Human T Lymphotropic Virus Type 1 Infection. Part 4
In the present study, conducted during a follow‐up period of 10‐years, HTLV‐1 infection was associated with a 3‐fold reduction in the risk of gastric cancer, suggesting that HTLV‐1 infection plays a role in reducing the risk for gastric cancer. We therefore looked at whether HTLV‐1 infection may reduce the risk of H. pylori infection. Isomoto et al. and Walker demonstrated that patients infected with HTLV‐1 had a low prevalence of H. pylori infection. Tachibana et al. showed that healthy carriers of HTLV‐1 exhibited significant diminution of delayed‐type hypersensitivity, suggesting the existence of subclinical immunosuppression even among healthy carriers of HTLV‐1. It is possible that, during long‐term infection with HTLV‐1, progression of immunosuppression provides a less suitable intragastric environment for H. pylori colonization and that the organism may gradually be eliminated from the stomach. Stuver et al. reported that significantly fewer HTLV‐1–positive patients had a past history of peptic ulcer, with odds ratios of 0.49 (95% CI, 0.27–0.89) and 0.81 (95% CI, 0.42–1.6) for male and female patients, respectively.
In this study, the rate of H. pylori positivity in the HTLV‐1–positive group was lower than that in HTLV‐1–negative group overall and for men and women; furthermore, the frequencies of gastric cancer among men, women, and both groups combined were greater among HTLV‐1–negative patients than among HTLV‐1–positive patients, although the differences were not significant. These findings suggest that HTLV‐1 infection may reduce the risk of H. pylori infection and proliferation. Among all men and HTLV‐1–positive women with gastric cancer, the number of patients with intestinal‐type carcinoma was greater than the number with diffuse‐type carcinoma. In contrast, among HTLV‐1–negative women, the number with diffuse‐type carcinoma was greater than the number with intestinal‐type carcinoma. The reason for the latter finding remains unclear.
Yamashita et al. determined the prevalence of H. pylori infection in healthy children from the Kyushu region in Japan. The prevalences of H. pylori seropositivity were 3% among children aged <1 year, 10% among those aged 1–4 years, 19% among those aged 5–9 years, 25% among those aged 10–14 years, and 29% among those aged 15–19 years. H. pylori infection is known to be acquired early during childhood. Infection frequently occurs before 10 years of age, and two‐thirds of individuals become infected before 7 years of age. Furthermore, family structure during early life (i.e., sibship size and birth order) is associated with a risk of future development gastric cancer among H. pylori–positive males. On the other hand, invasion by infected lymphocytes, which occurs via vertical infection (in 70% of cases), horizontal infection (in 20%), or transmission through blood (in 10%), is required for HTLV‐1 infection in vivo. A relatively high proportion of babies born to women positive for HTLV‐1 test positive for anti–HTLV‐1 antibody, although this antibody disappears within the first 9 months of life in many cases and by 2 years of age in nearly all cases. Among children with infection transmitted from their mother, there were no cases of seroconversion after the age of 3 years. These findings suggest that HTLV‐1 infection is frequently acquired before H. pylori infection. Early infection with HTLV‐1 may weaken gastric mucosal immune responses and thereby affect H. pylori infection and proliferation. In this study, we did not adjust for H. pylori infection, smoking, drinking habits, and salt intake, which could be related to the etiology of gastric cancer. Further studies of gastric cancer associated with HTLV‐1 seropositivity with adjustment for these factors are needed.