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4/12/23, 8:35 PM Antigenic shift - Wikipedia

Antigenic shift
Antigenic shift is the process by which two or more
different strains of a virus, or strains of two or more
different viruses, combine to form a new subtype
having a mixture of the surface antigens of the two or
more original strains. The term is often applied
specifically to influenza, as that is the best-known
example, but the process is also known to occur with
other viruses, such as visna virus in sheep.[1] Antigenic
shift is a specific case of reassortment or viral shift that
confers a phenotypic change.

Antigenic shift is contrasted with antigenic drift, which


is the natural mutation over time of known strains of
influenza (or other things, in a more general sense)
which may lead to a loss of immunity, or in vaccine
mismatch. Antigenic drift occurs in all types of
influenza including influenza A, influenza B and
influenza C. Antigenic shift, however, occurs only in
influenza A because it infects more than just
humans.[2] Affected species include other mammals
and birds, giving influenza A the opportunity for a
major reorganization of surface antigens. Influenza B
and C principally infect humans, minimizing the
chance that a reassortment will change its phenotype
drastically.[3]

In 1940s, Maurice Hilleman discovered antigenic shift, NIAID illustration of potential influenza genetic
which is important for the emergence of new viral reassortment
pathogens as it is a pathway that viruses may follow to
enter a new niche.[4][5]

Role in the transmission of influenza viruses from non-


human animals to people
Influenza A viruses are found in many different animals, including ducks, chickens, pigs, humans,
whales, horses, and seals.[3] Influenza B viruses circulate widely principally among humans, though it
has recently been found in seals.[6] Flu strains are named after their types of hemagglutinin and
neuraminidase surface proteins (of which there are 18 and 9 respectively), so they will be called, for
example, H3N2 for type-3 hemagglutinin and type-2 neuraminidase. Some strains of avian influenza
(from which all other strains of influenza A are believed to stem[2]) can infect pigs or other
mammalian hosts. When two different strains of influenza infect the same cell simultaneously, their
protein capsids and lipid envelopes are removed, exposing their RNA, which is then transcribed to

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4/12/23, 8:35 PM Antigenic shift - Wikipedia

mRNA. The host cell then forms new viruses that combine their antigens; for example, H3N2 and
H5N1 can form H5N2 this way. Because the human immune system has difficulty recognizing the new
influenza strain, it may be highly dangerous, and result in a new pandemic.[3]

Influenza viruses which have undergone antigenic shift have caused the Asian Flu pandemic of 1957,
the Hong Kong Flu pandemic of 1968, and the Swine Flu scare of 1976. Until recently, such
combinations were believed to have caused the infamous Spanish flu outbreak of 1918 which killed
40~100 million people worldwide. However, more recent research suggests the 1918 pandemic was
caused by the antigenic drift of a fully avian virus to a form that could infect humans efficiently.[7][8]
The most recent 2009 H1N1 outbreak was a result of antigenic shift and reassortment between
human, avian, and swine viruses.[9]

Role of pigs in Influenza antigenic shift


Pigs are especially important in antigenic shift of influenza viruses. Because pigs can be infected with
strains of influenza that infect various other species of animals, they act as 'mixing pots' for the virus.
When multiple virus strains, such as a duck and human influenza strain, infect the same pig, antigenic
shift is likely to occur. While most of the virus strains resulting from this will be dead-end strains, a
few have the potential to become pandemic viruses.[10]

See also
Coinfection

Notes
1. Narayan, O; Griffin, DE; Chase, J (1977). "Antigenic shift of visna virus in persistently infected
sheep". Science. 197 (4301): 376–378. Bibcode:1977Sci...197..376N (https://ui.adsabs.harvard.e
du/abs/1977Sci...197..376N). doi:10.1126/science.195339 (https://doi.org/10.1126%2Fscience.19
5339). PMID 195339 (https://pubmed.ncbi.nlm.nih.gov/195339).)
2. Treanor, John (15 January 2004). "Influenza vaccine--outmaneuvering antigenic shift and drift".
New England Journal of Medicine. 350 (3): 218–220. doi:10.1056/NEJMp038238 (https://doi.org/1
0.1056%2FNEJMp038238). PMID 14724300 (https://pubmed.ncbi.nlm.nih.gov/14724300).
3. Zambon, Maria C. (November 1999). "Epidemiology and pathogenesis of influenza". Journal of
Antimicrobial Chemotherapy. 44 (Supp B): 3–9. doi:10.1093/jac/44.suppl_2.3 (https://doi.org/10.1
093%2Fjac%2F44.suppl_2.3). PMID 10877456 (https://pubmed.ncbi.nlm.nih.gov/10877456).
4. Oransky, Ivan (14 May 2005). "Maurice R Hilleman" (https://www.thelancet.com/journals/lancet/art
icle/PIIS0140-6736(05)66536-1/abstract). The Lancet. 365 (9472): 1682. doi:10.1016/S0140-
6736(05)66536-1 (https://doi.org/10.1016%2FS0140-6736%2805%2966536-1). ISSN 0140-6736
(https://www.worldcat.org/issn/0140-6736). PMID 15912596 (https://pubmed.ncbi.nlm.nih.gov/159
12596). S2CID 46630955 (https://api.semanticscholar.org/CorpusID:46630955).
5. Kurth, Reinhard (April 2005). "Maurice R. Hilleman (1919–2005)" (https://doi.org/10.1038%2F434
1083a). Nature. 434 (7037): 1083. doi:10.1038/4341083a (https://doi.org/10.1038%2F4341083a).
ISSN 1476-4687 (https://www.worldcat.org/issn/1476-4687). PMID 15858560 (https://pubmed.ncb
i.nlm.nih.gov/15858560). S2CID 26364385 (https://api.semanticscholar.org/CorpusID:26364385).
6. Carrington, Damian (11 May 2000). "Seals pose influenza threat" (http://news.bbc.co.uk/1/hi/sci/te
ch/744945.stm). BBC.

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