University of Bonn researchers have come across a new bacterial compound that may very well impede the replication of the influenza virus.
Notably, viruses use the cluster of molecules in host cells that are already infected to collect and multiply. Apparently, the researchers were looking for novel ways to exploit this process of treating influenza viruses.
A team led by Professor Hiroki Kato, who happens to be from the Institute of Cardiovascular Immunology at the University Hospital Bonn, has come across a new bacterial compound that can halt the function of methyltransferase MTr1, an enzyme, thereby blocking the virus’s capacity to multiply.
This compound has been effectively used in lung tissue preparations as well as mouse studies. The researchers have also witnessed effects that are synergistic with influenza drugs that are already approved.
As and when the influenza virus infects a host cell, genetic information is transferred in the form of nucleic acids like DNA or RNA. This data is then used to manufacture novel viruses in the host cell. Own labelling system is used by the infested cell to differentiate its own nucleic acids from the foreign nucleic acids. This helps the immune system react in specific ways to varied threats.
Methylated nucleoside happens to be the molecular cap, a small molecule that is attached to the end of the RNA chain. It is well to be noted that once RNA is tagged in this way, no longer can an immune response be triggered. If in case the RNA is not capped, it gets recognised by the RIG-I immune system and thereby altered.
The influenza virus has created a unique mechanism to shun this immune system response. The virus takes away the molecular cap from the RNA molecules, which are cellular, and transfers the same to its own RNA. This entire process is called cap-snatching. A cap structure is provided by the MTr1 enzyme to the cellular mRNA so as to allow the enzymes to perform as nucleic acid labelers of the cells. This particular study shows how influenza viruses are dependent on the function of MTr1.
Although other viruses like the SARS-CoV-2 are able to put a cap on their RNA molecules on their own, the influenza virus completely relies on stealing existing caps, according to Yuta Tsukamoto, the paper’s lead author. He adds that if there happens to be a disruption in the cell pertaining to the functioning of MTr1, no caps will be available so as to transfer the viral RNA. Therefore, the activity of MTr1 is of prime importance for the exact duplication of the influenza virus in the cell.
It was this dependence on taking care of the influenza infections that the researchers were wanting to explore. The team looked out for halters that could particularly inhibit MTr1. They investigated as to how the infested tissue substances could have an effect on the number of virus particles which get created. All this was tested in human lung tissue preparations as well as mouse models.
Professor Kato said that among numerous candidates, they were able to pinpoint on a molecule that stops the growth of the MTr1 across human lung explants and also in the mice, therefore keeping the influenza replication in check.
The inhibitor that is suggested here is a natural bacterial product developer known as trifluromethyl tubercidin, which happens to be created by the genus Streptomyces bacteria.
The researchers came to the conclusion that in this study, trifluromethyl tubercidin works just fine with influenza drugs that are authorized. Many virus particles produced in the tissue also have a synergistic effect. Professor Kato opines that this study will surely lead to new treatment developments in the case of influenza.
