Influenza Virus: Evolution of the Mutant Predator


  • Influenza kills around 6,50,000 people every year worldwide
  • Three to five million flu cases of severe illness worldwide
  • The Spanish Lady in 1918 claimed more than 50 million lives


The fatal influenza virus triggers seasonal epidemics globally. A major reason for such epidemics is the ability of influenza virus to mutate itself genetically through diversification. A drawback of the host defence operation is that it can also evolve but probably over a longer span of time. This research looks at the influenza virus and its hosts, under the spectrum of a prey and predator correlation. The epidemiology of influenza has been studied substantially, but still the possibility of a pandemic cannot be ruled out. As influenza has caused such disasters in the past.

The flu virus, notoriously known as the “Spanish Lady” in the year 1918, affected 40% of the world population, eventually resulting in fifty million deaths, compared to 17 million deaths during the First World War It was called “Spanish Lady” as many people believed that the flu originated on the Iberian Peninsula. Spain was neutral during World War 1, other countries under a media blackout could read detailed reports only from Spanish news sources. Spanish King Alfonso fell sick during this pandemic phase, so it was but obvious for people to think that Spain was the epicentre of the influenza. However, researchers believe that China, France, Britain or the United States might have been the epicentre of the influenza.


Two more influenza pandemics occurred much later, the Asian flu in 1957 and the Hong Kong Flu in 1968. The death rates during these pandemics were lower as compared to the pandemic in 1918, where around two million people died. A new influenza virus the (H1N1) spread across the globe from Mexico causing much lesser death impact as enhanced lab testing capacity and medical treatment were available.

Viral genomes adapt themselves according to the host’s environment, as they are microscopic and flexible. This fact allows the pathogens to grow rapidly through transmission into other species or mutagenesis. These pathogens survive as they gradually develop a resistance to medical treatment and suddenly mutate becoming stronger and spreading further over a period causing pandemics. This research proves the fact, that influenza virus has coevolved with the human genomes.

Influenza Virus

Influenza viruses belong to the Orthomyxoviridae family, the genome is a single-stranded RNA, with a negative sense. The classification of the virus is done under A, B, C and D. The type A and type B affect the respiratory system in humans causing epidemics, whereas type C affects the upper respiratory tract in a mild manner. The D type virus has a major effect on cattle and does not affect humans. The type A virus affects marine mammals, birds, animals and such other hosts increasing the possibility of pandemics.

The type A influenza virus has two major subtypes, neuraminidase (NA) and hemagglutinin (HA) which are further divided into 11 NA and 18 HA subtypes.

This virus affects epithelial cells comprising of sialic acid (SA) receptors present in the respiratory tract. The influenza A virus show a penchant for such receptors resulting in death of cells during the viral replication process as the apoptosis and synthesis of protein is interrupted.

Clinical Indications

The symptoms of influenza occur suddenly after one to two days of set in period. Symptoms such as headache, chills, fever, sore throat, dry cough, nasal congestion, anorexia and malaise can be observed in the affected individuals. Fever can last for up to eight days. The influenza virus has various sub-types with different characteristics in terms of symptoms and effects on the upper and lower respiratory tracts which might result in severe or mild flu depending on the generic circumstances.

Immune System Retaliation to Viral Infection

The immune system cells respond immediately to the influenza virus. The Retionic Acid Inducible Gene-1 protein (RIG-1) receptors and Toll like receptors (TLR) recognize the pattern of the viral molecules taking further action launching the interferon regulatory factor (IRF) and kappa-B factors, which lead to pro-inflammatory cytokines and interferons to take anti-viral action. Natural Killer (NK) cells, dendritic cells, neutrophils and monocytes reach the infected site and retaliate against the viral molecules. A vivid combination of such antibodies becomes active, working as an initial phase defence mechanism against the influenza virus.

Nemesis Evolution: The Prey and Predator

The theory of evolution by Charles Darwin comes into play here. According to him, the natural selection concept in terms of transmutation of species is a crucial factor for evolution and

long-term survival of species. The predator and prey concept can be explained by an example of the deer and the tiger, where the deer has to be real fast to escape the tiger. As opposed to the tiger that needs to run faster to grab the deer in order to procure food, reproduce and survive. This explains the survival of the fittest notion, which is true for one type of species. The instability factor cannot be ruled out which actually boosts evolution process. The predator and prey concept can be applied to pathogens and host bodies. The fatal virus which survives through adaptation, mutagenesis and becomes resistant to medications is sort of a predator. It might not kill the human cells but cheat them by analysing the cell translation system, multiply and get out of the cells, but the cellular mechanism that works in defence also has the capability to evolve over a period. Genetic mutation of the influenza virus is a consistent process and the root cause of increase in the types of viral infections.

