Ancient viral remnants in DNA may mark Parkinson’s, be protective
Levels of HERV-K, one such retrovirus, low in patients' brain and blood cells
Levels of a retrovirus that entered the human genome via infections millions of years ago — an endogenous retrovirus called HERV-K that is still part of a person’s DNA — were lower in people with Parkinson’s disease and linked to more severe symptoms and longer disease duration, a study reports.
While further research is necessary to confirm these findings, “HERV-K is likely to be neuroprotective,” researchers wrote in the study “Human Endogenous Retrovirus K in Astrocytes Is Altered in Parkinson’s Disease,” published in the journal Movement Disorders.
“The fact that the human genome has conserved HERV … over millions of years may explain beneficial functions that HERVs provide to human hosts,” the scientists, all in Australia, added. “Their importance in human physiology is increasingly being recognized.”
HERVs, ancient viral remnants, thought to make up 8% of human DNA today
The human genome, or the complete set of genetic information found in human cells, contains HERVs, ancient viral remnants that are estimated to make up 8% of a person’s DNA. While usually inactive, HERVs can be activated under certain disease conditions. HERV-K, one group of these human endogenous retroviruses, is thought to be the most active and, as such, has been studied in relation to disease, particularly amyotrophic lateral sclerosis and frontotemporal dementia, the scientists noted.
However, it’s not known if and how HERVs link with Parkinson’s.
Researches with the University of Sydney aimed to find where HERV-K is located in the brain, if its brain and blood levels differ between Parkinson’s patients and other adults, and whether it could serve as a marker to track the disease. They also looked for links between HERV-K and the severity of Parkinson’s symptoms.
“Based on what we know of HERV in human physiology, we hypothesized that HERV-K is altered in PD [Parkinson’s disease] and is related to PD progression,” they wrote.
They analyzed postmortem brain tissue from eight people with Parkinson’s, ages 73-84, and from a control group of 10 adults, ages 67-92, who died of causes other than a neurological disease. They also looked into blood samples from 25 people with Parkinson’s and 25 age- and sex-matched healthy controls.
HERV-K less evident in nerve-supportive cells in blood, brain tissue
In two brain regions, the superior frontal and fusiform cortices, HERV-K was present in astrocytes — star-shaped cells that give support to nerve cells — in both groups. HERV-K levels in the brain, however, were lower in patients than in controls.
People with Parkinson’s also had lower blood levels of HERV-K than did controls.
In both brain tissue and blood samples from patients, moreover, the lower the HERV-K levels, the lower were those of glial fibrillary acidic protein (GFAP), a marker of astrocytes that can indicate a diminished presence or activity of these nerve-supportive cells.
Researchers also looked at how HERV-K might link to patients’ scores on the Hoehn and Yahr Scale, which rates disability from one (mild) to five (severe), and with MDS-UPDRS Part III scores, which measure disease motor symptoms on an ascending scale where higher scores again indicate more severe disease. Lower HERV-K blood levels linked with higher scores on both scales, they reported.
HERV-K levels linked with Parkinson’s severity and duration
People with a longer time since a Parkinson’s diagnosis also had lower blood levels of HERV-K, suggesting that it associated with how the disease progresses over time. These findings also raise the possibility of HERV-K as a potential marker to monitor Parkinson’s progression.
“We found that decreases in HERV-K protein correlated with decreases in astrocytic GFAP in PD, and that in peripheral blood the loss of HERV-K and GFAP was associated with PD severity and duration … [supporting] the idea that astrocytic HERV-K could be neuroprotective and has been altered in PD,” the researchers wrote.
“Although further work is needed to verify our findings in larger [groups of patients], our study has provided new insights into an unrecognized pathway in [Parkinson’s] and opened a new area of research for better understanding [Parkinson’s] and developing novel therapeutic strategies,” the researchers wrote.
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