Table 2.
Prevalence of EBV and HP co-infection (serological studies).
| Study/Country | Method | Disease | No. Tested | EBV Positivity | H. pylori Positivity | Co-Infection Positivity | Key Findings |
|---|---|---|---|---|---|---|---|
| Buza´s et al. 2015 [43] Hungary |
EBV: ELISA test (IgG and IgM) against EBV viral capsid protein (VCA) H. pylori: -Giemsa stain -IgG-chemiluminescence |
PUD | 40 | 75% | 72.5% | 60% | Higher prevalence of H. pylori + EBV co-infection along with higher anti-IgG levels found in duodenal ulcer. Could be attributed to an increased viral load or a stronger immune response |
| FD | 33 | 51.2% | 33.3% | 18.1% | |||
| GERD | 31 | 51.6% | 25.8% | 12.9% | |||
| Overall | 104 | 70.1% | 56.7% | 30% | |||
| Cárdenas-Mondragón et al. 2012 [10]. Mexico |
EBV: ELISA test (IgG and IgM) against EBV VCA H. pylori: ELISA test (IgG) against H. pylori whole-cell extracts and against CagA protein |
Non-atrophic gastritis (NAG) | 333 pediatric patients (median age 10.1 ± 3.7) |
64.3% | 53.4% | 1.8 (1–11.8) | EBV + H. pylori co-infection: significantly associated with severe gastritis. 2.4% (1%–9.7%) |
| Cárdenas-Mondragón et al. 2015 [45] Mexico and Paraguay |
EBV: ELISA test (IgG and IgM) against EBV VCA H. pylori: ELISA test (IgG) against H. pylori whole-cell extracts and against CagA protein |
Non-atrophic gastritis (NAG) | 225 patients (median age 30) |
32 (14.3%) | 18 (8%) | 175 (77.7%) | EBV collaborates with H. pylori to induce severe inflammation, increasing the risk of malignant transformation |