How the deadliest virus in human history paved the way for new cures

General Studies Paper 2

Introduction

• Influenza viruses are almost always circulating among humans. The nature of the virus means that every year, the virus’s genetic material undergoes some minor changes, rendering it a little different from the virus of the previous year. So scientists have to guess which changes are likely to survive the next year, and design or update their vaccines accordingly.

Nature of the virus

• An influenza virus can also infect birds, pigs, horses, and other domestic animals.
• It can assort the types of the two genes it contains – haemagglutinin (H) and neuraminidase (N) – in these animals to generate a new virus altogether, some of which may infect humans.
• All these complications ensure that designing an effective vaccine for influenza remains challenging.
• The virus mainly infected the lungs, and laid waste to them.
• While all eight pieces of the virus’s genetic material caused severe disease, two in particular stood out: the haemagglutinin and the RNA polymerase genes.

Haemagglutinin and RNA polymerase

• Haemagglutinin is the protein on the outer surface of the virus that docks with proteins on the cells of another organism.
• This way, the virus has a portal through to begin its invasion. The haemagglutinin segment of the 1918 strain contained modifications such that the virus could easily gain access to cells.
• The viral RNA polymerase, on the other hand, makes copies of the viral genetic material.
• In the H1N1 strain, the polymerase was extremely efficient at this process, allowing the virus to make numerous copies of itself in a very short span of time.
• This then took a heavy toll on the infected cell, since the virus hijacked the cellular machinery to replicate itself.

Unrivalled

• The full virus demonstrated a pathogenicity unrivalled by any other influenza virus scientists have ever studied – recombinant or natural.
• It was highly virulent: there were 39,000-times more virions (virus particles) in the lungs of the mice infected with the 1918 virus than those infected by the more benign laboratory strain.
• The former lungs were filled with fluid within days, causing extensive lung damage and resulting in death.
• The haemagglutinin and the RNA polymerase genes were important reasons for the extreme nature of the 1918 virus, by themselves they did not wreak just as much havoc as when they did in combination with the other gene segments.
• All viruses have to ensure they will be transmitted to more hosts. A virus that kills its host too soon will fail at this objective because a virus is only alive as long as it is inside a host.
• So a change in a virus that makes it more pathogenic will either kill the host faster or it will become an easier target for the host’s immune system. Both outcomes are detrimental to the virus’s long-term survival.
• So such genetic changes must be associated with alterations elsewhere in the genome that mitigate those effects on the creature’s long-term survival prospects.
• It could be a mutation that enhances its transmission rate, one that slows the viral life cycle, or something else that allows the virus to escape the immune system long enough for it to be transmitted.

Conclusion

• The 1918 influenza pandemic is a reminder to us all, especially in the wake of the COVID-19 pandemic, that ever so rarely, nature will arrive at that perfect, deadly combination after mixing thousands of genes and end up creating something as destructive as the 1918 H1N1 influenza virus. Ironically, nature’s ability to do so is at the very heart of evolution, and of all life on earth.