Animated Video by Hybrid Medical Animation
Antigenic shift is the process by which at least two different strains of a virus (or different viruses), especially influenza, combine to form a new subtype having a mixture of the surface antigens of the two original strains. The term antigenic shift is more often applied specifically, (but is not limited) to the influenza literature, as it is the best known example (e.g. visna virus in sheep). Antigenetic shift is a specific case of reassortment or viral shift that confers a phenotypic change.
In terms of virology, the marine ecosystem has been largely unstudied, but due to its extraordinary volume, high viral density (100 million viruses per mL in coastal waters, 3 million per mL in the deep sea) and high cell lysing rate (as high as 20% on average); marine viruses’ antigenic shift and genetic recombination rates must be quite high. This is most striking when one considers that the coevolution of prokaryotes and viruses in the aquatic environment has been going on since before eukaryotes appeared on earth.
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 influenzavirus A, influenza B and influenza C. Antigenic shift, however, occurs only in influenzavirus A because it infects more than just humans.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.
Antigenic shift is important as it is a pathway that viruses may follow to enter a new niche, and so should not be overlooked in the emergence of new viral pathogens. It could occur with primate viruses and may be a factor to consider for the appearance of new viruses in the human species such as HIV. Due to the structure of its genome HIV does not undergo reassortment, but it does recombine freely and via superinfection HIV can produce recombinant HIV strains that differ significantly from their ancestors.
Flu strains are named after their types of hemagglutinin and neuraminidase surface proteins, so they will be called, for example, H3N2 for type-3 hemagglutinin and type-2 neuraminidase. 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 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. 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. One increasingly worrying situation is the possible antigenic shift between avian influenza and human influenza. This antigenic shift could cause the formation of a highly virulent virus.
The WHO, NIH, CDC is now closely watching the new H1N1 Flu, as it circulates around the globe, and into the Southern Hemisphere. If it were to have an antigenic shift (mutate biologically), and return to the Northern Hemisphere in the fall of 2009, it could have become a very dangerous virus.
Role in transmission of influenza viruses from animals to people
Influenza A viruses are found in many different animals, including ducks, chickens, pigs, whales, horses, and seals. Influenza B viruses circulate widely principally among humans, though it has recently been found in seals.
There are 16 different hemagglutinin subtypes and 9 different neuraminidase subtypes, all of which have been found among influenza A viruses in wild birds. Wild birds are the primary natural reservoir for all subtypes of influenza A viruses and are thought to be the source of influenza A viruses in all other animals.Most influenza viruses cause asymptomatic or mild infection in birds; however, the range of symptoms in birds varies greatly depending on the strain of virus. Infection with certain avian influenza A viruses (for example, some strains of H5 and H7 viruses) can cause widespread disease and death among some species of wild and especially domestic birds such as chickens and turkeys.
Pigs can be infected with both human and avian influenza viruses in addition to swine influenza viruses. Infected pigs get symptoms similar to humans, such as cough, fever, and runny nose. Because pigs are susceptible to avian, human and swine influenza viruses, they potentially may be infected with influenza viruses from different species (e.g., ducks and humans) at the same time. If this happens, it is possible for the genes of these viruses to mix and create a new virus.
For example, if a pig were infected with a human influenza virus and an avian influenza virus at the same time, an antigenic shift could occur, producing a new virus that had most of the genes from the human virus, but a hemagglutinin or neuraminidase from the avian virus. The resulting new virus would likely be able to infect humans and spread from person to person, but it would have surface proteins (hemagglutinin and/or neuraminidase) not previously seen in influenza viruses that infect humans, and therefore to which most people have little or no immune protection. If this new virus causes illness in people and can be transmitted easily from person to person, an influenza pandemic can occur.
Each year’s flu vaccine contains three flu strains — two A strains and one B strain — that can change from year to year.
- After vaccination, your body produces infection-fighting antibodies against the three flu strains in the vaccine
- If you are exposed to any of the three flu strains during the flu season, the antibodies will latch onto the virus’s HA antigens, preventing the flu virus from attaching to healthy cells and infecting them.
- Influenza virus genes, made of RNA, are more prone to mutations than genes made of DNA.
