Release date: 2017-10-11
Experts say that the real goal of the vaccine is that even if you get the flu, you won't be as ill as you didn't. Image source: Michael Orrell
Although the flu virus has not yet hit the northern hemisphere, the season of flu shots has arrived. The banner outside the pharmacy urged: "Please vaccinate the flu now." However, it is not publicized that most of the vaccines are flat. The most commonly used flu vaccine can only protect up to 60% of vaccinates. In some years, the effectiveness of the vaccine has even dropped to 10%. Michael Osterholm, an epidemiologist at the University of Minnesota, said that considering the severe flu season, only 50,000 people will die in the United States. "10% to 60% of protection is better than nothing." However, for such a serious public health threat, the protection provided by the vaccine is seriously inadequate. Now, researchers are trying to understand why vaccines often lose efficacy and how to produce better-performing vaccines.
They are questioning the widely accepted view that vaccines fail when producers start working a few months before the flu season and mistakenly guess which strains will eventually spread. Instead, the researchers realized that even if the correct strain was used to produce a vaccine, the latter might fail. Part of the reason is the way it is produced, or the characteristics of the individual's immune system. "This is more complicated than we thought before." Osterholm said, "I know less about the flu than I did 10 years ago."
Vaccine effectiveness is exaggerated
The flu vaccine teaches the body to produce antibodies against the viral surface protein, the head of influenza hemagglutinin (HA). Ideally, these antibodies prevent HA from adhering to cellular receptors, thereby preventing infection. However, due to the highly variable head of the HA, vaccine manufacturers must propose new formulations each year.
For decades, researchers have argued that if the flu vaccine has a good match with the current strain, it will provide solid protection. At the same time, studies from the 1940s to the 1960s showed that the efficacy of influenza vaccines ranged from 70% to 90%. However, these studies rely on a misleading approach. Given that there is no easy way to detect viruses in the blood, researchers will measure antibody levels and look for peaks after infection. Then, in the 1990s, sensitive polymerase chain reaction tests allowed researchers to truly measure virus levels. They tell a different story. It turns out that some people did not show large antibody peaks after exposure to the virus and were therefore considered vaccinated successfully. But in fact, they showed a sudden rise in the level of the virus, which indicates the infection. Earlier evaluations exaggerated vaccine efficacy. More importantly, even if the vaccine and the strain that is becoming popular seem to match very well, its effectiveness is sometimes low. There are definitely other things happening.
After the vaccine is produced, the circulating virus strain continues to mutate, and the resulting "escape mutant" is generally considered to be the cause of vaccine failure. However, epidemiologist Arnold Monto of the University of Michigan School of Public Health expressed doubts about the important role played by escape mutants. In a recent article published in the bioRxiv preprint, the Monto team reported DNA sequencing results for 249 virus samples collected from humans during the five flu seasons. Unsurprisingly, they found a large number of HA mutations, but most of them weakened the virus, making it lose its ability to spread between humans. To this end, Monto suggests that surviving mutants that survive can be so rare that they cannot explain the vaccine failure seen year after year.
Ways to improve existing vaccines
Conversely, epidemiologist Danuta Skowronski of the British Columbia Center for Disease Control and Prevention in Vancouver blamed the vaccine for mutations in the vaccine strain itself. The most common flu vaccines contain "inactivated viruses," and manufacturers will let them grow in eggs. As the Skowronski team first reported in 2014, the virus mutates when grown in eggs, causing the vaccine to stop the growing strain.
"I think these mutations play an important role," said University of Pennsylvania virus immunologist Scott Hensley. His preliminary evidence shows that mutations adapted to eggs are the reason behind the weakening of vaccine protection in the 2016-2017 flu season. Hensley also pointed to another team's recent research: comparing vaccines grown in eggs with vaccines that contain genetically modified HA and circumvent the mutation problem. Genetically engineered vaccines provide more robust protection. According to Hensley, this provides a way to improve existing vaccines. "After 15 years, if our flu vaccine is still growing in eggs, I will be shocked."
At the same time, Hensley mentioned another way to reduce the chances of failure - to improve the technology for selecting vaccine strains. Vaccine producers rely heavily on an old technology: exposing ferrets to candidate vaccine strains and then assessing whether they can prevent strains isolated from humans that are naturally infected with the epidemic strain. Hensley said that genetic comparisons can achieve better matching.
Understanding immune response
Understanding the immune response associated with protection also helps to improve the vaccine. The immune response to the target, including the HA stem and another viral surface protein neuraminidase, rather than the HA head, did not attract much attention. Further complicating things is the multiple exposures to the flu from the vaccine and the wild-type virus from the annual "immune". “What is the impact of the first and subsequent exposure to the virus?†Adolfo GarcÃa-Sastre, a flu vaccine researcher at Icahn Medical School in Mount Sinai, New York, said, “This makes it very difficult to get solid data about what is happening.â€
The Hensley team confirmed that the immune system is also biased by the child's first exposure to the flu. The first exposure leaves a "ghost" that affects the response to subsequent vaccines. This may explain why in the 2013-2014 flu season, people in the middle of the year were attacked by unusual strains of virus variants that were not infected with most vaccinators. The team's research shows that at this age, the vaccine evokes similar but not identical HA antibodies seen in children, and the resulting immune response misses the target. "These first exposures really shape how we cope with the flu virus in our lifetime," Hensley said.
Other evidence suggests that multiple vaccinations can delay the immune response to some HAs. “Our understanding of this impact is not enough to make any recommendations at this time.†Edward Belongiab, an epidemiologist at the Marshfield Clinic in Wisconsin, who recently led a meta-analysis, said, “The best strategy is still to get it every year. A vaccine." This is especially important for older people or people with immunodeficiency: if they receive an immunization, even if the vaccine does not stop the infection, they may not be as serious.
Skowronski said many flu researchers are hesitant to discuss vaccine issues "because they are afraid of being affected by vaccination conflicts." She believes that this is wrong. "Unless we carry out these discussions, we will never be able to improve the vaccine."
At the same time, Skowronski believes that the field must be more aggressive in pursuing a generic flu vaccine. It will be resistant to a variety of virus strains and can be used for several years. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, agrees. He intends to accelerate the work by creating a coalition that includes top researchers, and hopes that next year's budget will provide funding for this. "In the next few years, I will make the production of generic flu vaccines a top priority." Fauci said, "We must do better."
Source: Science Network
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