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Immunomodulatory influence of HIV and EBV on Helicobacter pylori infections – a review

Helicobacter pylori is a Gram-negative, microaerophilic rod colonizing the stomach mucosa. In most cases, the colonization of this organ is asymptomatic, while some people may develop diseases, including gastritis, peptic ulcers and gastric cancers. The infection caused by H. pylori is accompanied by the secretion of pro-inflammatory cytokines and the strong response of Th1/Th17 cells. Because this bacterium colonizes more than half of the human population, co-infections with other pathogens are a relatively common phenomenon. One of such etiological factors are viruses that have an immunomodulatory effect on the infection caused by this microorganism. The relationship between H. pylori and HIV is antagonistic because there is an inverse relationship between the occurrence of this virus and the presence of H. pylori-dependent inflammations of the stomach. This is most probably caused by the HIV-related shift from a Th1 to a Th2 response and the reduction in Th17 cell counts. The reverse, synergistic interaction was demonstrated between H. pylori and EBV. Both of these pathogens are responsible for the recruitment of immune cells with a pro-inflammatory activity leading to the induction of gastric inflammation. The presence of the pro-inflammatory environment in the stomach supports the multiplication of both pathogens by maintaining H. pylori in the form of metabolically active, spiral forms and switching EBV from a latent into lytic phase. This review article discusses the epidemiology, pathophysiology and clinical consequences of H. pylori co-infection with HIV and EBV.