Steamy showers, herbal potions, chicken soup; people try almost anything to avoid getting the flu. While home remedies abound, vaccination is considered the most effective way to evade the infectious virus. But unfortunately, that flu shot you got last October just won't cut it this fall. Unlike vaccines for smallpox and polio that provide lengthy immunity, a new flu vaccine is required each year.
Influenza is an RNA virus, explains Michael Teng, Penn State assistant professor of biochemistry and molecular biology. That means its genetic material, the blueprint for the virus's structure and function, is single-stranded RNA. Unlike its counterpart in DNA, the familiar double-stranded helix, the RNA polymerase—the enzyme that copies the original strand of genetic code to replicate new material—lacks a "proof-reading function," Teng says. "In other words, viral RNA polymerases make more mistakes than viruses with a DNA genome because they don't have a way of checking whether they have made a mistake or not," he adds. In practice, that means new strains of influenza are mutating all the time.
For such a moving target, nailing the perfect vaccine formula is far from easy. Generally, annual vaccines for influenza are developed after careful evaluation of which strains will be most prevalent and harmful during that flu season. Large quantities of these strains are reproduced in the laboratory and then killed so that they lack the ability to successfully infect a host. The inactive particles make up the flu shot that is then injected into the human body. Ideally, a functional vaccine maintains a balance in which the virus is weak enough not to cause infection yet strong enough to trigger an immune response.
"The immune system is stimulated and remembers the virus," explains Teng. "So when you get exposed to the real virus, the body's response is much quicker."
For measles and mumps, one shot or a series of several shots is enough to immunize a person for life. To develop such a long-term vaccine for the flu, Teng suggests, will require a better understanding of virus-host interactions. To this end, he has been studying respiratory syncytial virus (RSV), an extremely common disease among infants and young children that leads to 100,000 hospitalizations per year in the United States alone.
Like influenza, RSV is an RNA virus that infects the respiratory tract. "They do the same things," Teng says. "They just happen to be in a different format."
His current research is aimed at learning how RSV interacts with the immune system by determining the function of each gene during infection.
He describes this work as akin to a seventh-grade shop experiment with a lawnmower. "A virus has all these parts, and what we're trying to do is take it apart and see what each one of the parts is responsible for," says Teng. By this deconstruction, Teng and his team hope to eventually be able to devise mutations that will weaken RSV's impact, and also to gain insights that may one day be applicable to influenza and other viruses. One such mutation, which Teng developed while working as a research fellow at the National Institute of Health, is already being tested in noninfectious RSV vaccine candidates. So far, he says, "It looks like the mutation is safe and immunogenic, providing a good starting point for making an effective vaccine."
If such a vaccine eventually pans out, it may be the first step toward devising a similar, long-term solution to the flu. However, until that day, Teng suggests, the best way to make it though flu season is to get that annual shot.
Michael Teng, Ph.D., is assistant professor of biochemistry and molecular biology. He can be reached at firstname.lastname@example.org.