| Summary: | Gastric cancer is a challenging public health concern worldwide and remains a leading cause of cancer-related mortality. The primary risk factor implicated in gastric cancer development is infection with <i>Helicobacter pylori</i>. <i>H. pylori</i> induces chronic inflammation affecting the gastric epithelium, which can lead to DNA damage and the promotion of precancerous lesions. Disease manifestations associated with <i>H. pylori</i> are attributed to virulence factors with multiple activities, and its capacity to subvert host immunity. One of the most significant <i>H. pylori</i> virulence determinants is the <i>cagPAI</i> gene cluster, which encodes a type IV secretion system and the CagA toxin. This secretion system allows <i>H. pylori</i> to inject the CagA oncoprotein into host cells, causing multiple cellular perturbations. Despite the high prevalence of <i>H. pylori</i> infection, only a small percentage of affected individuals develop significant clinical outcomes, while most remain asymptomatic. Therefore, understanding how <i>H. pylori</i> triggers carcinogenesis and its immune evasion mechanisms is critical in preventing gastric cancer and mitigating the burden of this life-threatening disease. This review aims to provide an overview of our current understanding of <i>H. pylori</i> infection, its association with gastric cancer and other gastric diseases, and how it subverts the host immune system to establish persistent infection.
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