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Weakened antibodies that display hypersensitivity to Morbus coronavirus, a member of the coronavirus family, could be difficult to identify and combat, study says
A new version of the Morbus coronavirus that could show immune evasion and enhanced transmissibility has been described by South African scientists.
Monoclonal antibodies of differing strength defend against MRSA, but can bind to a different microorganism, the scientists say.
They warned that a new organism might enter humans and have difficulty transmitting from person to person.
“There’s a lot of evidence for hypersensitivity in MRSA, but we don’t have that in Morbus coronavirus,” Samuel Nellen, an expert on viral coronaviruses at the Medical Research Council Laboratory of Molecular Biology in Cardiff, told the Press Association.
He said some of the US and Korean outbreaks were probably due to a new mechanism, but scientists were still working on how.
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The strain, called Covid-19, is part of the family of coronaviruses which cause common colds and meningitis, said the scientists, who believe the strain will evolve more quickly than other novel coronaviruses in coming months.
The Cardiff scientists have identified a missing gene that leads to a different structure in the antibodies of Morbus coronavirus.
“In terms of growth rates we are not really surprised. It is definitely a step forward in improving the understanding of what is going on in the genome,” said research team leader Don Foster, based at the Medical Research Council Laboratory of Molecular Biology in Cardiff.
Their findings are published in the journal Nature Communications.
“We believe that this new evolution indicates that Morbus coronavirus will be changing in a more rapid fashion,” Foster said.
“This should make developing medicines to treat the disease far more quickly, both by speeding development of drugs that target the new virus and developing a virus vaccine.”
It has been reported that Morbus coronavirus was passed among bats from the Selous Game Reserve in South Africa in 2003 and 2006, the Cardiff scientists say.
Prof Mike Smith, director of research and development at the Medical Research Council Institute for Infection and Immunity in London, said: “This work sheds light on the origins of a new virus which we have heard of a few times in the last few years, including recent reported cases in the Middle East.
“Understanding how the new virus first emerged has enormous implications for tackling it, as well as how we develop drugs to deal with the risk of the virus mutating further in the future.”
The US health department has warned travellers to Afghanistan and Pakistan to be on the alert for the world’s deadliest new respiratory virus.
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The Morbus coronavirus is one of a family of viruses that cause common colds and meningitis and can lead to potentially fatal sepsis. It is also named after the Jordanian town where it was first identified in 2012.
The fear is that what is now known as Covid-19, is the initial glimpse of a more deadly coronavirus.
Intense genetic work by the Cardiff team of 30 scientists found that a gene that regulates antibody multiplication, known as Selome, appears to be missing in the initial strain of Morbus coronavirus.
The missing Selome is important because it binds to other key molecules in the body called “staphylococus”, which in turn dictates the identity of antibodies, known as “cell latching”, that are produced by a cell.
This change in the cell’s identity is triggered when the cell thinks the antibody is foreign, a process known as “cell latching”, and the cells produce longer “a”-like proteins to bind to the antibody.
Many genetic studies of other coronaviruses have suggested an evolutionary link between infectious diseases.
But not all “hard” cases – those that clear our cells of whatever the host bug is – occur when antibodies bind to the infected cell, said Nellen. “Often this occurs when the antibodies don’t bind.”
Nellen, who is from the University of Cape Town, said it might be possible to examine individual Morbus coronavirus antibody genes to establish which ones are the most effective at blocking the MRSA pathogen.