SAN DIEGO — Statins, a common cholesterol-lowering medication, appear to be linked to a lower risk of developing severe COVID-19 symptoms and faster recovery time in general. That’s the takeaway from a new study by doctors at UC San Diego Health medical center.
The authors say that the molecule ACE2 resides on the outer surface of various human cells, similar to a doorknob on a door. Normally, ACE2 is a helpful molecule that contributes to blood pressure regulation. Unfortunately SARS-CoV-2 also uses ACE2 as its prime entryway into lung cells.
“When faced with this novel virus at the beginning of the pandemic, there was a lot of speculation surrounding certain medications that affect ACE2, including statins, and if they may influence COVID-19 risk,” comments study leader Dr. Lori Daniels, professor and director of the Cardiovascular Intensive Care Unit at UC San Diego Health, in a release. “We needed to confirm whether or not the use of statins has an impact on a person’s severity of SARS-CoV-2 infection and determine if it was safe for our patients to continue with their medications.”
Coronavirus patients who take statins much less likely to develop severe symptoms
Researchers retrospectively analyzed the medical records of 170 coronavirus patients who had been treated in San Diego between February and June of this year. They also used records from 5,281 COVID-negative patients as a control. For patients with COVID, the data encompasses the severity of their symptoms, how long they were hospitalized, the ultimate outcome of their hospital stay, any use of statins, and the use of any ACE or ARB inhibitors within the 30 days prior to being admitted.
Among COVID-positive subjects, 27% were taking statins when they were admitted. Another 21% were on an ACE inhibitor and 12% were on an ARB. Incredibly, the study shows that use of a statin before coming to the hospital is linked to more than a 50% drop in one’s risk of experiencing severe COVID-19 symptoms. Coronavirus patients using a statin also recover faster than other patients, researchers say.
“We found that statins are not only safe but potentially protective against a severe COVID-19 infection,” Daniels says of the study, published in the American Journal of Cardiology. “Statins specifically may inhibit SARS-CoV-2 infection through its known anti-inflammatory effects and binding capabilities as that could potentially stop progression of the virus.”
“I tell my patients who are on statins, ACE inhibitors or other ARBs to keep taking them,” she adds. “Fears of COVID-19 should not be a reason to stop, if anything our research findings should be incentive to continue with their medication.”
How cholesterol plays a role in COVID infections
In a related study, researchers explain that by removing cholesterol from cell membranes, statins essentially block SARS-CoV-2, the virus that causes COVID-19, from entering. Co-author Tariq Rana, PhD, professor and chief of the Division of Genetics in the Department of Pediatrics at UC San Diego School of Medicine and Moores Cancer Center, says he wasn’t focusing on statins at all initially.
At first, his team set out to see which genes “switch on” within human lung cells in response to SARS-CoV-2. Immediately, Rana noticed that a gene called CH25H turns “blazing hot” in response to the virus. CH25H is usually responsible for encoding an enzyme that modifies cholesterol.
“I got excited because with HIV, Zika, and a few others, we know that CH25H blocks the virus’ ability to enter human cells,” Rana says.
When CH25H activates, it produces a modified cholesterol called 25-hydroxycholesterol (25HC). This all starts a chain reaction that leads to the cholesterol on a cell’s membrane being depleted. Rana’s experiments show that adding 25HC to a group of human lung cells blocks the coronavirus from entering.
“The difference between untreated cells and those treated with 25HC was like day and night,” Rana explains.
These findings, published in The EMBO Journal, strongly suggest that SARS-CoV-2 needs some cholesterol, in addition to the ACE2 receptor, to bond with a host cell. This connects to statins because they also drain cell membranes of their cholesterol.
“This is already happening in our bodies on a regular basis, so perhaps we just need to give it a boost, with statins or by other means, to better resist some viruses,” Rana says. “It’s not unlike cancer immunotherapy — the idea that sometimes instead of attacking a tumor directly, it’s better to arm a patient’s immune system to do a better job of clearing away tumors on its own.”
The research team even says statins in general may not be necessary if 25HC can be turned into an antiviral medication.