Surviving an Influenza Supervirus – Chapter Two

Chapter Two

The Influenza Virus Strikes

Originally attributed to the “influence” of the heavenly bodies, the result of this devastating virus became known as Influenza early on in human history.

Transmitted through the air, the influenza virus, only 80 to 120 nm in size, produces a lower respiratory infection that inflames and damages the larynx, trachea and bronchi. Symptoms include fever, nasal and throat congestion, body aches, and possibly a rash. But that can be just the beginning. More violent symptoms, as seen in the 1918 epidemic described below, included profuse nosebleeds and hemoptysis, blood coughed up from the respiratory system. Some chroniclers noted bleeding from the ears, explosive coughing that tore apart abdominal muscles and rib cartilage; terrible headaches, skin changes including blue around the lips or fingertips signifying cyanosis (lack of oxygen), vomiting, intense body aches, writhing.*

One of the most devastating epidemics humankind has ever experienced, influenza struck during the last year of World War I and was erroneously nicknamed the Spanish Flu. An invisible killer of 50 million people, scientists have since been able to sort through the details. It is not pretty or reassuring. And it didn’t originate in Spain. It erupted in Fort Riley, Kansas, as men were getting ready to go overseas to fight:

It is March 11, 1918. There has been a dust storm that has mixed with burning manure from thousands of army horses and mules that are getting ready to go overseas to battle. There is a haze above the fort and the cook comes down with a bad cold. One hundred men also get sick with a similar presentation to the cook. But then forty-eight soldiers die, attributed to pneumonia. Before you know it 84,000 soldiers ship out to Europe and then 118, 000 the next month. Six soldiers die on the ship crossing the Atlantic Ocean. Now Europe is infected with soldiers on both sides beginning to die. By July whatever this is has struck soldiers and civilians in North Africa, Russia, India, China, Japan, the Philippines, as far as New Zealand.
The virus mutates, making it impossible for the immune system to fight back easily and when it arrives back across the Atlantic to the good ol’ USA it becomes a devastating situation. No one has seen anything like this before.
In late August and early September doctors at Chelsea Naval Hospital in Boston in are shaken to discover that bloody, foamy liquid is drowning the soldiers’ lungs. Three people in nearby Quincy die. The unknown assailant is an airborne virus and at the parade ‘A Win the War for Freedom’ it ends up spreading the disease to the rest of the population. One thousand people die within a month.

No one knows what to do since they haven’t even seen a virus under a microscope because an electron microscope won’t be invented for another 20 years!!

One doctor describes it as “a most vicious type of pneumonia” he had ever seen: “Two hours after admission they have the mahogany spots over the cheek bones, and a few hours later you begin to see cyanosis (blueness, lack of oxygen) extending from their ears and spreading all over the face. It’s only a matter of hours then until death comes and it is simply a struggle for air until they suffocate.”

During this time local governments took measures…people in San Francisco were forced by law to wear masks…elsewhere whole towns were quarantined, public places were closed.
In San Diego a law forced people to wear gauze masks in the street. A government rhyme went like this:

Obey the laws
And wear the gauze
Protect your jaws
From septic paws.

But by November 1918, eight months after it started, the pandemic died down, disappearing as fast as it came on.

Structure of an Influenza Virus

Influenza A, B and C are differentiated by their internal nucleoprotein and matrix (or outer) proteins. It is Influenza A virus that can infect humans, birds, swine along with seals and horses that we are concerned with in this handbook. (Influenza B affects only humans so now crossover concern and C can infect humans and swine but it is very rare.)

Like any virus, Influenza A virus has two particles: a protein coat that wraps around its genetic material, a nucleic acid core.

In influenza the genetic material is RNA, ribonucleic acid, rather than DNA, the nucleic acid that makes up other viruses. RNA has a very high rate of mutation (only the HIV virus that causes AIDS is higher). This can be a million times more that of DNA.

Influenza A virus is shaped like a corkscrew. There are eight twists, each containing some of the genetic material. Only two of these are of real concern, the ones that generate the viral coat protein. These two viral coat proteins are called antigens and are what the killer cells of our immune system react to: hemagglutinin (H) and neuramindase (N).

Hemagglutinin and neuramindase have various subtypes. H has fourteen and N nine, each drastically different from the other.

This ability to conjure new strains is what makes the influenza viruses so dangerous, this ever changing, always evolving ability. This unpredictability, or antigenic drift, means the immune system is always trying to catch up, to get to know a new virus. Meanwhile the virus travels through the air, circulates within a family, a school, or a community looking for new host cells to infect.

However this doesn’t happen during one bout of disease. This happens when the RNA segments are actually…get ready for it…swapped between different viral strains of pigs and ducks.

Thus as they outwit us at every turn by changing their structure not only internally it is when our genetic material is swapped with some from a pig or a bird is where the real danger lies.

In 1918, this “Spanish” Flu, was ground zero for H1N1 although no one knew to categorize it that at the time.

And although it can happen within ducks and other water birds, it seems pigs are what the Zimmerman brothers call in their book Killer Germs, “nature’s true mixing bowl for flu viruses.” Apparently if a human flu virus replicates inside a pig it could get an H or N gene from a duck. This is why the 1918 pandemic would ultimately be called the first swine flu.

It’s easy for us in North America to keep pigs and humans apart but not so easy in countries in Asia where their farming practices rely on polyculture, meaning hens are kept above pigs and feed on their feces. These pig feces then fertilize ponds where ducks swim…well, you get the picture.

What seems to be true as well as frightening is that influenza viruses can thrive in the digestive tract of these critters—pigs and ducks —with no harmful effect on them. So they don’t die off.

In 1976 there was another scare of swine flu, something no one had seen since 1918 but it turned out to be mostly H3N2, and the H1N1 was not as transmissible as in 1918, not nearly as virulent.

It is the proficiency of spreading, the transmission of the viral vector that is often the determining factor. For instance, the H5N1 (bird) flu cannot spread between humans (it first jumped from birds to humans in 1997 ) but it was a major scare in 2005 (from ducks in Vietnam). This particular flu virus is poorly adapted to its human host because of its inability to transmit efficiently. It does not become airborne; it is not therefore transmissible when people sneeze or cough.

In the last one hundred years there have been five influenza pandemics. In the H1N1 of 1918 all new recombinant genes came from birds; the H2N2 “Asian” flu of 1957 added new genes including H and N from birds; the H3N2 “Hong Kong” flu of 1968 added genes from wild ducks; and the “Russian” flu of 1977, a 1950s version of H1N1, that is supposed to have escaped from a Russian lab. And then there was another H1N1 “swine” flu, in 2009 in Mexico.

This continuing ability to make changes genetically is why there are regular yearly outbreaks of the “flu” and then every decade or so an epidemic of some level of influenza. The past century has seen pandemics from viruses of the H1, H2 and H3 subtypes but not H5 although it is circulating in flocks of birds throughout the world and needs only five mutations in its gene code to possibly become transmissible between humans. If this happens or two different strains of another subtype recombine into a new version of the influenza virus capable of illness in humans we are in serious trouble.

But before we all get our knickers in a twist or hyperventilate let’s look at the obstacles a virus must contend with before it can establish itself with a new host population.

First it has to find the right host cell receptor molecule to unite with…something that stops the virus in its tracks right there…and then it also has to use the cell’s machinery, also a possible detriment to a successful mission.

And so we can develop our host response, build our immune system before we get anywhere near an influenza virus A with any subtype. We can harness our reserves through increasing optimal immunity, what this handbook is all about.