ISLAMABAD: Genetic simplicity and defective replication machinery of viruses make them masters of changing forms and these in turn cause failure of our diagnostic and therapeutic strategies. The ‘gene pools’ of viruses change over time by recombination or random mutations giving rise to new viral strains with different properties.
To understand how viruses evolve, the 2009 H1N1 swine flu pandemic caused by Influenza virus offers a classic example of Influenza virus evolution by recombination.
When two influenza viruses infect the same cell at the same time, some of the new viruses made inside of the cell may have a mix of genetic segments thus exhibiting different properties. Pigs are ‘mixing vessels’ for influenza viruses.
Apart from the Pig Influenza virus, the pig cells can be infected with the human and birds Influenza viruses at the same time. At a given time, if a cell is infected with two different Influenza viruses, the newly formed progeny of viruses would have a mixture of genetic material. Scientists found out that H1N1 Influenza virus had genetic segments from human, birds and pigs viruses mixed up together in steps which would have taken years.
SARS CoV-2 – commonly referred to as the novel coronavirus – responsible for Covid-19, is the seventh coronavirus to infect human beings.
Previously, the SARS epidemic of 2003 and MERS outbreak in 2014 are well documented. Being an RNA virus-like SARS and MERS coronaviruses which originated in bats, CoV-2 also has originated in bats and is highly prone to mutations thus evolving rapidly.
The rate of evolution of CoV-2 is being assessed but still, the initial assessment indicates that as compared to SARS, it evolves slowly. However different polymorphisms in strains isolated from China, Italy and USA indicate that it can accumulate 2 to 3 mutations per month which means that it will continue to challenge our control strategies in future and has got the potential to re-emerge too.
The emergence of novel and variant viruses from the wild animals has been predicted by scientists, particularly after the SARS outbreak. The current outbreak started in November 2019 in China and within 2 months the infection reached 146 countries. What makes CoV-2 as the most dangerous pathogen is the ease of transmission and its severe complications which are like SARS and MERS. Epidemiologists have estimated that if the virus were not contained, it can infect half the world population in a matter of a month.
Globalisation has challenged our control strategies for infectious diseases. The rise of free social media platforms in the global world has intensified the flow of information and propaganda at the same time. Conspiracy theories are always very thrilling because these are not close to reality. As soon as the CoV-2 outbreak started, the conspiracy theorists started their job to come up with alternative explanations mainly focusing on the power struggle between China and the US.
As the state of affairs between the two countries is well known around the globe, conspiracy theorists started connecting the dots in order to prove that CoV-2 was a man-made pathogen which was engineered in the US to target China.
People in power and politics usually do propaganda as it suits them to influence public opinion but scientists are always looking for facts. Several scientific investigations in January and February indicated that CoV-2 is not new in entirety and that similar coronaviruses have been characterised long before from different animal species as well as human beings.
A study by Chinese scientists analysed more than 100 genomic sequences of CoV-2 along with other coronaviruses and found out that its genomic sequence was 96% similar to coronavirus of Bats origin indicating without a doubt that it originated in bats just like MERS and SARS. However, they found variations in the Spike gene between CoV-2 and Bat Co-V.
Spike protein binds with human receptor ACE2 and is considered as most important for its virulence. Here some people started speculations that probably the spike gene was introduced into Bat Co-V in the lab in order to make the most virulent CoV-2. However, other scientists thoroughly analysed the sequencing data for finding any evidence of genetic manipulation in CoV-2 but they failed.
A recent scientific investigation led by Kristian G Andersen of the Scripps Institute conclusively proved that the Spike gene of CoV-2 has resulted from natural selection and evolution and that there is no evidence of it being manipulated by techniques of genetic engineering.
The investigators rejected the idea on two grounds:
1. If the strain had been manipulated using any of the known techniques in genetic engineering, there would have been left over traceable elements of the systems used which in this case are none.
2. The binding domains of the Spike genes and their affinity to bind strongly to the human ACE2 receptors were previously unknown, although only recent studies identified a similar Spike gene in Pangolin Coronavirus with same binding domains but its binding affinity studies have never been performed before.
It is therefore not possible that CoV-2 has been manipulated in any way. The study further highlighted several possible scenarios for the viral evolution including animal to human, human to human and accidental escape of mutants from cell cultures in BCL1/2 labs.
The most plausible explanation seems to be transmission from bats to pangolins and from pangolins, the mutated form jumped into humans. Remember that CoV-2 has 96% similarity with Bat coronavirus indicating that the later is ancestor, while in pangolins the Spike gene sequence of the Pangolin coronavirus has the same genomic sequence as CoV-2 which indicates that the Spike gene of this virus had undergone natural selection and mutation thus acquiring the most virulent binding domains from the Bat coronavirus.
It ends the speculations about genetic manipulation of CoV-2 and its use as a biological weapon. We do not know about the entire spectrum of viruses in many wild species including bats, pangolins etc. Several animal species are hosts for the yet un-encountered viral species and also serve as ‘mixing vessels’ for the existing strains to give rise to newer ones. It is therefore very much likely that many more viruses having an affinity for human cells will probably emerge in future.
Dr Ijaz Ali is an Associate Professor of Virology at COMSATS University Islamabad and a Fulbright scholar.