k l m n o p} Scholtissek, C (1995). "Molecular evolution of influenza viruses". Virus Genes 11 (2–3): 209–215. DOI:10.1007/BF01728660. PMID 8828147. http://springerlink.metapress.com/content/v5747t6n11622627/fulltext.pdf. 
3. ^ ^{a b} Reid, A; Fanning, T; Hultin, J; Taubenberger, J (1999). "Origin and evolution of the 1918 "Spanish" influenza virus hemagglutinin gene". Proceedings of the National Academy of Sciences USA 96 (4): 1651–1656. DOI:10.1073/pnas.96.4.1651. PMC 15547. PMID 9990079. http://www.pnas.org/content/96/4/1651.full.pdf. 
4. ^ Gorman, O; Donis, R; Kawaoka, Y; Webster, R (1990). "Evolution of influenza A virus PB2 genes: implications for evolution of the ribonucleoprotein complex and origin of human influenza A virus". Journal of Virology 64 (10): 4893–4902. PMC 247979. PMID 2398532. http://jvi.asm.org/cgi/content/abstract/64/10/4893. 
5. ^ ^{a b} Simonsen, L; Viboud, C; Grenfell, B; Dushoff, J; Jennings, L; Smit, M; Macken, C; Hata, M et al. (2007). "The genesis and spread of reassortment human influenza A/H3N2 viruses conferring adamantane resistance". Molecular Biology and Evolution 24 (8): 1811–20. DOI:10.1093/molbev/msm103. PMID 17522084. http://mbe.oxfordjournals.org/cgi/content/full/24/8/1811#SEC4. 
6. ^ ^{a b c} Holmes, E; Ghedin, E; Miller, N; Taylor, J; Bao, Y; St George, K; Grenfell, B; Salzberg, S et al. (2005). "Whole-Genome Analysis of Human Influenza A Virus Reveals Multiple Persistent Lineages and Reassortment among Recent H3N2 Viruses". PLoS Biology 3 (9): 1579–1589. DOI:10.1371/journal.pbio.0030300. PMC 1180517. PMID 16026181. http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0030300. 
7. ^ Vana, G; Westover, K (2008). "Origin of the 1918 Spanish influenza virus: A comparative genomic analysis". Molecular Phylogenetics and Evolution 3: 1100–1110. 
8. ^ ^{a b} Fitch, W; Bush, R; Bender, C; Subbarao, K; Cox, N (2000). "Predicting the evolution of human influenza A". Journal of Heredity 91 (3): 183–185. DOI:10.1093/jhered/91.3.183. PMID 10833042. http://jhered.oxfordjournals.org/cgi/reprint/91/3/183. 

This biographical article needs additional citations for verification. Please help by adding reliable sources. Contentious material about living persons that is unsourced or poorly sourced must be removed immediately, especially if potentially libelous or harmful. (June 2010)

Christy Carlson Romano
Romano in May 2010
Born	Christina Michelle Romano (1984-03-20) March 20, 1984 (age 28)
Other names	Christy Romano
Occupation	Actress, singer, author
Years active	1996–present

Christy Carlson Romano (born March 20, 1984) is an American stage and film actress and singer. She is perhaps best known for her roles in the sitcom Even Stevens and the animated series Kim Possible, in which she is the voice of the title character, as well as the voice of Yuffie Kisaragi in Kingdom Hearts and Final Fantasy VII Advent Children. She got engaged to writer/actor Brendan Rooney in September of 2011.

Career[link]

In 1998, Romano made her Broadway debut in the musical Parade by Alfred Uhry and Jason Robert Brown in the role of Mary Phagan.^[1] In 2002, Romano became the first person to act in three Disney Channel projects simultaneously, supplementing her work at Even Stevens with a starring role in a movie named Cadet Kelly (alongside Hilary Duff) and voice acting as the title character in Kim Possible. She is also the voice of Yuffie Kisaragi in the English version of the movie Final Fantasy VII Advent Children, as well as in the Disney/Square game Kingdom Hearts.

On February 17, 2004, Romano began a 31-week run of playing Belle in Disney's Beauty and the Beast on Broadway where she replaced Megan McGinnis as Belle. She left the production on September 12, 2004, and was succeeded by Brooke Tansley.

Romano recently starred in the Broadway company of Avenue Q, in which she played Kate Monster, Lucy the Slut, and two of the singing moving crates, among other characters. She began her run on September 29, 2008, replacing Carey Anderson, and stayed with the show until November 23, 2008.^[2]

She most recently starred as Michelle in the new Off-Broadway show White's Lies, which began previews at New World Stages on April 12, 2010, and officially opened on May 6, 2010.^[3][4] The show closed on June 13, 2010.^[5]

Singer[link]

While working at Disney, Romano has recorded songs in the soundtracks of some Disney movies and TV series such as Kim Possible and Teacher's Pet. Romano first sang on the Disney Channel on a first season episode of Even Stevens (in 2000) which led to more singing on the series and with Disney in general. In 2004, Walt Disney Records released Romano's debut album Greatest Disney TV & Film Hits, featuring her new single "Dive In" (which was written by Christian music singer Cindy Morgan) and her other song, "Could It Be" from the television movie, Kim Possible: So The Drama.

Filmography[link]

Film[link]

Television[link]

Broadway[link]

Off-Broadway[link]

Discography[link]

Albums[link]

• Greatest Disney TV & Film Hits (2004)

MySpace Music[link]

Shared Songs (in order of when released):

Soundtracks

Awards and nominations[link]

References[link]

External links[link]

Wikinews has related news: Wikinews attends Christy Carlson Romano concert Sesame Place

• Official website
• Disney discography Christy Carlson Romano (2004)
• Christy Carlson Romano at the Internet Movie Database
• Christy Carlson Romano at the Internet Broadway Database
• BroadwayWorld.com interview with Christy Carlson Romano, October 3, 2008