COVID-19 and CMV coinfection caused the premature aging of immune systems, leading to a greater risk of cardiovascular disease at an earlier age, the study authors said.
There is an increased risk of cardiovascular disease during a coinfection of COVID-19 and cytomegalovirus (CMV), according to a paper published in The Journal of Infectious Diseases. The evidence suggests that a COVID-19 vaccination can protect against this phenomenon.
These study findings came nearly in tandem with today’s US Food and Drug Administration (FDA) approval of letermovir for prophylaxis of CMV disease in high-risk adult kidney transplant recipients (Donor CMV-seropositive/Recipient CMV-seronegative [D+/R-]). Letermovir (Prevymis) is a first-in-class non-nucleoside that inhibits viral replication by specifically targeting the viral terminase complex.
Investigators from the University of Cordoba in Spain wanted to determine the effects of COVID-19 and CMV coinfection. The study authors explained that as a common herpesvirus which causes chronic infection, CMV can affect between 40 and 90% of the world’s population but it depends on factors such as age, socioeconomic status, race, and education. CMV is also associated with cardiovascular disease (CVD) and increased risk of cardiovascular death, the study authors added. However, it does not produce symptoms in otherwise healthy people.
For the study, the investigators included 30 healthy donors, 56 non-hospitalized COVID-19 patients, and 30 patients with severe aortic stenosis (AS) as controls for CVD. Participants with and without CMV infection provided blood samples at 3 and 12 months after a mild or asymptomatic COVID-19 infection. The investigators used the samples to analyze the T cell response from the immune system, which were found to be elevated after CMV infection and additionally elevated following a COVID-19 infection.
This elevation can generate inflammation and damage the vascular endothelium, the study authors explained in a statement.
“COVID-19 also has medium- and long-term consequences in people who had the disease without complications, and that we should take this into account,” the study’s lead author, Dr. Alejandra Pera, added in the press release.
The study authors noted that many studies have suggested a link between COVID-19 infection and elevated risk of CVD, with their study adding to that knowledge base.
“Here we show that SARS-CoV-2 infection is, in fact, an accelerating factor of CMV-associated T cell senescence that may lead to an increased risk of CVD in CMV-positive individuals,” they wrote.
There was no evidence that this varied depending on the COVID-19 variant, nor was their evidence to support vaccination status made a difference. But the study authors highlighted that vaccine adherence was near 90% in the region where the study was conducted (Andalusia). For example, among participants who became infected with COVID-19 after vaccination, there was no increased T cell response observed.
“Our results alert us to a noteworthy worldwide potential health problem,” the study authors concluded. “CMV-positive individuals infected with SARS-CoV-2 in 2020–2021 exhibit, to some extent, accelerated T cell immunosenescence that may contribute to the development of inflammatory diseases such as CVD at earlier-than usual-ages.”