People hospitalised with serious bouts of Covid-19 are more likely to develop heart disease and Parkinson’s, finds a major new study led by New Zealand geneticists. Photo / 123RF
People hospitalised with serious bouts of Covid-19 are more likely to develop heart disease and Parkinson’s, finds a major new study led by New Zealand geneticists. Photo / 123RF
People hospitalised with serious bouts of Covid-19 are more likely to develop heart disease and Parkinson’s, finds a major new study led by New Zealand geneticists.
The new research, just published in the journal Scientific Reports, sheds fresh light on the complex interplay of genetics and the long-termcomplications of Covid-19, at a time scientists are still trying to understand its many concerning lingering impacts.
In their study, a team from the University of Auckland’s Liggins Institute drew on publicly-available genetic data from 8500 people with serious cases of Covid-19.
“In the early days of the pandemic, when global scientific collaboration was at its peak, a wealth of genome data from severely ill Covid patients became available,” explained the study’s leader, Rachel Jaros.
“It became evident that certain individuals were more vulnerable to developing a severe infection due to their genetic makeup.”
Moreover, clinicians highlighted that individuals with pre-existing conditions like cardiovascular disease and diabetes faced a higher risk.
“The problem was we had a lot of genetic information and no real mechanistic information about how genetic changes were interacting together to increase risk.”
That raised an urgent need to reveal the mechanisms at play.
By using sophisticated computational techniques to explore the data, the researchers gained new insights into the behaviour of proteins working together, and how certain genes could be turned on.
“This meant we could make tissue-specific gene regulatory maps that showed how susceptibility to Covid interacted with other conditions.”
This revealed genetic factors that began to explain observed connections between Covid-19 outcomes and conditions like Parkinson’s disease and coronary artery disease.
“This significant finding is backed by previous clinical research, which indicates a direct association between acute Covid infections and the risk of developing cardiovascular diseases, even up to a year after the infection,” she said.
“What sets this study apart is the discovery of the mechanisms that potentially underly these connections.”
This, she said, opened up avenues for two vital actions: assessing patients’ predisposition to comorbidities before or after a Covid infection, and identifying targetable mechanisms that could mitigate these risks.
University of Auckland geneticist Professor Justin O'Sullivan. Photo / Supplied
Study co-author Professor Justin O’Sullivan said that, in some cases, heart disease or Parkinson’s could be evident before Covid infection, but in other instances, the virus might activate the conditions.
“While our analysis has confirmed many of the known genetic risk factors for severe or fatal Covid-19 infections, it also throws up new genetic risk factors,” says Professor O’Sullivan of the Liggins Institute.
“Of great concern is the genetic risk for Parkinson’s.”
He said it was known that rates of Parkinson’s went up dramatically in the years following the 1918 Spanish flu epidemic, which also killed millions worldwide.
Epidemiologists later found a three-fold increase of Parkinson’s among Spanish influenza survivors compared with those who hadn’t been exposed to the virus.
Since then, a number of other triggers, including pesticides and viruses, such as influenza A, which causes the common flu, have been linked to later development of Parkinson’s.
Still, O’Sullivan said, there was much to learn.
“We really don’t understand the long-term impacts of viral infections and the Covid-19 virus is no exception,” he said.
“We need better ways to understand why some people have symptoms that persist even after the infection subsides.”
What we knew as Long Covid – a constellation of persisting symptoms thought to accompany 10 to 20 per cent of infections – had been shown to affect nearly every organ system in our bodies.
Yet there remained no established treatment or cure for the condition, nor did there appear to be any clearly-understood, single cause.
One possibility was that Covid-19 infection caused the immune system to go haywire, triggering a long-lasting inflammatory response.
O’Sullivan said the latest study, at least, told us more about the role our genetics played in determining both the likelihood of severe infection, and the potential development of long-term complications, such as cardiovascular diseases and Parkinson’s.
“In the medium to long-term, we think the insights from our research might help scientists stratify people who are at risk of Covid complications, and potentially highlight therapeutic targets that may reduce the long-term impacts of the virus.”
Jamie Morton is a specialist in science and environmental reporting. He joined the Herald reporting team in 2011 and has spent the last decade writing about everything from conservation and cosmology to climate change and Covid-19.
