Post by Andras Donaszi-Ivanov, University of East Anglia
Researchers have found that respiratory syncytial virus (RSV) can manipulate levels of regulatory genetic material, called microRNAs, in host cells, helping the virus suppress the immune response to aid its survival. This research, published in the Journal of General Virology, is an important step in understanding host-virus interactions, and in the future could lead to development of vaccines or treatments for RSV.
MicroRNAs are short strands of RNA (21-22 nucleotides long), that are very important in fine-tuning gene expression. They do this by binding to complementary messenger RNA molecules within the cell, which can suppress protein synthesis. Several human viruses have been shown to be able to change the amount of microRNAs present in host cells to help their own replication, but how this happens is not well understood.
RSV causes infection in the lower respiratory tract, and is the most common cause of respiratory illness in children and infants. It only causes mild cold-like symptoms in the majority of cases but 2-3% of infected children need to be hospitalized. In rare cases it can turn into a life-threatening illness. RSV is highly contagious and can spread rapidly, causing epidemics mostly over winter months in childcare facilities and hospitals. Despite its medical and economic importance there is no vaccine or effective treatment available.
Researchers from the University of Georgia and the University of South Florida Health investigated changes in microRNA levels in human cells, in response to RSV infection. They identified particular microRNAs that decreased or increased in number, which is an indicator that they might play a role in infection. The scientists also demonstrated how one specific RSV protein directly upregulated a specific microRNA called Let-7f.
By comparing the sequences of the affected microRNAs to computer databases, the scientists could predict the target genes of these molecules. They showed that most of these microRNAs were involved with genes that are important in cell cycle regulation and cytokine expression. This could explain how RSV is able to arrest the cell cycle during infection, and repress the cellular immune response.
A better understanding of how viruses interact with their host cells is crucial for developing vaccines and cures, yet almost nothing is known about the role of microRNAs in this interaction. Exploring this new field is a promising step towards effective treatments of RSV (and other viral) infections.