Excerpt – Studying genetics and virulence

COVID 19: Coronaviruses have historically caused mild common colds, outside incidents like the SARS and MERS outbreaks. Mutations in 2019 have turned this less harmful Coronavirus into the more malevolent COVID 19 version. The COVID 19 spike proteins had evolved to effectively target a molecular feature on the outside of human cells called ACE2 , a receptor involved in regulating blood pressure, 10 times more efficiently. This coupled with another mutation to use human enzymes like Furin, to spit its RNA into the cell, makes this virus particularly potent.

The COVID 19 virus seems to have been evolved rapidly in the last few decades. Looking at the diagram below, which depicts mutations and the emergence of new strains over time, the COVID 19 virus is more similar to viruses from Bats than from Pangolins. A mutated version that infected bats or pangolins probably began the human outbreak.

Source: https://evolution.berkeley.edu/evolibrary/news/200305_coronavirus

Another interesting fact uncovered by Chinese researchers is that the COVID 19 virus is evolving as we speak, in front of our eyes. After the Wuhan outbreak, the virus has further mutated into 2 types, the L type (70% of cases) and S type (30% of cases). Whereas the L type was more prevalent in the early stages of the outbreak in Wuhan, the frequency of the L type decreased after January 2020. Human intervention may have placed more severe selective pressure on the L type, which might be more aggressive and spread more quickly. On the other hand, the S type, which is less aggressive, might have increased in relative frequency due to relatively weaker selective pressure. Later I argue that viruses that are extremely virulent do not fare as well as viruses that are less virulent. Less virulent viruses can spread and survive in populations longer.

SARS: Looking at the diagram below, the SARS virus infecting humans (SARS 4 and SARS 3) seems closer to viruses infecting civets (SARS 2) more than even those infecting bats (SARS 1 and SARS 5-8). The current thinking is that deadly strain probably originated in China’s horseshoe bats and later passed through masked palm civets sold in Guangdong’s animal markets.

Virulence of viruses: Typically, malignant viruses have less interest in harming their host humans in the long term. Natural selection balances this trade-off, selecting for pathogens virulent enough to produce many offspring (that are likely to be able to infect a new host if the opportunity arises) but not so virulent that they prevent the current host from presenting them with opportunities for transmission. Where this balance is struck depends, in part, on the virus’s mode of transmission.

Sexually-transmitted pathogens, for example, will be selected against if they immobilize their host too soon, before the host has the opportunity to find a new sexual partner and unwittingly pass on the pathogen. Some biologists hypothesize that this trade-off helps explain why sexually-transmitted infections tend to be of the lingering sort. Even if such infections eventually kill the host, they do so only after many years, during which the pathogen might be able to infect a new host. On the other hand, diseases like cholera (which causes extreme diarrhea) are, in many situations, free to evolve to a high level of virulence. Cholera victims are soon immobilized by the disease, but they are tended by others who carry away their waste, clean their soiled clothes, and, in the process, transmit the bacterium to a water supply where it can be ingested by new hosts. In this way, even virulent cholera strains that strike down a host immediately can easily be transmitted to a new host. Accordingly, cholera has evolved a high level of virulence and may kill its host just a few hours after symptoms begin. it suggests how we might sway pathogen evolution towards less virulent strains. In situations where high virulence is tied to high transmission rates (e.g., cholera), reducing transmission rates (e.g., by providing better water sanitation) may favor less virulent forms. The idea is to create a situation in which hyper-virulent strains that soon kill or immobilize their hosts never get a chance to infect new hosts and are turned into evolutionary dead ends. In fact, biologists have observed this phenomenon in South America: when cholera invaded countries with poor water sanitation, the strains evolved to be more virulent, while lineages that invaded areas with better sanitation evolved to be less harmful.

Virulence, and link with evolutionary history: Tracing the history of viruses, tracking their virulence and mutations also gives insight into human evolution, primate evolution, vertebrate evolution and ultimately the evolution of surface life. This becomes evident when studying some viruses like HPV, Herpes, and Hepatitis.

HPV: Human papillomavirus (HPV) is an STD causing virus with just 8 genes. It impacts 79 million Americans, but around 90% of infections cause no symptoms and resolve spontaneously within two years. But the trouble is for the remaining 10%. When a high-risk HPV infection persists for many years, it can lead to cell changes that, if untreated, may get worse over time and become cancer. Around 5.2% of all cancers are caused by HPV. HPV causes about 610,000 cancers annually worldwide, including virtually all cervical cancers, and many anogenital and head and neck cancers. 

