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The global tuberculosis mortality rate has dropped by 72%! How does antiretroviral therapy change the fate of HIV patients?
The co-epidemic of tuberculosis (TB) and human immunodeficiency virus (HIV) is one of the major global health challenges today. According to the World Health Organization (WHO), tuberculosis remains the leading cause of death among people living with HIV. In 2019, TB caused 30% of the 693,000 HIV/AIDS-related deaths. And of the 1.4 million global tuberculosis deaths, 15% are people living with HIV or AIDS.
The combined effects of the two diseases result in HIV causing a decline in immune function, while tuberculosis develops rapidly due to poor immune status.
For HIV patients, low levels of CD4 T cells significantly increase the risk of tuberculosis infection. When the CD4 T cell count is less than 200, the risk of contracting TB increases 25-fold. This situation is particularly serious in the case of multidrug-resistant tuberculosis (MDRTB) and extensively drug-resistant tuberculosis (XDRTB), which are difficult to treat and lead to increased mortality.
Even after the introduction of effective antiretroviral therapy (HAART), the threat of tuberculosis to HIV patients remains. According to a 2021 report, the initiation of HAART reduced the incidence of tuberculosis by 60% and the mortality rate by 72%. HAART reduces the risk of tuberculosis infection by 67-84% in HIV patients.
Impact of TB and HIV infectionTraditionally, TB often affects the upper lobes, but in HIV patients the presentation is often unusual. After HIV infection causes immunosuppression, tuberculosis lesions may shift to the lower lobes and enlarged lymph nodes may appear. In people with advanced HIV/AIDS, chest X-rays may appear normal. People who have both HIV and TB are more likely to develop systemic TB (TB that spreads to the blood or other organs).
The mortality rate of tuberculous meningitis in HIV patients can be as high as 40%.
HIV patients with latent TB have a 5-10% chance of developing active TB. If left untreated, active pathogens have a mortality rate of up to 50%.
Pathological mechanisms of co-infection between HIV and tuberculosis
The development of tuberculosis is associated with the inability of the immune response to control the growth of mycobacteria. Normally, CD4+ helper T cells secrete the cytokine IFN-γ, which attracts macrophages and stimulates them to destroy TB bacteria. The macroscopic structures that fight TB are called granulomas, which help limit the spread of infection. However, in HIV-infected people, granuloma formation is often impaired, allowing tuberculosis to spread throughout the body.
HIV infection leads to a significant decrease in IFN-γ production, increasing the risk of tuberculosis reactivation or reinfection.
Thus, people with HIV and TB infection are at increased risk for systemic TB (hematogenous mycobacteremia). Tuberculosis can also affect the progression of HIV, and proinflammatory cytokines (especially TNFα) in tuberculosis granulomas have been shown to accelerate HIV progression.
Prevention and treatment measures
For HIV-negative children, taking isoniazid can reduce the risk of tuberculosis infection. A study of HIV-positive children found that taking isoniazid was effective in reducing the risk of active tuberculosis and death in children who were not receiving antiretroviral treatment.
For people infected with HIV, standard treatment consists of at least six months of rifampicin-based therapy. Combination therapy for HIV-infected patients with TB is widely recommended regardless of CD4 cell count. However, the initial period of antiretroviral therapy may increase the risk of immune reconstitution inflammatory syndrome (IRIS), making it particularly important to ensure timely management.
Providing antiretroviral treatment early can effectively reduce early mortality and prevent tuberculosis recurrence and the emergence of drug resistance.
Future Research and Challenges
At the molecular level, the study found that genotypes associated with increased IL-10 expression make HIV-infected people more susceptible to tuberculosis. The need for thorough research at all levels to improve allopathic treatment is emphasized. Given the coexistence of tuberculosis and HIV, future medical and public health strategies need to pay more attention to this high-risk group. Then, in the face of curbing the co-prevalence of these two diseases, can we find more effective measures to reduce the infection rate?
