Column: The Natural View; What’s the big deal with the bird flu?
Imagine a heavy White Pages phone book for a large metropolitan area. Imagine each name in the phonebook represents a species in the world and each number to the right of the name represents a virus that infects only that species.
A phone number is a simple code and, similarly, a virus is a capsule containing a simple genetic code: short DNA or RNA segments. Each virus has specific surface proteins arranged to connect to the cell membranes of their host species, like a key to a lock. This surface structure allows a virus to break into the host’s cell wall, insert its genetic code, then take over the cell’s machinery to replicate. Acute sickness or death of the host may follow, but eventually the host’s immune system may organize a defense known as antigens that maintain some control over the virus. Stable host/virus relationships are the norm in most natural populations.
But researchers are beginning to realize that human environmental impacts are releasing viruses from a once-stable host/virus condition. Changing land-use patterns, global warming, increasing populations, pollution, animal markets, misused antibiotics and poverty are all strongly linked to infectious disease outbreaks.
Human encroachment into the tropical forests of Africa allowed Ebola and AIDS viruses to jump from native wildlife to humans. Deforestation and global warming are expanding the geographic range of malaria and dengue fever. The examples are endless, but geneticists are finding common patterns in most of the world’s deadliest viruses: viral strains persisted relatively unchanged for centuries and then … Bang! An explosion of new variation began erupting in the 1800s and has only been accelerating.
Still, human-to-human viral transmission is difficult, as many of the world’s infectious diseases depend on blood-to-blood contact or intermediate hosts such as mosquitoes and ticks. So what is the big deal about bird flu?
Most “Influenza A” viral strains (bird flu) are not dangerous to humans, and if they are, transmission from bird to human is unusual. But if the conditions are right, a highly virulent avian flu strain can combine with other flu strains – from birds, pigs or humans.
When an organism is infected with multiple influenza strains, the viruses may recombine in new ways. (Similar to when a man and a woman produce a baby, the recombined genetic code produces a baby with a unique mixture of genes.) Because of the already high mutation rate of influenza viruses, further genetic recombination produces an explosion of new variation.
This explosion of new variation increases the chance the virus will evolve the surface protein structure needed to penetrate and infect human cells that have no antigens for the foreign strain … a pandemic is born.
The 1918 “Spanish Flu” avian influenza was the worst human pandemic in recorded history, killing around 50 million people; 10 percent of the human population at the time. (Possibly up to 100 million; influenza statistics were rarely accurately because initial infection was often masked by a secondary infection such as bacterial pneumonia.)
This 1918 virus was named H1N1, referring to the structure of the surface proteins (HA) hemaglutinin and (NA) neuraminidase.
Lesser avian flu pandemics occurred in 1957 (H2N2) and 1968 (H3N2). In 1997, scientists in Hong Kong began tracking an astonishing number of new strains in local domestic bird markets (~500 strains). Out of this reservoir of viral variation, an unusually deadly strain, H5N1, emerged killing scores of wild and domestic fowl and six humans.
Hong Kong officials responded, killing 1.5 million domestic fowl. But H5N1 reemerged in 2002 along with a less deadly H9N2. In a phenomenon called “cross protection,” some infected chickens did not develop symptoms of H5N1 because of antibodies produced in response to the similar H9N2, effectively masking the disease while continuing to shed H5N1. Worse yet, some wild migratory waterfowl have now developed outright immunity while still spreading the virus, becoming an H5N1 “Trojan Horse.”
In 2003, an H5N1 “super strain” reemerged with even more virulence. In lab tests, this new strain (Z genotype) was not limited to respiratory cells like the catastrophic H1N1. Shockingly, tests revealed H5N1 had the ability to infect cells in the blood, heart and brain; potentially evolving into a systemic disease.
As of March 9, 2006, the World Health Organization recorded 175 human H5N1 cases with 96 deaths (~50 percent mortality), and hundreds of recent H5N1 animal cases have been reported spreading from Asia to Western Europe, and may reach North America sooner than expected. Because H5N1 is so especially virulent, with 50 percent mortality in human cases, the threat is very serious.
Of the 15 HA and 9 NA possible flu virus surface proteins, a new combination may result in human-to-human transmission and there is no way of knowing which one until it happens. Because of this, health officials may be left without an effective vaccine.
Infectious disease experts are calling for pharmaceutical companies to ready influenza “seed viruses” of all possible HA and NA combinations for quick vaccine development and stockpiling more general anti-viral agents as opposed to specific vaccines. If these anti-viral agents can be readied and administered to the young and old in advance of a spreading flu, mortality could be reduced dramatically.
There is no need to panic, but federal, state and local governments are developing plans to stockpile anti-viral agents, outline effective quarantine procedures and procedures to close schools and daycare facilities for extended periods. Wildlife and agricultural officials are developing plans for infection risks associated with migratory waterfowl, domestic birds, and pigs.
To review information provided by the WHO, CDC, state of Utah and USU, see links:
http://www.cdc.gov/
http://www.who.int/en/
http://health.utah.gov/
http://extension.usu.edu/files/factsheets/BirdFlu0308.pdf
Send comments or questions to jmgoodell@cc.usu.edu.