Genetic Variation of the Flu Virus

Molecular mechanism is a source of diverse influenza pathogens. Genetic recombination, re-assortment and mutation are the molecular patterns for the influenza virus. An extensive research carried out reveals that, these genetic mechanisms are a result of antigenic shift. This shift is a rapid change in the antigenicity and the structure of the virus, which caused flu pandemics in the past. Mutagenesis occurring at a fast rate escalates the chances of widening the range of host cells for the virus. The type a influenza mutates under negative pressure which happens because of inborn immune recognition, a process that is not common with the evolution of the B type influenza. Antigenic drifts are more common with type A influenza. Antigenic drifts are slow changes in the viral properties but these drifts might occur at a faster pace. According to recent extended research on the influenza virus, affected people are, actually attacked by a diverse combination of flu viruses and not by a single strain of the virus. The medication kills the strain that is dominant but not the whole group of viruses. The other viral strains can stay in the human body or the host species, where they have an ample scope to genetically mutate and adapt themselves to the host system, eventually emerging stronger.

Humans and Influenza Virus: A Predator-Prey Correlation

There are different types of viruses that stay and evolve inside the human cell without damaging it. The set of chromosomes in humans is constituted by viral sequences as they get adequate time to mutate inside the human body. Vaccines for influenza are created and modified, based on the immunity level and strategy of the antibodies, but the vaccines may not have a hundred percent efficacy rate. The health and basic immunity of every person differs with age, gender and geographical location globally. The variation in antibodies is a genetically complicated process. The people, who survive pandemics, do carry viral strains of the flu or such other viral infections. These unstable viral strains in micro molecular form stay for long periods in the human body and are capable of transforming without harming the host cells. Mutations give rise to types of viral infections as human antibodies also evolve to retaliate these viral types but comparatively, the flu pathogens mutate at a much faster rate. The predator virus has been emerging as a winner against the human antibodies. The influenza epidemics and pandemics in the past have proved this fact and there is always a possibility of such flu epidemics in the future.

Congenital Bottlenecks

Genetic bottleneck with context to population is a common phenomenon of evolution, where a small part of a large population of individuals migrates to another region. It carries only a subset of genetic statistics of that population. As a result, genetic diversity can be seen across various geographical locations. Isolation and congenital mutations modify the cell structure of the new population.

The process of virus transmission in host bodies insinuates three types of genetic bottleneck aspects.

  • The set of chromosomes is significant in terms of human host antibodies. The efficacy of the antibodies should be at the highest level but in case of bottlenecks, a subset of MHC genes of the paternal part will be transferred to the migrated part of the region.
  • The initial pool of viruses is not transferred, but only a sub group of viral strains is transferred when human sub groups or individuals migrate to other geographical locations.
  • People who survive after epidemics carry viral strains of the virus. According to research, major variants are transferred with minor variants under transmission bottlenecks. Mutagenesis is a process through which the minor variants mutate and transforming into major variants. Virus entry and virus replication are the two elements which happen inside the host cells creating new variants.


The eventual combination of these factors will determine the host and virus equation as far as human population is concerned. Human migrations are a part of human evolution and this equation will keep changing as new bottlenecks take place globally.


Influenza virus cannot be underestimated as pandemics and seasonal epidemics have claimed several lives in the past. According to medical experts, influenza virus is as hazardous as the coronavirus and should not be underestimated. Mutagenesis is a continuous process where the influenza virus sub-types regenerate within the host cells and may cause more damage than their previous forms to humans. The flu virus is surely a predator as it lurks inside the human body and attacks whenever the immunity decreases. The host cells evolve and become powerful over a long period, which could only be protected by the use of enhanced vaccines. Though our knowledge about the influenza virus and its evolution process has surely increased over the years but we are still not fully equipped with adequate measures in terms of vaccination. Medical experts and researchers have been consistent in exploring new insights with context to the ever-transforming influenza virus. An awareness needs to be created among people around the world against this virus as millions of people die due to influenza every year. Third world countries also report cases of influenza which are a major concern but influenza cases are not limited to third world countries only but affect people all around the world. Evolution algorithms related to the influenza virus will surely help in developing stronger vaccines and treatment facilities globally.