Mammals have evolved several mechanisms to fight viral infections, and insight into how humans and animals successfully limit virus spread helps to develop effective anti-viral drugs and vaccines.
The scientists are set to further investigate a mechanism that may be able to stop so-called retroviruses in their tracks. Retroviruses, during their life cycle, spread by permanently inserting their genetic material into healthy cell's DNA.
The scientists, led by Professor Massimo Palmarini from the University of Glasgow's Faculty of Veterinary Medicine, are investigating how some endogenous retroviruses ('benign' retrovirusese present in the genome of all mammals) protect hosts by interfering with the infection by related disease-causing retroviruses.
The new grant will boost the study of how an 'endogenous' retroviruses (ERV) named enJS56A1 interferes with a pathogenic 'exogenous' retrovirus (JSRV), the cause of major infectious diseases of sheep. enJS56A1 forms viral particles that 'stick' together and cannot exit the cell and spread to other cells. JSRV instead forms particles normally able to exit the cell.
However, when JSRV and enJS56A1 are present in the same cell only defective 'sticky particles' are formed, effectively blocking viral infection. Understanding the mechanisms of enJS56A1-induced block can lay the foundation to develop new drugs that stop production of viruses from infected cells.
The research is set to shed light on how retroviruses evolve and will help explain late steps in the retroviral life cycle. Understanding how enJS56A1 functions co
Contact: Jenny Murray
University of Glasgow