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Understanding the Seasonal Influenza Virus
- Joshua A.
- Apr 30
- 5 min read
As the weather begins to warm, many people are relieved to leave behind the dreary winter cold in favor of the spring and summer sunshine. People can also be relieved to leave behind what the CDC has described as one of the most intense Influenza seasons in over a decade. 8% of the United States population is diagnosed with an influenza infection on average annually, with incidence rates climbing up to 11% depending on the time of year (i.e. the “flu season”). With the estimated US population of 341.5 million, that means about 27.3 million people in the US are infected with influenza annually. To put that in perspective, 27.3 million is more than the top 8 most populated United States cities combined (based on data from the 2020 US Census). Given the prevalence of influenza, it is important to understand what the virus is, how it infects people, how it is transmitted, and how infections can be prevented. This article attempts to discuss all of those topics through the lens of microbiology.
The Structure of Influenza
Influenza viruses are classified into 4 groups: influenza A, influenza B, influenza C, and influenza D. This article will mostly focus on Influenza A as it is known to contribute most to the annual “flu season.”
The Influenza A virus can be thought of as a “spiked” pouch containing instructions for making copies of itself. The instructions, or genetic material, of the virus comes in the form of 8 RNA molecules. These RNA molecules are enveloped by a sack of water-hating fatty molecules, called phospholipids, that act like a protective barrier preventing the external environment from damaging the precious genetic contents.
Sticking out of the phospholipid layer are chains of complexly tangled amino acids called proteins. 2 of those proteins, called Hemagglutinin (pronounced “he-ma-glu-ti-nin”) and Neuraminidase (pronounced “neur-a-mi-ni-dase”), play a pivotal role infecting host cells.
With these structures in mind, let's consider how the Influenza A virus infects humans.
The Infection Process
An inflection begins with an Influenza A virus entering a person’s respiratory tract, specifically in areas where air enters and exits the lungs when breathing. Parts of the respiratory tract - specifically the inside of the nose (a.k.a. the nasal cavity) and windpipe (a.k.a the trachea), have special cells that line the surface of the organs called pseudostratified ciliated columnar epithelial cells. While that name is a mouthful, what's important to remember is that Hemagglutinin surface proteins on Influenza A viruses are able to “recognize” and bind to the special respiratory epithelial cells. Think of this as a “lock and key” type of interaction: the Hemagglutinin proteins are “keys” that can only fit into respiratory epithelial cell “locks”. When Hemagglutinin binds with an epithelial cell, the entire virus molecule is “ingested” by host cells (via a process called endocytosis).
The virus’ phospholipid layer is then disintegrated, releasing the viral RNA into the host cell's cytoplasm. Once the genetic material finds its way into the host cell’s nucleus, the nucleic machinery begins to process the virus RNA. Since the virus’ genetic material is made from the same amino acids as a human’s genetic material, the machinery in the host cell “reads” the virus’s instructions as it normally would. The processing of virus RNA by the host cell machinery results in identical copies of the virus genetic code and surface proteins. In essence, the virus takes advantage of the host cell’s machinery to create the materials for replica copies of itself.
Once the materials are made, the components are coalesced at the host cell’s phospholipid layer. In a process called budding, the host’s phospholipid layer (now “spiked” with new viral Hemagglutinin and Neuraminidase proteins) surrounds the new RNA molecules until the layer “pinches,” creating a new protective “pouch.” Not only did the virus hijack the host cell’s machinery to create more copies of itself, it also steals some of the host’s own membrane to protect the new copies. The new virus molecule is finally released when the “lock and key” bond between the host cell and Hemagglutinin is broken by Neuraminidase. This new virus can then go on to infect more respiratory epithelial cells and create even more copies of itself.
Influenza Transmission and Prevention
Influenza viruses are most commonly transmitted through saliva and mucus droplets released from the cough or sneeze of an infected person (referred to as respiratory droplet transmission). This makes sense when considering that the infection site of influenza is near or at the same place where mucus and saliva are made. As such, the symptoms associated with influenza are the means through which the virus can infect more people. This is the reason why covering one’s mouth when coughing and sneezing is important. Moreover, virus molecules in respiratory droplets can survive on surfaces anywhere from 8 hours to 2 full days depending on the surface material, exposure to light, and moisture content among other factors. This is why surface disinfecting and hand washing can go a long way in preventing the spread of the influenza virus.
Another way to prevent an infection is by taking the annual influenza vaccine. While the biology of vaccines won’t be discussed in detail, the rationale for the vaccines is as follows: by introducing harmless or weakened virus molecules, the immune system can “learn to recognize” the virus (usually through its surface proteins like Neuraminidase or Hemagglutinin) so that it is prepared to fight off an infection from the real, full-strength virus.
However, vaccines are ineffective after an influenza infection has already taken place. Influenza patients admitted to a hospital can be given medication to mitigate the symptoms of an influenza infection while the immune system works to exterminate the virus molecules. One such medication is Tamiflu (also known by its pharmacological name Oseltamivir phosphate). Tamiflu is a neuraminidase inhibitor, meaning the drug is a “key” that can fit into the neuraminidase surface proteins “lock.” When Tamiflu binds to neuraminidase, the virus surface protein’s function is inhibited: the neuraminidase can no longer break the Hemagglutinin-Host Cell bond, essentially anchoring the new virus molecules to the host cell. The benefit is 2-fold: 1) the new virus molecules cannot infect new cells, and 2) immune cells can better find and destroy the stationary molecules.
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