Latent tuberculosis infection (LTBI) is an asymptomatic mycobacterial infection defined on the basis of cellular immune responses to mycobacterial antigens. Currently, the tuberculin skin test (TST) and interferon gamma release assay (IGRA) are used to diagnose LTB. However, neither TST nor his IGRA are useful in distinguishing between active and latent TB. Furthermore, these tests cannot be used to predict whether a patient with LTBI will develop active tuberculosis (TB) or whether treatment for LTBI will be effective in reducing the risk of active tuberculosis. . Therefore, in this article, we review current approaches and some of the current approaches to identify immunological markers that may help distinguish between LTBI and tuberculosis and assess the efficacy of LTB treatment against the risk of progression to active tuberculosis. Review some efforts. prologue
About 5-10% of people infected with M. tuberculosis develop the disease within the first 2-5 years after infection. In the remaining cases, the innate immune response either completely eliminates the infection without leaving a trace of an immunological response (resistance to TB infection) or immunizes against M. tuberculosis antigens without clinical signs. A situation arises in which the response persists. Active disease. In fact, this last result underlies the assumption that his quarter of the world’s population is infected with her M virus. tuberculosis. These people have persistent immunoreactivity for latent tuberculosis infection (LTBI) even after bacterial elimination has been achieved, making them potential carriers of active tuberculosis. In this context, there is a clear need for a diagnostic test for her LTBI that can also be used to identify people at risk of developing active tuberculosis and monitor their response to LTBI treatment.
Identifying people who had contact with an active tuberculosis patient during her first two years of infection is important for her two reasons.
First, identifying individuals at increased risk of developing active tuberculosis will enable the implementation of public health disease control policies. especially recently infected persons. Second, it may lead to a deeper understanding of immune responses during infection, which may be important for the development of better therapeutic and preventive interventions.
The dominant paradigm of LTBI has long been the balance between host immune responses and pathogen metabolism, and disruption of this balance results in active disease. However, in the past decade, evidence has emerged that tuberculosis infection has been redefined in terms of a spectrum of immune responses rather than static conditions .
Several factors increase the risk of developing active tuberculosis in patients with LTBI. Most of these are associated with decreased immune responses such as HIV co-infection, cancer, immunosuppressive therapy or kidney transplantation, and diabetes. This last condition is especially important. The incidence of diabetes is increasing in countries where the prevalence of tuberculosis is also high, as people with diabetes are approximately three times more likely to develop tuberculosis than non-diabetics. However, several other factors are related to specific components of host responses. B. Activation of macrophages, maintenance of granuloma architecture, CD4 T cells, CD8 T cells, interferon gamma (IFN-γ) and tumor necrosis factor alpha (TNF-). α) production, all of which are important for pathogen control during LTBI (9). Recently, whole blood transcriptome profiling studies have been performed to identify features that distinguish LTBI from active tuberculosis and may predict different treatment outcomes.
