Genital herpes linked to thinning of the cerebral cortex

American scientists investigated the relationship between exposure to cytomegalovirus, herpes simplex viruses type 1 and 2, Chlamydia pneumoniae and Helicobacter pylori and three indicators of magnetic resonance imaging (MRI) – the thickness of the entire cerebral cortex, the volume of the hippocampus and signs of Alzheimer’s disease. It turned out that increased titers of antibodies to herpes simplex virus type 2 (HSV-2), which causes genital herpes, are associated with a decrease in the thickness of the cerebral cortex. In addition, combined infection with HSV-2 and C. pneumoniae thins the bark even more. Research results published V Journal of the Neurological Sciences.

The neuroinflammatory hypothesis of Alzheimer’s disease posits that chronic central and peripheral inflammation are key factors in the pathophysiology of the disease. Neuroinflammation can be caused by either acute or chronic infection. Studies have shown that high serological indicators, which reflect the infectious load, for Chlamydia pneumoniae, Helicobacter pyloricytomegalovirus (CMV), herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2) connected with impaired cognitive functions, including memory.

It is noteworthy that in other studies, scientists have found morphological changes in the brain due to these infections. For example, American doctors discovered C. pneumoniae in the brains of people with Alzheimer’s disease. HSV-1 also was discovered in the brains of people with this disease. In addition, some infections have been associated with specific changes in brain matter, but it is unclear to what extent such changes are visible on neuroimaging and what prognostic potential they have.

A group of scientists led by Jose Gutierrez from Columbia University studied how various infections affect the brain, and how this effect is reflected in MRI scans. To do this, they analyzed tomograms of 455 people with known serological test results. The average age of the participants was 70 years. Participants were most often seropositive for HSV-1.

Several models showed that the titer of class G antibodies to HSV-2 was inversely related to the thickness of the cortical layer of the cerebral hemispheres. In addition, high levels of immunoglobulin A C. pneumoniae also appeared to be associated with decreased cortical thickness, although in adjusted models, this observation was not statistically significant. Other infections did not affect the thickness of the cerebral cortex. However, the presence of antibodies to H. pylori in one model it was associated with an increase in hippocampal volume. Neither pathogen is associated with MRI features of Alzheimer’s disease.

Considering the overall effect of HSV-2 and C. pneumoniae on the thickness of the cerebral cortex, scientists tested how their co-infection could affect neuroimaging of the brain. It turned out that co-infection with two pathogens leads to greater thinning of the cerebral cortex. Other neuroimaging parameters were not affected by coinfection.

Overall, these results may help clinicians identify risk groups of people who are susceptible to morphological changes in the cerebral cortex and subsequent cognitive impairment.

We previously reported that the herpes virus caused symptoms of Alzheimer’s disease in a three-dimensional brain model, and also disrupted the processes of differentiation of neural stem cells and the formation of the cerebral cortex.