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Covid virus, vaccines does not enter human DNA: Study

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SYDNEY: Covid-19 cannot enter a person’s DNA, say Australian researchers refuting claims of SARS-CoV-2, the virus that caused the infectious disease, integrating its genetic material into the human genome.
The study, published in the journal Cell Reports, showed there was no evidence of Covid-19 — or the Pfizer or AstraZeneca vaccines — entering DNA.
The claims have led to “scaremongering” and people should not hesitate to be vaccinated, said researchers from University of Queensland.
The research confirmed there was no unusual viral activity and the Covid-19 behaviour was in line with what was expected from a coronavirus.
“The evidence refutes this concept being used to fuel vaccine hesitancy,” said Geoff Faulkner, Professor at the varsity’s Queensland Brain Institute.
“We find no evidence of SARS-CoV-2 integration suggests such events are, at most, extremely rare in vivo, and therefore are unlikely to drive oncogenesis or explain post-recovery detection of the virus.
“From a public health point of view, we would say that there are no concerns that the virus or vaccines can be incorporated into human DNA,” Faulkner said.
In his previous research, published in the Proceedings of the National Academy of Sciences, Faulkner suggested that positive Covid-19 tests long after recovery are due to the virus being incorporated into DNA.
“We looked into their claims that the human cells and machinery turned Covid-19 RNA into DNA, causing permanent mutations.
“We assessed the claims in cells grown in the laboratory, conducted DNA sequencing and found no evidence of Covid-19 in DNA,” he added.
In May, researchers from the Purdue University in Indiana, US, showed that although throughout human history there have been viruses capable of integrating their genetic material into human genes, the Covid virus lacks the molecular machinery to integrate its RNA into human DNA.



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In-host mutations in Covid-19 virus reflecting in variants, finds study

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NEW DELHI: Changes that happen in the genome of the SARS-CoV-2 virus in an infected person reflect at the population level as a variation, according to a study that researchers say will be “of enormous utility” in predicting the spread and infectivity of viral Covid strains.
Tracking the changes that happen in the virus inside a host in individuals and populations might provide important leads to the viral sites that are favourable or disadvantageous for the survival of SARS-CoV-2 that causes Covid-19, the researchers said.
The team behind the recent study included researchers from the National Centre for Disease Control and the CSIR-Institute of Genomics and Integrative Biology (CSIR-IGIB) in Delhi, as well as the Institute of Life Sciences in Bhubaneswar, the Academy for Scientific and Innovative Research in Ghaziabad, the CSIR-Centre for Cellular and Molecular Biology (CSIR-CCMB) in Hyderabad and the Indian Institute of Technology, Jodhpur.
Reacting to the findings of the study, virologist Upasana Ray explained that the emergence of viral variants is dependent on its successful reproduction in the host.
“Mutation is a very common phenomenon in the life cycle of any virus. While a virus undergoes replication and multiplies inside the host cell, small nucleotide alterations occur,” Ray, a senior scientist at Kolkata’s CSIR-Indian Institute of Chemical Biology told PTI.
“As a virus gets transmitted more and more, within its host it gets plenty of chances to accumulate such changes and thus variants emerge,” Ray, who was not involved in the study, said.
In the yet-to-be-published study posted on the preprint repository BioRxiv on July 27, the researchers analysed samples of Covid-19 diagnosed patients from two different time periods of the pandemic.
In phase 1 of the study, the team analysed 1,347 samples collected latest by June 2020 from China, Germany, Malaysia, UK, US and different subpopulations of India to perceive a genome-wide intra-host single nucleotide variation (iSNV) map in SARS-CoV-2 infected populations.
A single nucleotide variation (SNV) is a substitution of a nucleotide — a basic building block of the genetic material of the virus.
According to Ray, iSNV are the variations happening inside the host. She added that these mutations might or might not ultimately reflect at the population level.
“For an intra-host SNV to survive, such a variant should be able to multiply and spread and hence establish itself,” the scientist said.
The researchers observed 18,146 iSNV sites spanning the viral genome, including those that defined the B.1 and B.6 lineages.
The Alpha variant, first identified in the UK, the Beta variant first found in South Africa and Delta variant, first reported from India, belong to this lineage of SARS-CoV-2.
“Interestingly, 41 per cent of all unique iSNVs identified in these samples were found to be reported as an SNV by 30th September 2020 in one or more samples submitted in GISAID, increasing to 80 per cent by 30th June 2021,” the authors of the study noted.
GISAID is a global science initiative and primary source that provides open access to genomic data of influenza viruses and the coronavirus responsible for the Covid-19 pandemic.
In phase 2 of the study, the authors analysed 1,798 samples sequenced in India between November 2020 and May 2021.
They found evidence that iSNVs can over time manifest into SNVs in populations.
“In these samples, iSNVs could be recorded to be present in the population in most of the Delta (B.1.617.2) and Kappa (B.1.617.1) lineage-defining genomic positions prior to their fixation as SNVs by February 2021,” the researchers said.
“These results highlight the importance of recording iSNVs as an extension to the genomic surveillance programmes to enable more accurate models for viral epidemiology,” they said.
The authors also observed iSNVs in 87 per cent of the sites in the spike protein — which the virus uses to enter and infect the human cells — that have been recently reported to confer antibody resistance.
Current vaccines are directed against the spike protein of SARS-COV-2 virus.
“These mutations can have major implications in vaccine response as they could alter the immunogenicity,” the authors said.
Immunogenicity is the ability of a vaccine to provoke an immune response in the body.
“The study reveals important insights about residues favourable or not favourable for the survival of this virus and thus might help to engineer the next generation therapeutics which targets these mutation prone proteins,” Ray added



