A future vaccine or treatment that attacks a specific HIV strain by priming the immune system's "killer" blood cells may be ineffective if the person is then exposed to a different, but related, strain, according to a study published on Thursday in Nature, the British science weekly.
The evidence has been detected in only one patient and needs further research, but the authors fear there could be major implications for the fight against the pandemic.
About 42 million people around the world have HIV or Aids, according to figures published by United Nations agencies this week ahead of World Aids Day on Sunday.
Those with the virus are condemned to death or a lifetime of taking antiretroviral drugs - if they have access to them - that can reduce the presence of HIV to below detectable levels, but not eliminate it.
A team led by Bruce Walker of Harvard medical school were monitoring a patient who was following a "stop-start protocol" of treatment.
Under this, a patient takes a course of antiretrovirals to dampen the virus levels.
He then suspends the course and, during this time, his blood samples are regularly checked to see when the virus starts to sneak out from its refuge, believed to be the lymph glands, and venture out across the body once more.
Once the viral levels rebound beyond a certain threshold, the treatment is resumed to bring them down, and so on.
The main point behind this on-off protocol is to give patients a break, usually lasting several weeks or hopefully months, from the side-effects of the powerful drugs.
Some theorise that stop-start helps to stimulate "killer" white blood cells called CD8 T-cells, which are the body's heavy artillery against an invader by priming a key component of the immune system and which are aided by so-called CD4 "helper" cells.
The unnamed patient showed a remarkably strong response until, at one point, his viral levels suddenly shot up and the response of his CD8 cells to the infection dramatically plummeted.
The culprit was eventually found to be a cousin to the initial virus that the man had apparently picked up through unprotected sex.
Both the initial virus
and the second virus he had caught were members of the B clade, or group, of
HIV-1, the predominant family of Aids viruses in
Cross-protective immunity lacking
This finding could be bad news indeed, because it appears to shows that a "strong and broadly directed" priming of the CD8s fails to provide protection for HIV strains that are even closely related, say the authors.
By inference, it implies that vaccines that are geared to trigger a CD8 response to specific proteins on a given strain of HIV may fail to provide a shield if you come into a contact with a different strain.
"The lack of cross-protective immunity for closely related HIV-1 strains... has important implications for public health and vaccine development," they say.
Priming the T-cells is the favourite path taken by designers today in the elusive quest for a vaccine. It would not prevent infection, but could keep viral replication level down and discourage the onset of full-blown Aids.
The Walker team add a large caveat, saying the cross-protective problem, arising from a double infection, had been seen in only one person, and that this patient's immune system already had been damaged by HIV infection.
Someone with a healthy immune system, who had received an HIV vaccination, might react differently, they said.