In recent years, scientists have discovered many convincing links between diseases such as cancer, multiple sclerosis or Alzheimer’s disease and infectious pathogens. In some cases, these relationships are clear causal relationships. For example, we know that human papillomavirus (HPV) infection directly causes 90% of cervical cancers, and new HPV vaccines promise to virtually eliminate this form of cancer in the near future.
Other relationships may be more of a factor among the many elements that contribute to the disease. One of the most groundbreaking scientific discoveries of 2022 to date is a major study that affirms a link between Epstein-Barr virus (EBV) infection and multiple sclerosis (MS).
This landmark study shows that EBV infection is not the only cause of multiple sclerosis, after all, the virus is so common and not everyone who is infected ends up developing the neurodegenerative disease. Instead, the study confirmed that while not all EBV infections lead to multiple sclerosis, all cases of multiple sclerosis may precede EBV infection. This means that a vaccine against the virus has the potential to prevent most cases of multiple sclerosis from occurring.
Epstein-Barr virus is a member of the larger herpesvirus family. Eight types of herpesviruses are known to cause disease in humans, including the varicella-zoster virus (HHV-3, which causes chickenpox and shingles). All of these herpes viruses are known to cause latent infections, meaning that once a person is infected, the virus can remain relatively “dormant” in the body for a lifetime.
The new study aimed to investigate whether there is any association between latent herpesvirus infection and the development of prediabetes, a metabolic state that often precedes the onset of type 2 diabetes. To do this, the researchers analyzed data from a long-term health study that followed several thousand people for about seven years.
The presence of seven herpesviruses was followed at baseline, and diabetes biomarkers were measured at follow-up several years later. Over nearly seven years of follow-up, the researchers found that about 360 subjects developed markers of prediabetes. In those who develop prediabetes, infection with two herpes viruses is frequently detected: herpes simplex virus type 2 (HSV-2) and cytomegalovirus (CMV).
“Multivariate analysis showed that the two viruses consistently and complementary contributed to the development of (pre)diabetes, with sex, age, BMI,educate, smoking, physical activity, parental diabetes, hypertension, lipid levels, insulin resistance, and fasting glucose were not associated with the , BMI, cholesterol, and fasting blood glucose, but both HSV2 and CMV added additional supplemental risk information, despite high viral prevalence and co-occurrence. “
HSV-2 was the strongest association, with infected people being 59 percent more likely to develop prediabetes. And those infected with CMV were 33 percent more likely to develop prediabetes.
The researchers make it clear that their current finding is only a preliminary observational association. Several other known risk factors for diabetes, such as cholesterol and obesity, apparently play a larger role than the herpes virus in determining a person’s likelihood of developing metabolic disease. However, the new findings do provide some signals that certain types of herpesviruses may be contributing.
How exactly do these viruses affect the development of diabetes? It’s unclear, at this point, researchers can only hypothesize underlying mechanisms, such as the herpes virus regulating immune responses in a way that affects the body’s endocrine system.
A lot of work is needed to unravel this potential link between the herpes virus and diabetes, but the researchers did stress that these findings require more public health work to prevent people from getting infected in the first place. Moreover, the development of a herpes virus vaccine appears to serve as a preventive tool to reduce the incidence of diabetes in the future.
The new study was published inDiabetes(Diabetologia) magazine.