The last month, the World Health Organization (WHO) officially announced the conclusion of the global emergency status concerning Covid-19, yet cautioned nations against complacency and urged them to maintain their defense mechanisms against the virus.
This significant declaration by the global health institution symbolically concludes a pandemic that’s thought to have claimed at least 20 million lives over the past three years.
Despite marking the end of the emergency phase, the WHO emphasized that the pandemic has not ended entirely, drawing attention to recent surges in Covid-19 cases in Southeast Asia and the Middle East.
Dr. Tedros Adhanom Ghebreyesus, the Director-General of WHO, optimistically announced,
“It’s with great hope that I declare Covid-19 over as a global health emergency.
“That does not mean Covid-19 is over as a global health threat.”
He further elaborated that the virus continues to exist, mutate, and still killing people.
Amid these developments, a study published in the Journal of Infectious Diseases on May 30 pointed towards a potentially worrisome issue – individuals with co-infection of Covid-19 and another pathogen might face premature aging of their immune systems. This could heighten their risk of experiencing cardiovascular diseases at an earlier age.
Cytomegalovirus (CMV), a pervasive strain of the herpesvirus family, impacts a significant portion of the global populace. This virus is widespread, infecting between 40% and 90% of individuals across different regions. Although it typically doesn’t cause symptoms in healthy individuals, maintaining control over this chronic infection demands a continuous effort from the immune system to suppress it.
In a collaborative study conducted by the University of Cordoba (UCO) and the Maimonides Biomedical Research Institute (IMIBIC) of Cordoba, researchers assessed the impact of SARS-CoV-2, the virus causing COVID-19, on patients with mild or asymptomatic COVID-19 who were concurrently infected with CMV. The findings of this research reveal that dual infection with these viruses may accelerate the aging of the immune system. This is associated with an increased likelihood of developing cardiovascular disease earlier in life.
Dr. Alejandra Pera, the lead investigator of the study, emphasizes that the dual infection does not automatically imply these individuals will develop cardiovascular issues. Nonetheless, considering the widespread occurrence of both viruses, it underscores an important consideration for a patient’s medical profile. This dual infection should be recognized alongside other risk factors, including alcohol and tobacco use, regular consumption of foods high in saturated fats, and a sedentary lifestyle.
The research scrutinized the immune response in individuals with and without enduring cytomegalovirus infection, at both 3 and 12 months post mild or symptom-free infection by SARS-CoV-2, the virus causing COVID-19. The findings reveal that when co-infected with both viruses, there’s a surge in highly functional T-cells. T-cells are a type of white blood cell crucial for our body’s defense mechanism. Yet, when overly stimulated, these cells can lead to inflammation and potentially damage the vascular endothelium – the cell lining inside blood vessels.
“Cytomegalovirus alone causes these cells to increase. Now we have found that SARS-CoV-2 has an added effect,” note the authors.
One notable highlight of this research is the detection of this effect in people with mild or even no symptoms of the coronavirus. While most studies focus on severe cases, the researchers stress the importance of considering COVID-19’s medium and long-term effects in those who experienced the disease without complications.
“We are seeing that 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,” underline the authors of the study.
The recent research, led by UCO predoctoral scholar Pablo Álvarez, revealed that individuals with a prior cytomegalovirus infection saw an escalation in cells linked to heart disease following a SARS-CoV-2 infection. Interestingly, this effect was not observed in those who contracted COVID-19 post-vaccination.
Despite these findings, Dr. Pera emphasized the need for further research to consider the impacts of varying waves and strains of the virus. Preliminary evidence, however, suggests that COVID-19 vaccines might play a crucial role in preventing and moderating the unchecked growth of T cells that could potentially cause harm to the cardiovascular system.
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