Let's look at pathogenicity first.

Contemporary, 'normal' flu viruses require the presence of the enzyme trypsin in their human host, in order to replicate.

The 1918 virus instead could proliferate even in the absence of trypsin, making it more pathogenic than other viruses.

The Spanish flu also displayed a unique capacity to proliferate at high rates inside human bronchial cells – and that explains its virulence.

Little by little, a picture of the killer was emerging, thanks to modern researchers in the role of crime scene investigators, or criminal profilers.

The next step was to understand how Mr Type A H1N1 of the 1918 class actually killed: what was its modus operandi.

Enter Dr David Morens of the National Institute of Allergy and Infectious Diseases in Maryland.

In 2007 he reviewed autopsy records for influenza casualties in the 1918-1919 period and identified two overlapping syndromes which caused the death of the infected hosts.

In at least 85% to 90% of cases, patients suffered from an acute viral infection, that spread down the respiratory trait, causing severe tissue damage inside the lungs.

The damaged tissue was then invaded by a so-called secondary invasion.

Not viruses this time, but bacteria: pathogens like Streptococcus Pneumoniae or Staphylococcus aureus would invade the damaged lungs, causing cases of aggressive bronchopneumonia.

In other words, the killing virus did not act alone, but had accomplices.

The actions of these cohorts eventually led to severe pulmonary haemorrhage and necrosis – or tissue death – within the bronchi.

The remaining 10 to 15% of fatal cases suffered from ARDS, or 'acute respiratory distress—like syndrome'.

Patients with this syndrome could be easily identified by their peculiar blue-grey facial discoloration: a typical sign of drowning.

Because that's essentially what was happening: the virus caused the pulmonary blood vessels to exude huge amounts of thin, watery droplets, which clogged the lung tissue.

In other words: these patients were drowning in a liquid created by their own bodies.

Now that we have clarified the modus operandi of this killer, we have to understand its peculiar choice of victims.

Normally flu epidemics claim most of their victims among the elderly, but the Spanish Flu had a clear predilection for a younger demographic, those aged between 15 and 34.

A lower than expected mortality among the elderly may have been explained by acquired immunity.

Individuals aged 40 and over, may have been exposed to one of the three flu pandemics of the 19th Century, in 1830, 1847 or 1889.

Although not everybody agrees: unlike the 1918 strain, these previous viruses did not cause aggressive bronchopneumonia nor lung haemorrhage.

We may have more convincing answers explaining why the death rate was higher among the young ones.

Dr Robert Snelgrove from Imperial College London, among others, has theorised the notion of the so-called 'cytokine storm'.

Cytokines are proteins released by cells to interact with each other and to trigger specific processes.

For example, internal inflammation – a common reaction of the body against infections.

A younger organism would naturally release more cytokines than and elderly one.

In the case of the Spanish flu, the cells of infected younger patients released a deleterious excess of cytokines, leading to excessive inflammation of the lungs, and more importantly, tissue necrosis.

Ironically, younger, fitter organisms deployed a stronger reaction to protect themselves – a reaction which eventually claimed their lives.

Shortly after the last wave had died down, the scientific community tried to take stock of the magnitude of the disaster.

American bacteriologist Edwin Oakes Jordan was one of the first to calculate the death toll, which he estimated to be in the vicinity of 21.5 million.

This number in itself is staggering.

Compare it to the casualties of the Great War: about 10 Million dead soldiers, killed over a period of four years and a half.

The Spanish Flu killed twice as many people over little more than a year.

Now let's compare it to the world's population in 1918.

At that time there were 1.8 Billion on the planet. The Spanish flu killed 1.2% of them.

If we apply that ratio to today's population we would have a death toll of more than 93 million.

Oakes Jordan's estimate stood for decades, but it was later challenged as being too low.

First, a 1986 publication calculated the mortality in India alone to be at 18 million.

Subsequently, in 1991 authors David Patterson and Gerald Pyle proposed another estimate, placing the death toll between 25 and 40 million victims.

Was that the definitive number? Probably not.

A 2002 study by Dr Niall Johnson and Dr Juergen Mueller suggested that previous numbers may have been underestimated due to common issues such as missing records, misdiagnosis or death certificates compiled by non-medical personnel.

Not only that: deaths among indigenous populations in colonial dominions may have been overlooked, ignored or simply not reported by colonial authorities.