The interactions of HTLV‐1 and humans are complex. Only 0.1%–3% of HTLV‐1 infections result in T cell leukemia. Most often infection is chronic and indolent with little viral replication, exceeded by larger amounts of latent, integrated provirus. HTLV‐1 infection also is associated with some degree of immunosuppression, possibly because of its propensity to establish a clinically silent low‐grade infection in T lymphocytes distorting cytokine production. HTLV‐1 also stimulates polyclonal activation of lymphocytes without infecting them, can transform cells because of its transactivating tax protein, and, uncommonly, may infect cells other than T lymphocytes. HTLV‐1 infection may also have nonmalignant consequences, including tropical spastic paraparesis (HTLV‐1–associated myelopathy), polyarthritis, and uveitis. Each of these manifestations is characterized by substantial local lymphocytic infiltration.
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How then might HTLV‐1 decrease the prevalence of H. pylori infection (in males) and decrease the incidence of gastric cancer in males and females? An effect of the virus on the microenvironment affecting H. pylori growth or on gastric epithelial cells might account for Matsumoto and colleagues’ observation. Although it is possible that HTLV‐1 might decrease H. pylori–induced chronic inflammation, HTLV‐1 usually induces lymphocytic infiltrates, despite its association with immunosuppression. Comparison of gastric histologic findings in the presence or absence of HTLV‐1 and H. pylori might provide initial clues as to the nature of the interaction.
HTLV‐1–specific cytotoxic lymphocytes are present in the blood of asymptomatic infected individuals. Cross‐reacting immunity might modify responses to H. pylori, or an immune response to the virus might activate innate immune mechanisms that could modulate the preneoplastic process. Some viruses are biologically active even when not replicating, and HTLV‐1 may disrupt normal cellular functions. In addition to its potential for integration within a gene encoding a host protein, the HTLV‐1 tax protein can modulate several cellular signaling pathways; viral polypeptide translation might interfere with cellular protein functions or, if expressed on the cell surface, render it susceptible to cytotoxic CD8 lymphocytes. Archival sequences of human endogenous retroviruses are present in the human genome, and RNA transcripts of these sequences can be detected at low levels in the plasma of some healthy individuals and at much higher levels in immunosuppressed patients infected with HIV. Cytotoxic lymphocytes directed against peptides encoded by these retroviral genes can be detected in the blood of HIV‐infected individuals.
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What are the implications of finding an interaction between HTLV‐1 and H. pylori? Both microbes are rapidly disappearing because of public health measures (in the case of HTLV‐1) and because of changes extant in modern life, possibly driven by antibiotic use (in the case of H. pylori). As such, the epidemiologic significance of the interaction between these 2 microbes may lessen over time. Nevertheless, the linkage has important implications in human cancer biology. The concept of a protective effect suggests that HTLV‐1 may be a form of viral commensal of humans, protecting hosts through interference with H. pylori‐induced pathology. The value of our indigenous commensal microbiota has been recognized at least since the 19th century, but only now are we beginning to understand its scope and complexity. Most attention has focused on the bacterial species that are major constituents of our microbiota, with bacterial cells substantially outnumbering “human” cells in our bodies. Research efforts such as the recently announced Human Microbiome Project (HMP), sponsored as part of the National Institutes of Health Roadmap, and parallel efforts in other countries will provide new knowledge and insights into the relationships.