Using Host Factors to stop the spread of the Flu
Influenza (also known as the common flu) , is caused by a virus that annually infects 5 percent to 20 percent of the U.S. population where thousands die from flu-related illness. Globally it is even more of an epidemic , where between 291,000 and 646,000 people worldwide die from seasonal influenza-related respiratory illnesses each year . Despite the widespread national and global suffering caused by influenza there is no effective drug or medication to protect from it, outside of the yearly flu shot.
The flu shot is a common (an unpleasant) part of our yearly medical checkups. Like any other vaccine it contains a weakened version of the influenza virus. However each year the viruses that are selected are based off of an estimation. The vaccine is designed to protect against the three or four influenza viruses that research indicates are most likely to spread and cause illness among people during the upcoming flu season.Through extensive testing and global surveillance activities, the Food and Drug Administration (FDA) identifies the strains and makes the final decision about the influenza vaccine viruses to be distributed in the United States. Based on that decision, candidate vaccine viruses are prepared in labs and then distributed to the public . Due to this, there is no guarantee that the vaccine will actually prevent an individual from getting sick.
Research on lung cells conducted in The University of Tokyo have raised hopes for the development of a more effective protection against influenza. Viruses (unlike bacteria) are not classified as living creatures, so they are unable to create their own proteins. Therefore, upon entry to the human body they attach to a host cell where the insert their genetic material for the forced production of viral proteins. Host factors are certain proteins that interact with the viral components and are crucial to their life cycle.In a previous version of this study Nucleoporin 93(NUP93) is the host factor found to interact with influenza virus in lung epithelial cells.
Using small interfering RNA (SiRNA), the expression of NUP93 was reduced to observe the effect on infected lung cells. The results indicate that NUP93 plays an important role in influenza virus replication and is involved in the early steps of the influenza virus life cycle. NUP93 also contributes to the nuclear export of influenza virus RNA to infect further cells in the body. However, NUP93 was not found to be necessary for the virus binding and internalization steps right after the initial interaction. So, although NUP93 is not involved in the actual infection of influenza in the cells, it does play an important role in the advancement of the virus to further cells.
Current antiviral drugs are only directed towards viral proteins which have the potential to lead to drug- resistant viruses (due to the tendency of viruses to rapidly mutate). Manufacturing antiviral drugs and medication that target host factors instead could not only prevent the possibility of dangerous mutations, but also may create produce more effective results. Further exploration and research in this area will lead to increased knowledge on viral life cycles and host-virus interaction, which could be applicable to other strains of viruses as well. In other words, it is possible that in the foreseeable future a trip to the doctors office for a flu shot will mean guaranteed protection from a fever and headache filled seasonal experience.
2 Comments
Natalie Badillo
September 29, 2018Reading this article reminded me of exactly why I chose my major, biomed engineering. This backward way of thinking about a problem is a method I really am inspired by given the standards set by science to follow a certain route or classical model when devising an experiment or a question. The fact that they decided to investigate the “substrate” or “acceptor” in a sense when they chose to utilize RNA interference on the host factors was, in my opinion, extremely interesting compared to the traditional “let’s study the virus and stop it” train of thought. By approaching a widespread problem from another angle, they happened to have stumbled upon what seems like a new source for the virus to grow and thrive in the human body. This could open up a door to new methods of thinking about how to approach health problems by instead of focusing on the pathogen, understanding how they anchor themselves to and thrive in the human body.
I enjoyed how you broke down the information with the broad influenza background to introduce the flu shot and how you brought it back together in the end by addressing the concern of the flu shot’s ineffectiveness juxtaposed with the idea that a future flu shot has the potential to “guarantee (d) protection” against this seasonal pathogen.
Sarah Taj
October 1, 2018This is a fantastically written piece for it brought to light what not many people take into account when they plan to take their annual influenza shots. The fact that the weakened viruses may or may not have the ability to protect the immune system from potential foreign bodies raises many alarms that i did not even know were ringing. The fact that current antiviral drugs are only directed towards viral proteins which MAY have the potential to lead to drug-resistant viruses because of their rapid rate of mutation is not only alarming, however, but a reason to delve into the specifics and find a better alternative. The aforementioned solution of manufacturing antiviral drugs that instead focus on host factors may be the solution. This would not only be effective but it resolves the solution of the mutations that would render the vaccine useless. Not only did you explain the topic fruitfully, but you explained it well which deserves great admiration!