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Covid-19 virus highly adapted to infect human cells, says study

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MELBOURNE: The SARS-CoV-2 virus, which causes Covid-19, is most ideally adapted to infect human cells, rather than bat or pangolin cells, according to a study that raises questions about the origin of the virus.
The researchers from Flinders University and La Trobe University in Australia used high-performance computer modelling of the form of the SARS-CoV-2 virus at the beginning of the pandemic to predict its ability to infect humans and 12 domestic and exotic animals.
The study, published in the journal Scientific Reports on Thursday, aimed to help identify any intermediate animal vector that may have played a role in transmitting a bat virus to humans.
The researchers used genomic data from the 12 animal species to painstakingly build computer models of the key ACE2 protein receptors for each species.
These models were then used to calculate the strength of binding of the SARS-CoV-2 spike protein to each species ACE2, which acts as the receptor for SARS-CoV-2 and allows it to infect the cell.
The results showed that SARS-CoV-2 bound to ACE2 on humans cells more tightly than any of the tested animal species, including bats and pangolins.
The researchers explained that if one of the animal’s species tested was the origin, it would normally be expected to show the highest binding to the virus.
Humans showed the strongest spike binding, consistent with the high susceptibility to the virus, but very surprised if an animal was the initial source of the infection in humans, said David Winkler, a professor at the La Trobe University.
The computer modelling found the virus’s ability to bind to the bat ACE2 protein was poor relative to its ability to bind human cells, Winkler said.
This, the researchers said, argues against the virus being transmitted directly from bats to humans.
If the virus has a natural source, it could only have come to humans via an intermediary species which has yet to be found, said Professor Nikolai Petrovsky from Flinders University.
The team’s computer modelling shows the SARS-CoV-2 virus also bound relatively strongly to ACE2 from pangolins, a rare exotic ant-eater found in some parts of South-East Asia.
Winkler said pangolins showed the highest spike binding energy of all the animals the study looked at, significantly higher than bats, monkeys and snakes.
The researchers said it was incorrectly suggested early in the pandemic by some scientists that they had found SARS-CoV-2 in pangolins.
This was due to a misunderstanding and this claim was rapidly retracted as the pangolin coronavirus they described had less than 90 per cent genetic similarity to SARS-CoV-2 and hence could not be its ancestor, Petrovsky said.
This study and others have shown, however, that the specific part of the pangolin coronavirus spike protein that binds ACE2 was almost identical to that of the SARS-CoV-2 spike protein.
This sharing of the almost identical spike protein, which allows the virus to enter the cells, almost certainly explains why SARS-CoV-2 binds so well to pangolin ACE2, according to the researchers.
Overall, putting aside the intriguing pangolin ACE2 results, our study showed that the Covid-19 virus was very well adapted to infect humans, Petrovsky said.
The study also suggests that some domesticated animals like cats, dogs and cows are likely to be susceptible to SARS-CoV-2 infection too.
The extremely important and open question of how the virus came to infect humans has two main explanations currently, they said.
The virus may have passed to humans from bats through an intermediary animal yet to be found (zoonotic origin), according to the researchers.
However, it cannot yet be excluded that it was released accidentally from a virology lab, they said.
A thorough scientific, evidence-based investigation is needed to determine which of these explanations is correct, the researchers added.



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Researchers led by Indian-origin scientist identify genes that fight the virus

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WASHINGTON: US researchers led by an Indian-origin scientist have identified a set of human genes that fight SARS-CoV-2, the virus which causes Covid-19, a study that could help in understanding the factors that affect disease severity and suggesting possible therapeutic options.
The study by scientists at Sanford Burnham Prebys Medical Discovery Institute in San Diego, California, was published in the journal Molecular Cell.
The genes in question are related to interferons, the body’s frontline virus fighters.
“We wanted to gain a better understanding of the cellular response to SARS-CoV-2, including what drives a strong or weak response to infection,” says Sumit K. Chanda, professor, and director of the Immunity and Pathogenesis Program at Sanford Burnham Prebys and lead author of the study.
“We’ve gained new insights into how the virus exploits the human cells it invades, but we are still searching for its Achilles heel so that we can develop optimal antivirals,” he said.
Knowing which genes help control viral infection can greatly assist researchers’ understanding of factors that affect disease severity and also suggest possible therapeutic options, the institute said in a press release.
Soon after the start of the pandemic, clinicians found that a weak interferon response to SARS-CoV-2 infection resulted in some of the more severe cases of Covid-19.
This knowledge led Chanda and his collaborators to search for the human genes that are triggered by interferons, known as interferon-stimulated genes (ISGs), which act to limit SARS-CoV-2 infection.
Based on knowledge gleaned from SARS-CoV-1, the virus that caused a deadly, but relatively brief, outbreak of disease from 2002 to 2004, and knowing that it was similar to SARS-CoV-2, the investigators were able to develop laboratory experiments to identify the ISGs that control viral replication in Covid-19, the statement said.
“We found that 65 ISGs controlled SARS-CoV-2 infection, including some that inhibited the virus’ ability to enter cells, some that suppressed manufacture of the RNA (Ribonucleic acid) that is the virus’s lifeblood, and a cluster of genes that inhibited assembly of the virus,” Chanda said.
“What was also of great interest was the fact that some of the ISGs exhibited control across unrelated viruses, such as seasonal flu, West Nile and HIV, which leads to AIDS”.
As a next step, the researchers will look at the biology of SARS-CoV-2 variants that continue to evolve and threaten vaccine efficacy.
The overall global Covid-19 caseload has topped 139.6 million, while the deaths have surged to more than 2.99 million, according to the Johns Hopkins University.

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