“In each year’s flu season, most deaths are in infants and the aged, but none of the first ones in Mexico were in people over 60 or under 3 years old, a W.H.O. spokeswoman said. When a new virus emerges, deaths may occur in healthy adults who mount the strongest immune reactions. Their own defenses — inflammation and leaking fluid in lung cells — can essentially drown them from inside.” The New York Times

Pathogenicity is a complex question and a delicate balance of host response and virus load.

Cytokines play an extremely important role in the immune system’s defense against infection. We don’t fully understand the effects of intervening with the cytokine response, since this can alter the balance between the protective and damaging effects of these signaling molecules during an infection. We need to learn much more about the role and effects of cytokines during an infection. Much more work remains to be done to understand the interplay between the highly pathogenic virus and the host.

When the immune system is fighting pathogens, cytokines signal immune cells such as T-cells and macrophages to travel to the site of infection. In addition, cytokines activate those cells, stimulating them to produce more cytokines. Normally, this feedback loop is kept in check by the body. However, in some instances, the reaction becomes uncontrolled, and too many immune cells are activated in a single place. The precise reason for this is not entirely understood but may be caused by an exaggerated response when the immune system encounters a new and highly pathogenic invader. The body must limit the multiplication of the virus itself as well, as not create a cytokine storm, by an over reactive immune system.

A cytokine storm is a blizzard of signaling proteins called cytokines that is generated by various immune system cells as they coordinate an attack on an invading microorganism. But if this response runs out of control, it can cause potentially fatal inflammation and damage to the lungs. And that is what many researchers have thought kills people who are infected with flu virus. Perhaps, this is why many Mexicans have died from the swine flu, whereas people from other countries have not.

We think of external microbes as our worst enemy during an outbreak of influenza or bronchitis but our own immune system can be potentially lethal, as well. When our body detects pathogens, indicating an infection, our body might respond by over-protecting the site of infection.

The body may race so many antibodies to the infection site that they collect in a cytokine storm. When the infection is in the lungs, for example, a cytokine storm can potentially block airways and result in suffocation. Medical researchers have identified the causes and stages of the cytokine storm and are working on treatments to weaken an overactive immune response.


At all times, white blood cells circulate in the bloodstream and are the first to sense if a virus or bacteria has infiltrated the body. Immediately, our body sends immune cells, including T-cells and macrophages, to attack the infection. During this stage, our immunity functions properly, and immune cells attack the microbes so they do not get too strong a foothold in our lungs.

For reasons not completely known, too many immune cells can be sent to the infection site. This happens when a particular type of molecule in the body, known as cytokines, activate the immune cells at the infection site and cause more immune cells to flood the site of infection. This propagates what is referred to as a cytokine storm where far too many immune cells are caught in an endless loop of calling more and more immune cells to fight the infection. The cytokine storm ends up inflaming the tissue surrounding the infection.

When the infection is in the lungs, severe inflammation caused by a cytokine storm can cause permanent lung damage. A prolonged cytokine storm will eventually shut down breathing altogether. Airducts get clogged and cells no longer properly absorb oxygen. This is what makes the cytokine storm so deadly in certain epidemic strains, such as bird flu.

Even bronchitis, other varieties of influenza, pneumonia, sepsis and possibly rheumatoid arthritis are susceptible to triggering a cytokine storm.
Of course, flu vaccines are usually effective at preventing the flu during its peak season. But they are no guarantee, especially when flu strains mutate after the vaccine has been manufactured. Therefore, researchers are pursuing other methods of preventing the cytokine storm by bioengineering a drug that could slow the snowball effect of antibodies. They hope to force the cytokines to recirculate in the bloodstream, rather than pool in the lungs. Experts predict that a major influenza pandemic could kill millions of people worldwide as it has done in centuries past.

Technician Working on Egg-Based Production of Inflluenza Vaccine

Aventis Pasteur MSD/Getty Images.

A train in Mexico City, ground zero of the epidemic;


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