The discovery may help explain why the risk of developing neurological difficulties increases as AIDS patients live longer, and may also help predict which patients are at greatest risk for the problem, according to the U.S. scientists.
They said the two newly-identified HIV types aren’t being detected in HIV that circulates in a patient’s blood, and one type may be present cerebrospinal fluid years before the onset of HIV-linked dementia.
The fact that the two HIV types can be detected in the CSF indicates that they grow in the central nervous system, the researchers said.
The finding might also help explain while highly active antiretroviral therapy — the drug “cocktails” that HIV-positive patients take to stay healthy — can help prevent some of the neurological troubles associated with infection, but not all.
The study, which appears in the Oct. 6 issue of the journal PLoS Pathogens, was led by researchers at the University of North Carolina at Chapel Hill School of Medicine.
Besides spotting the two types of HIV in cerebrospinal fluid, the team also made another discovery: While HIV is known to infect and replicate within immune system T-cells, one of the two HIV types found in CSF does so in another immune cell, called macrophages.
“This is the first time that anyone has demonstrated active replication of HIV virus in a cell type other than T- cells,” study senior author Ronald Swanstrom, a professor of biochemistry and biophysics and director of the UNC Center for AIDS Research, noted in a university news release.
The finding could enhance scientists’ understanding of why some patients respond better than others to HIV treatment.
“We know that HIV in the blood disappears quickly when you go on therapy, and that’s because the virus is growing in T-cells, which have a very short half-life,” the amount of time it takes for the level of virus to drop by half, Swanstrom explained.
But half of the patients In the new study showed a much slower rate of decay when it came to the amount of virus in their CSF. “This is evidence the virus is actually being produced by a cell with a longer half-life, and not a T-cell,” Swanstrom explained.
The next step is to determine how relevant all of this might be to HIV-linked neurological issues.
“Is it bad to have these viruses around even if you don’t get a diagnosis of dementia?” Swanstrom said. “And are they potentially causing cognitive damage that can be reversed with treatment?”