Details of the Influenza Virus
Introduction:
- Influenza viruses travel between humans almost always. Due to the nature of the virus, it undergoes a few minute genetic changes every year, making it slightly distinct from the virus of the year before. Scientists must therefore make educated assumptions about which changes are likely to continue over the course of the ensuing year in order to develop or update their vaccines.
The kind of virus:
- Flu viruses can infect birds in addition to domesticated animals like pigs and horses.
- These creatures can mix and match the two genes it possesses—haemagglutinin (H) and neuraminidase (N)—to produce an entirely new virus, some of which may infect humans.
- It is challenging to develop an effective influenza vaccination due to all of these problems.
- Mostly, the virus attacked and ravaged the lungs.
- Among the eight genetic components of the virus, the haemagglutinin and RNA polymerase genes stood out as causing severe sickness.
Hemoglobin and RNA polymerase:
- Haemagglutinin is the name of the virus’s outer-surface protein that interacts with proteins on the cells of a different organism.
- Now that there is a portal open, the virus may begin its invasion. The haemagglutinin section of the 1918 strain was altered, making it simpler for the virus to enter cells.
- The viral RNA polymerase, on the other hand, duplicates the genetic makeup of the virus.
- Because the polymerase in the H1N1 strain was so good at accomplishing its job, the virus was able to make a lot of copies of itself in a short period of time.
- The infected cell suffered significant harm as a result of the virus’ exploitation of the cellular machinery to replicate itself.
Unrivalled:
- No other influenza virus, whether recombinant or wild, that researchers had ever examined could equal the pathogenicity of the complete virus.
- It was exceedingly virulent; mice exposed to the 1918 virus had 39,000 times more virus particles in their lungs than mice exposed to the less hazardous laboratory variety.
- Within days, the patient’s former lungs started to fill with fluid, seriously harming them and leading to death.
- When they were absent, the haemagglutinin and RNA polymerase genes did not inflict as much damage as they did when they were present along with the other gene segments, which contributed significantly to the severe nature of the 1918 virus.
- All viruses must be capable of infecting more hosts. A virus that kills its host too rapidly will fail to achieve its goal because viruses can only thrive inside of living things.
- The host will therefore either pass away sooner or the virus will be an easier target for the host’s immune system if the virus receives a transformation that makes it more destructive. Both effects are detrimental to the virus’s long-term survival.
- Therefore, in order to minimise their detrimental effects on the creature’s long-term survival chances, these genetic mutations must also be accompanied by other genomic changes.
- It could have a mutation that causes the viral life cycle to accelerate or decelerate, or it could have another mutation that allows the virus to avoid the immune system long enough to spread.
Conclusion:
- The 1918 influenza pandemic should serve as a reminder to us all that periodically, nature will mix millions of genes until it finds the perfect fatal combination and create something as destructive as the 1918 H1N1 influenza virus. This is especially true in the wake of the COVID-19 pandemic. Ironically, evolution and all life on Earth depend on nature’s ability to achieve this.
