Research led by the University of Adelaide studied how and why these HIV fibrils, known as semen-derived enhancers of viral infection (SEVI), enhance infection and cause toxicity in the body's cells.
"Amyloid fibrils play an important role in a number of prominent diseases, such as Parkinson's, Alzheimer's and others, and it's absolutely essential that we understand how they work if we have any hope of developing new drugs to stop them," said lead author Dr Ian Musgrave, from the University's School of Medical Sciences.
"This suggests that you can't just prevent one part of SEVI from aggregating and being toxic to cells. You need to shut the whole thing down or stop it from forming in the first place," Musgrave said.
Researchers also tested the fibrils against another major type of body tissue, epithelial cells, and found they were not toxic to these cells.
More From This Section
"Epithelial cells are a major barrier to HIV entry. There have been theories that the fibrils can damage the epithelial layer, making it much easier for the virus to enter the body and infect the immune cells, but our findings show that healthy epithelial cells are resistant," Musgrave said.
"We now have a better understanding of the role of these protein enhancers in HIV infection. However, it's clear that much more research is needed in this area," he said.
The study is published in the journal Biochimica et Biophysica Acta.