Abstract
Human herpesviruses (HHV)-6A, HHV-6B, and HHV-7 are considered to be involved in the pathogenesis of the
frequent neurological disorder epilepsy. Prognosis of the disease depends on the pathogen, the diverse routes of CNS
entry, viral tropism, and immune system state of the host. The aim of this study was to determine the role of
roseoloviruses infection in pathogenesis of epilepsy, analysing 53 patients with epilepsy and 104 apparently healthy
controls.
Methods: To determine the presence of virus-specific antibodies ELISA and IFA was used. Virus-specific genomic
sequences were revealed by nPCR and restriction endonuclease, but viral load was determined by qPCR, virus gene
expression by RT-PCR.
Results: Seroprevalence of HHV-6 and HHV-7 IgG class antibodies were similar between patients with epilepsy and
control group individuals (81.1% vs 78.8% and 81.7% vs 83.0%, respectively). Roseolovirus genomic sequences in DNA
samples from whole blood were found in 86.8% of patients with epilepsy versus 64.4% in control group individuals.
HHV-6A was identified in two epileptic patients and HHV-6B in 13/15 epileptic patients and in all positive for HHV-6
control individuals’ blood samples. Plasma viremia (marker of infection active phase) was revealed only in patients with
epilepsy (9/46, 19.56%). Significantly higher viral load was detected not just in patients compared to the controls, but
was also higher in patients with persistent viral infection in active phase than in those with latent phase. HHV-6
U89/90 immediate early gene expression in PBMC was found in 73.3% (11/15) of the epileptic patients with previously
detected HHV-6 genomic sequence in blood DNA samples, but was not found in any of the HHV-6 positive samples
from control individuals. HHV-7 U57 gene expression, was detected in 37.5% (15/40) of epileptic patients positive for
HHV-7 genomic sequences and in (1/63) control samples. Changes in the levels of pro-inflammatory and antiinflammatory cytokines were determined in patients with elevated viral load.
Conclusion: Results on frequent active HHV-6 and HHV-7 infections in epileptic patients' peripheral blood indicate
possible involvement of these viruses in the disease development. However, more evidence is required, such as data on
viral presence in tissue from specific regions of the brain.
frequent neurological disorder epilepsy. Prognosis of the disease depends on the pathogen, the diverse routes of CNS
entry, viral tropism, and immune system state of the host. The aim of this study was to determine the role of
roseoloviruses infection in pathogenesis of epilepsy, analysing 53 patients with epilepsy and 104 apparently healthy
controls.
Methods: To determine the presence of virus-specific antibodies ELISA and IFA was used. Virus-specific genomic
sequences were revealed by nPCR and restriction endonuclease, but viral load was determined by qPCR, virus gene
expression by RT-PCR.
Results: Seroprevalence of HHV-6 and HHV-7 IgG class antibodies were similar between patients with epilepsy and
control group individuals (81.1% vs 78.8% and 81.7% vs 83.0%, respectively). Roseolovirus genomic sequences in DNA
samples from whole blood were found in 86.8% of patients with epilepsy versus 64.4% in control group individuals.
HHV-6A was identified in two epileptic patients and HHV-6B in 13/15 epileptic patients and in all positive for HHV-6
control individuals’ blood samples. Plasma viremia (marker of infection active phase) was revealed only in patients with
epilepsy (9/46, 19.56%). Significantly higher viral load was detected not just in patients compared to the controls, but
was also higher in patients with persistent viral infection in active phase than in those with latent phase. HHV-6
U89/90 immediate early gene expression in PBMC was found in 73.3% (11/15) of the epileptic patients with previously
detected HHV-6 genomic sequence in blood DNA samples, but was not found in any of the HHV-6 positive samples
from control individuals. HHV-7 U57 gene expression, was detected in 37.5% (15/40) of epileptic patients positive for
HHV-7 genomic sequences and in (1/63) control samples. Changes in the levels of pro-inflammatory and antiinflammatory cytokines were determined in patients with elevated viral load.
Conclusion: Results on frequent active HHV-6 and HHV-7 infections in epileptic patients' peripheral blood indicate
possible involvement of these viruses in the disease development. However, more evidence is required, such as data on
viral presence in tissue from specific regions of the brain.
| Original language | English |
|---|---|
| Pages | 37 |
| Number of pages | 1 |
| Publication status | Published - 24 Jun 2019 |
| Event | 11th International Conference on Human Herpesvirus HHV-6&7 - Quebec, Canada Duration: 23 Jun 2019 → 26 Jun 2019 Conference number: 11 https://hhv-6foundation.org/uncategorized/2019-conference |
Conference
| Conference | 11th International Conference on Human Herpesvirus HHV-6&7 |
|---|---|
| Abbreviated title | HHV-6&7 |
| Country/Territory | Canada |
| City | Quebec |
| Period | 23/06/19 → 26/06/19 |
| Internet address |
Field of Science*
- 1.6 Biological sciences
Publication Type*
- 3.4. Other publications in conference proceedings (including local)