- If the HA gene changes, so can the antigen that it encodes, causing it to change shape
If the HA antigen changes shape, antibodies that normally would match up to it no longer can, allowing the newly mutated virus to infect the body’s cells. This type of genetic mutation is called “antigenic drift.”
The genetic change that enables a flu strain to jump from one animal species to another, including humans, is called antigenic shift. Antigenic shift can happen in three ways:
Antigenic Shift 1
- A duck or other aquatic bird passes a bird strain of influenza A to an intermediate host such as a chicken or pig.
- A person passes a human strain of influenza A to the same chicken or pig.
- When the viruses infect the same cell, the genes from the bird strain mix with genes from the human strain to yield a new strain.
- The new strain can spread from the intermediate host to humans.
Antigenic Shift 2
- Without undergoing genetic change, a bird strain of influenza A can jump directly from a duck or other aquatic bird to humans.
Antigenic Shift 3
- Without undergoing genetic change, a bird strain of influenza A can jump directly from a duck or other aquatic bird to an intermediate animal host and then to humans.
The new strain may further evolve to spread from person to person. If so, a flu pandemic could arise.
Graphic credit: National Institute of Allergy and Infectious Diseases (NIAID).
Influenza viruses are extremely changeable. Their RNA often mutates and acquires subtle changes that alter the characteristics of the virus enough so that it can evade host antibodies.
Influenza can also undergo major, rapid changes that cause it to change so dramatically that host defenses are practically useless.
These major changes or “antigenic shifts” can occur when two separate strains of influenza infect the same cell simultaneously. When this happens, a new strain, combining characteristics of the two previous strains can emerge.
Here you see viral particles of two separate influenza strains: H3N2, which commonly infects humans and H5N1, which commonly infects birds. H5N1 has recently been known to also infect humans with a fatality rate of 40%. Fortunately, so far, the H5N1 virus does not transmit easily between humans like an H3N2 virus does.
To infect a cell, the virus particles must cross the cell membrane. The hemagglutinin (H) proteins help the virus to attach to the membrane. It may be that the H5N1 virus is so virulent (deadly) to humans because the H5 hemagglutinin is particularly efficient at attaching to human host cells.
Once inside the cell, the virus can go to work. Here, you can see that particles of both the H5N1 virus and the H3N2 virus have infected this cell.
First, the viral particles are uncovered. The lipid envelope and protein capsid are removed.
The RNA strands are transcribed.
The host cell’s machinery contructs the new viral proteins coded for by the viral DNA.
New influenza particles are assembled from the new viral proteins. The lipid envelope is formed from host cell materials.
The newly assembled viral particles bud off from the host cell. The protein neuraminidase (N) seems to be important in the budding process and may be involved in determining transmissability of the virus.
GoogleNews.com, May 13, 2009, by Paul Douglas — You’ve heard the expression before: “bolt from the blue” or “out of the blue”. I’m referring to a weather phenomenon that claims more lives in the USA than tornadoes and hurricane combined – lightning. Every year nearly a dozen people are killed by lightning, struck dead with blue sky directly overhead, a thunderstorm 5-10 miles away. Lightning can travel horizontally up to 10 miles away from the parent thunderhead. The solution? Wait at least 30 minutes after hearing the last thunderclap before heading back outside, to be absolutely safe. Remind your kids about the 30-30 Rule. If you can count 30 seconds between seeing the “flash” of lightning and hearing the “bang” of thunder, you’re in danger – time to head indoors. And at the tail end of a storm wait at least 30 minutes after the last thunder before venturing back outside. Just because the rain has subsided does NOT mean the lightning risk has passed.
Here are more tips that a thunderstorm may be especially severe:
- Lightning can be detected on your AM radio. These electromagnetic bursts show up as static on your AM radio dial. If you hear nearly continuous static it’s a tip-off that a line of thunderstorms may be approaching.
- Thunderstorms are most likely around the dinner hour, when the atmosphere is most unstable.
- Before a storm strikes winds at the ground usually blow from the south or southeast. T-storms are rare when surface winds are blowing from the west, northwest or north.
- Look for cues in nature: the old proverb “birds fly low before a storm” has some scientific merit: apparently birds fly near the ground to relieve air pressure in their ears; the barometer usually falls sharply ahead of a T-storm.
- An eerie, greenish color to the sky and large hail are tip-offs that a storm may be especially severe, even capable of spinning up a tornado.