In a research of how HIV mutates in response to immune system, scientists claim to have found evidence that the virus can take several escape routes, not one preferred route.

The human immune system has the ability to temporarily overpower HIV in early infection. Recent studies showed that most newly infected patients develop neutralising antibodies.

But, the problem is HIV’s ability to mutate, disguising itself enough to get away from the antibodies.

Now, a team has claimed that if a vaccine component is identified which can stimulate neutralising antibodies, HIV’s capacity for rapid mutation can still be a confounding factor.

“A single type of neutralising antibody may not be enough to contain HIV. These neutralising antibodies work really well — they hit the virus fast and hard. But so far, every time we look, the virus escapes,” lead researcher Prof. Cynthia Derdeyn of Emory University School of Medicine said.

Prof. Derdeyn and her colleagues collaborated with a public health programme which provides thousands of couples counselling and condom supplies every three months. Despite these measures, a low level of HIV transmission still occurs.

The collaboration allowed the team to take blood samples a few weeks after infection occurred and then later as two participants’ immune responses continued.

The scientists isolated individual viruses over the first two years of HIV infection and tested how well the patients’ own antibodies could neutralise them.

“In one patient where we had very early samples, there was evidence that neutralising antibody came up within weeks, and that’s earlier than what was previously thought,” Prof. Derdeyn said.

In both patients, some viruses mutated part of their outer proteins so that after the mutation, an enzyme would be likely to attach a sugar molecule to it. The sugar interferes with antibody attack.

However this tactic, known as the “glycan shield,” was not observed in all cases. Other viruses mutated the part of the outer protein that the neutralising antibodies stick to directly. In both patients, many changes in the virus’ genetic code were necessary for escape.

“We need to understand early events in the immune response if we are going to figure out what a potential vaccine should have in it. What we can show is that even in one patient, several escape strategies are going on.

“That means that in order to be immune to HIV infection, someone may need to have several types of neutralising antibodies ready to go. Seeing how the virus mutates will allow researchers to choose the best parts to put in a vaccine,” Prof. Derdeyn said.