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Influenza A virus subtype H3N2
H3N2 is a subtype of the influenza A virus. Its name derives from the forms of the two kinds of proteins on the surface of its coat, hemagglutinin (H) and neuraminidase (N). H3N2 viruses can infect birds and mammals. In birds, humans and pigs the virus has mutated into many strains. H3N2 exchanges genes for internal proteins with other influenza subtypes. The annual flu (also called "seasonal flu" or "human flu") kills an estimated 36,000 people in the United States each year. Flu vaccines are based on predicting which mutants of H1N1, H3N2, H1N2, and influenza B will proliferate in the next season. Separate vaccines are developed for the northern and southern hemispheres in preparation for their annual epidemics. In the tropics, influenza shows no clear seasonality. In the past ten years, H3N2 has tended to dominate in prevalence over H1N1, H1N2, and influenza B. Measured resistance to the standard antiviral drugs amantadine and rimantadine in H3N2 has increased from 1% in 1994 to 12% in 2003 to 91% in 2005.[1]
Seasonal H3N2 fluSeasonal H3N2 flu is a human flu from H3N2 that is slightly different from one of last year's flu season H3N2 variants. "Seasonal influenza viruses flow out of overlapping epidemics in East and Southeast Asia, then trickle around the globe before dying off. [Identifying] the source of the viruses allows global health officials to better predict which viruses are most likely to cause the most disease over the next year. [An analysis of] 13,000 samples of influenza A/H3N2 virus that were collected across six continents from 2002 to 2007 by the WHO's Global Influenza Surveillance Network [showed that] newly emerging strains of H3N2 appeared in East and Southeast Asian countries about 6 to 9 months earlier than anywhere else. The strains generally reached Australia and New Zealand next, followed by North America and Europe. The new variants typically reached South America after an additional 6 to 9 months, the group reported." [2] Swine flu
Pigs can harbor influenza viruses adapted to humans and others that are adapted to birds, allowing the viruses to exchange genes and create a pandemic strain. Avian influenza virus H3N2 is endemic in pigs in China and has been detected in pigs in Vietnam, increasing fears of the emergence of new variant strains. Health experts say pigs can carry human influenza viruses, which can combine (i.e. exchange homologous genome sub-units by genetic reassortment) with H5N1, passing genes and mutating into a form which can pass easily among humans. H3N2 evolved from H2N2 by antigenic shift and caused the Hong Kong Flu pandemic of 1968 and 1969 that killed up to 750,000 humans. The dominant strain of annual flu in humans in January 2006 is H3N2. Measured resistance to the standard antiviral drugs amantadine and rimantadine in H3N2 in humans has increased to 91% in 2005. A combination of these two subtypes of the species known as the avian influenza virus in a country like China is a worst case scenario. In August 2004, researchers in China found H5N1 in pigs.[4] Hong Kong Flu (1968-1969)The Hong Kong Flu was a category 2 flu pandemic caused by a strain of H3N2 descended from H2N2 by antigenic shift, in which genes from multiple subtypes reassorted to form a new virus. The Hong Kong Flu pandemic of 1968 and 1969 infected an estimated 500,000 people with a low death rate.[5][6] Fifty million people were infected in the United States, resulting in an estimated 34,000 deaths.[7] Both the H2N2 and H3N2 pandemic flu strains contained genes from avian influenza viruses. The new subtypes arose in pigs coinfected with avian and human viruses and were soon transferred to humans. Swine were considered the original "intermediate host" for influenza, because they supported reassortment of divergent subtypes. However, other hosts appear capable of similar coinfection (e.g., many poultry species), and direct transmission of avian viruses to humans is possible. H1N1 may have been transmitted directly from birds to humans (Belshe 2005).[8] The Hong Kong flu strain shared internal genes and the neuraminidase with the 1957 Asian Flu (H2N2). Accumulated antibodies to the neuraminidase or internal proteins may have resulted in much fewer casualties than most pandemics. However, cross-immunity within and between subtypes of influenza is poorly understood. The Hong Kong flu was the first known outbreak of the H3N2 strain, though there is serologic evidence of H3N? infections in the late 19th century. The first record of the outbreak in Hong Kong appeared on July 13, 1968 in an area with a density of about 500 people per acre in an urban setting. The outbreak reached maximum intensity in 2 weeks, lasting 6 weeks in total. The virus was isolated in Queen Mary Hospital. Flu symptoms lasted 4 to 5 days.[5] By July 1968, extensive outbreaks were reported in Vietnam and Singapore. By September 1968, it would reach India, Philippines, northern Australia and Europe. That same month, the virus entered US California from returning Vietnam War troops. It would reach Japan, Africa and South America by 1969.[5] "Three strains of Hong Kong influenza virus isolated from humans were compared with a strain isolated from a calf for their ability to cause disease in calves. One of the human strains. A/Aichi/2/68, was detected for five days in a calf, but all three failed to cause signs of disease. Strain A/cal/Duschanbe/55/71 could be detected for seven days and caused an influenza-like illness in calves."[9] Fujian flu (2003?2004)
Diagram of influenza virus nomenclature. Fujian flu refers to flu caused by either a Fujian human flu strain of the H3N2 subtype of the Influenza A virus or a Fujian bird flu strain of the H5N1 subtype of the Influenza A virus. These strains are named after Fujian, a coastal province of the People's Republic of China that is across the Taiwan strait from Taiwan.[10] A/Fujian (H3N2) human flu (from A/Fujian/411/2002(H3N2) -like flu virus strains) caused an unusually severe 2003?2004 flu season. This was due to a reassortment event that caused a minor clade to provide a haemagglutinin gene that later became part of the dominant strain in the 2002?2003 flu season. A/Fujian (H3N2) was made part of the trivalent influenza vaccine for the 2004-2005 flu season and its descendants are still the most common human H3N2 strain. 2004-2005 flu seasonThe 2004–05 trivalent influenza vaccine for the United States contained A/New Caledonia/20/99-like (H1N1), A/Fujian/411/2002-like (H3N2), and B/Shanghai/361/2002-like viruses.[11] 2005-2006 flu seasonThe vaccines produced for the 2005–2006 season use:
2006-2007 flu seasonThe 2006–2007 influenza vaccine composition recommended by the World Health Organization on February 15, 2006 and the U.S. FDA's Vaccines and Related Biological Products Advisory Committee (VRBPAC) on February 17, 2006 use:
2007-2008 flu seasonThe composition of influenza virus vaccines for use in the 2007–2008 Northern Hemisphere influenza season recommended by the World Health Organization on February 14, 2007[13] was:
"A/H3N2 has become the predominant flu subtype in the United States, and the record over the past 25 years shows that seasons dominated by H3N2 tend to be worse than those dominated by type A/H1N1 or type B." Many H3N2 viruses making people ill in this 2007-2008 flu season differ from the strains in the vaccine and may not be well covered by the vaccine strains. "The CDC has analyzed 250 viruses this season to determine how well they match up with the vaccine, the report says. Of 65 H3N2 isolates, 53 (81%) were characterized as A/Brisbane/10/2007-like, a variant that has evolved [notably] from the H3N2 strain in the vaccine?A/Wisconsin/67/2005."[16] See alsoFurther reading
Sources
de:Hongkong-Grippe es:Gripe de Hong Kong it:Influenza di Hong Kong nl:Hongkonggriep ja:H3N2?? pt:Gripe de Hong Kong zh:???? Source: Wikipedia | The above article is available under the GNU FDL. | Edit this article
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