HIV can avoid the immune system by mutating into a slightly different form that isn't recognised -- but this disguise comes at a cost to the virus, a new study has revealed.
An international team has carried out the study and found that when HIV mutates to hide from the immune system, it is slightly less able to reproduce and cause harm, a finding that is a step closer to understanding how to develop vaccines against AIDS.
According to lead author Liyen Loh of Melbourne University, the study focussed on the interplay between virus and the immune system and how this affected the number of copies of the HIV virus in the body.
"Our research revealed that maintaining a weakened strain of the virus during the early stages of HIV infection may help body's immune system to control virus replication. Knowing what factors are important for controlling HIV replication can also help guide vaccine studies," Loh said.
Killer T-cells are a major player in the host immune system as they have the ability to identify and attack virus infected or cancerous cells.
However HIV can 'out-smart' killer T cells by mutating to a slightly different form that can no longer be recognised by the killer T cells. These viruses are known as escape mutants.
The study discovered these changes usually come at a 'fitness cost' to the virus resulting in slower replication and fewer copies of the virus.
"When HIV is transmitted to a new host, the mutations often revert to the original wild-type virus, allowing the virus to regain a fitter state, or the changes may be retained, depending on the individual's immune system. This explains why some individuals have better clinical outcomes than others," said Loh.
The team measured the length of time it took for transmitted escape mutant virus to return to its fitter wild-type state in a new host. "We have identified several 'rules' governing how HIV escapes being detected by killer T cells.
"Once HIV gets into an individual, it undergoes mutation to 'adapt' to the immune response of that person. All of our immune systems are subtly different so what is 'well adapted' in one patient is often slightly slow growing in a new patient.
"Therefore, over the first few weeks or months of infection of a new patient, the virus 'reverts' from this slow growing form to a fast growing form, while at the same time adapting to the new immune response," Loh said.
The study is published in the Public Library of Science Pathogens journal.