The major evolutionary separation between some papillomaviruses found only in humans, has now been observed in animals. The presence of these two major divisions of papillomaviruses in both human and monkey hosts strongly suggests that this diversification predated the evolutionary split between monkeys and apes. This would imply that at least two different groups of papillomavirus have evolved separately in their respective primate hosts for more than 22 million years with only moderate sequence changes since their genesis. The closest relatives of human papillomaviruses are the papillomaviruses that infect chimpanzees, our closest living relatives. And the next closest relatives of human papillomaviruses infect our next closest relatives, the gorillas. It is therefore likely that the common ancestor of humans, chimpanzees, and gorillas-an ape that lived some eight million years ago-carried its own strain of papillomavirus. The genealogy of HPV reflects the genealogy of our species. The oldest lineage of the virus is most common in living Africans, for example. Native Americans descend from East Asians, and their viruses share the same kinship.

Herpes: The Herpes virus is an example of how it has evolved along with humans. Approximately two-thirds of the human population is infected with at least one herpes simplex virus. The viruses are most commonly presented as cold sores on the mouth or lips or blisters on the genitals. Humans are the only primates we know of that have two herpes simplex viruses and researchers wanted to know why. They compared the HSV-1 and HSV-2 gene sequences to the family tree of simplex viruses from eight monkey and ape host species. It became clear that HSV-1 has been present in humans far longer than HSV-2, prompting the researchers to further investigate the origins of HSV-2 in humans. The viral family tree showed that HSV-2 was far more genetically similar to the herpes virus found in chimpanzees. This level of divergence indicated that humans must have acquired HSV-2 from an ancestor of modern chimpanzees about 1.6 million years ago, prior to the rise of modern humans roughly 200,000 years ago. In addition, some genes of this virus were found in bacteriophages, suggesting a common origin. The most common ancestor of all known Herpes viruses seems to have existed around 400 million years ago.

Hepatitis: Approximately one in every 12 individuals, or 500 million people worldwide, is living with chronic viral hepatitis. The Hepatitis B virus (HBV) specifically infects the liver cells of many primates (including humans), causing severe flu-like symptoms. Although most people fully recover, roughly 5 percent remain infected throughout their lives; acting as carriers who can infect others whilst also suffering a variety of serious liver diseases, including cancer. In fact, HBV is second only to tobacco amongst known human carcinogens. According to genomic analysis, scientists came up with 2 scenarios: the first ancestral HBV became trapped in avian DNA quite early: the common ancestor of all the bird species carrying this particular viral fossil lived about 82 million years ago. It infected birds way longer than it infected mammals by switching hosts. The other scenario was that the virus infected the first amniotes (ancestors of reptiles, birds, and mammals) and split into separate lineages more than 324 million years ago when the early bird and mammal lineages split.

Source: http://www.immpressmagazine.com/viruses-and-us-evolving-by-infection/

Spanish flu: The 1918–1919 influenza pandemic killed more people than any other outbreak of disease in human history. One of the first casualties was the British prime minister and war leader, David Lloyd George. On 11 September 1918, Lloyd George, riding high on news of recent Allied successes, arrived in Manchester to be presented with the keys to the city. Female munitions workers and soldiers home on furlough cheered his passage from Piccadilly train station to Albert Square. But later that evening, he developed a sore throat and fever and collapsed. He spent the next 10 days confined to a sickbed in Manchester town hall, too ill to move and with a respirator to aid his breathing. Lloyd George, then aged 55, survived, but others were not so lucky. Recent scholarship estimates the death toll from 50 to 100 million dead. When it was reported in May 1918 that King Alfonso XIII was ill in Madrid, most people dismissed the Spanish flu as a joke. The main advice was to gargle with salt water and to isolate yourself until the fever had passed. However, these rules did not apply to munitions workers who were urged to “carry on” for the sake of the war effort.

When researchers analyzed the genome of the Spanish flu recently, they found that most of its genes were derived from a bird flu virus. The 1918 virus was also found to be the common ancestor of human and classical swine H1N1 influenza viruses, which continue to haunt us to the present day. Haskell County, Kansas was pointed as one of the places of origin of the Spanish flu, being close to the first outbreak at Camp Funston, Fort Riley. There the smell of manure meant civilization. People raised grains, poultry, cattle, and hogs. A rival theory, favored by the British virologist John Oxford, is that the pandemic began at Étaples, a huge British military camp an hour south-west of Boulogne. With accommodation for up to 100,000 soldiers, Étaples lay on a migratory bird flyway close to the Somme estuary and had all the necessary conditions for a spillover event: wild waterfowl, plus chickens and pigs, living in close proximity to men packed into airless barracks. Étaples also had several hospitals where soldiers whose lungs had been compromised by mutagenic gases deployed on the battlefield.

This flu had long term impact. Economist Douglas Almond has estimated that people exposed in the womb to the Spanish flu in received less education, earned lower incomes, and were likelier to have disabilities than people who missed the pandemic in the womb. Its mortality rate ranged from 2% in developed countries to 6% in India where 18.5 million people perished.


Photo: Image © iStockphoto.com/Dr_Microbe

Published by Vinod Aravindakshan

Engineer, Economist and Manager

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