Goodbye Rinderpest, Hello Measles

Variola virus, the agent of smallpox, once held a lonely spot on the list of globally eradicated diseases. Now it is joined by rinderpest, the cattle plague. The OIE (Organization for Animal Health) declared the disease eradicated and the UN’s Food and Agriculture Organization (FAO) is expected to adopt a resolution in June declaring it eradicated. The disease affects cloven-hoofed animals and can have an extremely high mortality rate in some cattle and buffalo. It is also extremely contagious, so its rapid spread through livestock can have an obviously large impact on animal health, food production and livelihood of cattle farmers. Thanks to an intensive word-wide vaccination effort, rinderpest virus can now be added to the list of organisms we actually intended to make extinct.

Rinderpest is caused by rinderpest virus, a member of the Morbillivirus genus. Another member of that genus is measles virus. Oh, and there is a vaccine for that too. In fact North America was free of measles in 2002 and perhaps it was on track for global eradication. But not anymore.

My son recently turned one, so I took him to get his measles, mumps and rubella (MMR) vaccine, feeling confident that Im helping protect him from three pretty nasty viruses, and not giving him Autism. In fact, before he turned one, I’d been feeling a little anxious about getting him the vaccine soon enough. My email inbox keeps filling up with notices from ProMED mail (Program to Monitor Emerging Diseases) with news of various measles outbreaks across the globe.

There are outbreaks all over Europe, especially in France, the UK, Spain and Switzerland. The epidemic in France that started in 2008 has now reached over 14,000 people, with 9000 of those infections reported in the last 6 months. (France has a vaccination rate of about 60%. Vaccination rates in the UK bottomed out at 80% and are slowly on the rise again). Outbreaks in the USA and Canada have been small, the vaccination rates are higher but not high enough. Many of these can be tracked to travel of unvaccinated individuals to areas where measles is still endemic or flaring up. In Minnesota, an outbreak counting 21 people has sent 13 people to the hospital (an unusually high number). Of the 21 people, 8 were old enough to be vaccinated but weren’t, 7 were too young to be vaccinated, 1 was vaccinated and the status of the others is unknown.

The Minnesota outbreak emphasizes an important point: it is necessary to maintain a sufficiently high level of herd immunity to prevent outbreaks and protect those who can’t be vaccinated. For most diseases, vaccination rates need to be at or above 95% to prevent outbreaks, and may need to be even higher for measles. Virus transmission depends on the virus finding a susceptible host. If a population is primarily made up of immune individuals, the virus has a hard time maintaining a chain of transmission.

Vaccination is therefore not just a matter of personal health, but community health. Maintaining high herd immunity helps protect babies too young to be vaccinated by limiting the chances that they ever encounter the virus. Don’t just get your kids vaccinated to protect themselves, do it to protect us all.

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Swine Flu: New and Improved!

Contributed by guest blogger: Marni Hershbain ’11

Flu season is never enjoyable, but some seasons are certainly worse than others. The 2009 swine flu outbreak was particularly serious because the 2009 H1N1 strain was a novel virus, formed via the reassortment of swine, avian and human flu viruses. There were over 600,000 confirmed cases of H1N1 and over 18,449 deaths during the course of the pandemic. While this sounds pretty bad, it could have been much worse. The transmission efficiency of H1N1 was actually much lower than those of other pandemic strains, such as the 1918 H1N1 strain. Unfortunately, recent research demonstrates that this could change.

Flu strains are characterized by the hemagglutinin and neuraminidase found on their surfaces, hence names like H1N1. In order for the virus to infect a cell, hemagglutinin on the surface of the virus must bind to glycan receptors on the cell. Therefore, to explain the low transmission efficiency of 2009 H1N1, researchers looked to its hemagglutinin.
In most flu strains, the amino acids at positions 219 and 227 within the hemagglutinin are both hydrophobic or both charged. In 1918 H1N1 both are hydrophobic. However, the 2009 H1N1 strain has isolucine, a hydrophobic molecule, in position 219 and glutamic acid, a charged molecule, in position 227. Researchers hypothesized that lacking either hydrophobic or ionic interactions at these positions would disrupt the positioning of neighboring residues and decrease the hemagglutinin’s binding affinity. They further hypothesized that if they replaced isolucine with the charged amino acid lysine, stable inter-residue interactions would occur and binding affinity would increase.

When researchers compared the ability of wild type and isolucine→lysine mutant strains to bind to an array of glycans representing human binding sites, they found the binding ability of the mutant strain was 30 times greater. The mutant version also bound more intensely to receptors in human tracheal tissue. Researchers also infected ferrets (commonly used as models in human influenza studies) with either wild type or mutant virus. Only the ferrets infected with mutant virus spread the infection to all of the previously uninfected ferrets placed in close proximity to them.

The mutation of just one amino acid could greatly impact the transmission efficiency of 2009 H1N1. Flu viruses tend to mutate frequently, which is why a new vaccine needs to be developed every year. Predicting what these mutations will be is not an easy task, but mutations at the positions in this study will certainly be monitored closely.

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