Possible Role of Epstein-Barr Virus (EBV) and Human Herpesvirus 7 (HHV-7) Infection in Pathogenesis of Recurrent Aphthous Stomatitis

Objectives*
Recurrent aphthous stomatitis (RAS) is a multifactorial disease that affects approximately 25% of the population. It is characterized by mucosal destruction linked to immune response dysregulation and stimulation by unidentified antigens. This work explores a possible role of EBV and HHV-7 in aphthous stomatitis pathogenesis.
Materials and Methods
The cohort comprised 31 adult patients diagnosed with recurrent aphthous stomatitis who visited the RSU Clinic of Oral and Maxillofacial Surgery and Oral Medicine between dates 21.06.2021- 05.08.2024. Data were collected from patient medical records, structured interviews and clinical evaluations. Saliva samples were taken on the first visit, stored at -80oC degrees and later transported to the Institute of Microbiology and Virology for the quantitative detection of EBV and HHV-7 genomic DNA using real time PCR with corresponding primers. Descriptive statistics were used to identify clinical patterns and correlation with laboratory indices.
Results
The cohort comprised 31 patients. Ulcer occurrences ranged between 1 and 5, with a median of 2 per patient.
Ulcer Severity Scores (USS) predominantly clustered between range 12 to 37. Gastroesophageal reflux disease
(GERD) emerged as the most frequently associated chronic condition, often coexisting with stress,
hypertension, and celiac disease. EBV genomic sequences were detected in 25 (81%) and HHV-7 genomic
sequences in 30 (97%) patients saliva samples. The median for EBV was 2063.35 copies/mL (7 patients > 10⁵
copies/mL) and HHV-7 was 112348.955 copies/mL (17 patients> 10⁵ copies/mL). USS showed a skew toward
higher severity in 14 patients with high viral load (1 with EBV, 9 with HHV-7, and 4 with both).
Conclusions
This study suggests a possible link between the presence of EBV and HHV-7 genomic sequences in saliva and RAS pathogenesis. Co-occurrence with conditions like GERD, stress, and celiac disease highlights its multifactorial nature, with viruses likely contributing rather than causing the disease. Larger studies are needed to confirm these findings.