AIDS patients are prone to opportunistic infections after the immune system is destroyed by HIV virus, and PTB is one of the most common opportunistic infections. A total of 939 AIDS patients were included in this study, of which 68 (7.24%) were combined with PTB, which was slightly lower than that in parts of Tanzania (8.5%) [11] and significantly lower than that in Ethiopia (27.7%) [12]. HIV/TB co-infection is not a simple superposition of the two diseases, but a mutually reinforcing process, resulting in a significantly higher mortality risk in co-infected patients than in pure HIV or TB infection [13]. HIV infection increases the risk of TB from latent infection to active TB by 30 times. HIV-negative Mycobacterium tuberculosis infected people have a 10% chance of developing active TB in their lifetime, while HIV-positive people have a 15% chance of developing active TB within 1 year [14]. Studies have found that specific CD4 + T lymphocytes are first decreased in HIV-infected TB patients, and HIV infection can lead to severe and rapid pulmonary interstitial CD4 + T lymphocyte loss. Loss of interstitial CD4 + T lymphocytes, especially effector memory CD4 + T lymphocytes and M. tuberculosis-specific CD4 + T lymphocytes, may be an important factor contributing to the increased risk of transmission of TB infection [15, 16]. After the body is infected with Mycobacterium tuberculosis, the immune activation is increased, and the release of cytokines such as IFN-γ, TNF-α, interleukin-1 (IL-1), and IL-2 is increased, and the toxicity of natural killer cells is reduced, so that the HIV replication is enhanced and variability increases [17, 18]. Therefore, exploring the risk factors of AIDS complicated with PTB is of great significance to prevent the occurrence of PTB in AIDS in the later stage.
There are also many reports on factors associated with AIDS complicated by PTB, such as CD4 + cell count, type of tuberculosis, smoking, body mass index, place of residence, compliance, and educational level [19–23]. Through retrospective analysis, this study found that AIDS/PTB and AIDS groups were not significantly different in gender, residence, occupation, annual income, educational level, marital status, drinking history, history of diabetes, history of BCG vaccination, homosexuality, and the presence of multiple sexual partners at the same time. However, the differences in smoking history and CD4 + cell count were significant and statistically significant.
Smoking is significantly associated with PT and increases the risk of death during PT treatment [24–28]. In addition, smoking increases the severity of PT, affects its treatment efficacy, and predisposes to relapse, while smoking cessation may reduce the risk of relapse and secondary transmission [29]. Studies have found that the biological mechanism by which smoking increases PTB susceptibility may be related to changes in cellular and humoral immune responses [30]. To a certain extent, smoking can alter mucociliary clearance and inhibit the phagocytic activity of monocytes, thereby increasing the risk of PTB in patients [31–33] and increasing the probability of PTB treatment failure [34]. In addition, smoking is also a risk factor for HIV/AIDS, increasing its morbidity and mortality, and increasing the risk of co-infection with TB [35]. Smoking impairs the immune activation and function of T cells, and co-infection with HIV can lead to more severe immune damage [36], thereby increasing the risk of PTB [37].
The main target cells invaded by HIV-infected patients are CD4 + T cells, which lead to a decrease in the number of CD4 + T cells and thus destroy the body's immunity. In AIDS patients, the level of CD4 lymphocytes in peripheral blood is significantly correlated with the immune status of the body. When the CD4 lymphocyte count decreases, the body's defense mechanism can be destroyed, making various opportunistic infections more likely to occur [38]. Studies have found that the severity of AIDS patients and the quality of prevention are related to the number of CD4 + T lymphocytes. The fewer CD4 + cells, the more severe the patient's immune function damage, the more atypical clinical manifestations of the patient with PTB, and the probability of other opportunistic infections in the patient will increase significantly [39]. In addition, the level of CD4 + cells in peripheral blood can be used to evaluate the level of the immune status of the body. When the number of CD4 + cells is less than 200 cells/mm3, it indicates that HIV-infected patients enter the AIDS stage, and the CD4 count < 200 cells/mm3 can be used as the cutoff for typical HIV co-infection [40]. This study found that the number of CD4 + cells < 200/mm3 was a risk factor for AIDS/PTB. Nie et al. [41] conducted a study on 19,512 AIDS patients and found that 1,109 patients had PTB, and the infection rate was 5.68%. Among them, AIDS patients with a baseline CD4 value of ≤ 200 was more prone to PTB co-infection. Du et al. [42] found that AIDS patients with a history of tuberculosis had a risk of developing tuberculosis 12.76 times that of those without a history of tuberculosis, and the risk of tuberculosis in AIDS patients with the recent CD4 value ≥ 200 cells/µl was 0.34 times that of those with CD4 value < 200 cells/µl. Therefore, it is recommended to pay attention to the TB screening of AIDS patients, and to strengthen the follow-up of AIDS patients with a history of TB and the latest CD4 < 200 cells/µl to prevent the occurrence of TB. Mo et al. [43] analyzed and compared the data of AIDS and AIDS/PTB patients and found that there were statistically significant differences in CD4 + lymphocyte count, clinical features, and chest CT findings (P < 0.05), suggesting that the decrease of CD4 + T lymphocytes plays an important role in the evolution of AIDS complicated with PTB disease.
The Mycobacterium tuberculosis rpoB gene and mutation detection kit (Xpert MTB/RIF) technology can rapidly and sensitively detect Mycobacterium tuberculosis-specific nucleic acid and rifampicin resistance gene rpoB and has been vigorously promoted [44–46]. Further research found that the Xpert MTB/RIF detection technology in bronchoalveolar lavage fluid has high application value in the diagnosis of HIV/PTB patients, and it is a rapid, time-saving, highly sensitive and specific detection method for rapid detection of Mycobacterium tuberculosis[47]. At present, the preferred treatment strategy for patients with AIDS and PTB co-infection is: rifampicin-based anti-tuberculosis regimen combined with efavirenz plus two nucleoside reverse transcriptase inhibitors antiviral regimen. Susceptible tuberculosis bacteria are usually treated with isoniazid + rifampicin/rifabutin + ethambutol + pyrazinamide for 2 months of intensive treatment, followed by isoniazid + rifampicin/rifabutin regimen 4 months of consolidation therapy. Regardless of the patient's immune status, it is recommended to start highly active antiretroviral therapy (HAART) as soon as possible, and anti-tuberculosis therapy should be performed first, followed by HAART. For patients with severe immunodeficiency with CD4 + T lymphocytes < 50/µl, it is recommended to start HAART within 2 weeks of anti-tuberculosis; for patients with CD4 + T lymphocytes ≥ 50/µl, it is recommended to start HAART as soon as possible within 8 weeks[10]. Studies also found that active ART was significantly associated with increased CD4 counts in HIV-infected individuals [48] and reduced the incidence of TB [49.50]. Sanhueza-Sanzana et al. [51] found that among Chilean AIDS patients, the survival rate of PT-infected patients was lower, especially for those patients with delayed initiation of ART. In a meta-analysis, Burke et al. [52] found that starting ART earlier (≤ 4 weeks) had no significant effect on mortality compared with later (> 4 weeks). In HIV with CD4 ≤ 50 cells/mm3, early ART reduced mortality. However, if CD4 > 50 cells/mm3), early ART may not have a significant effect on death. In March 2021, World Health Organization recommended that antiretroviral therapy (ART) should be started within two weeks of TB treatment start, at any CD4 count[53]. The prevention of AIDS and TB co-infection can be carried out through two-way screening, publicity and education, multi-sectoral cooperation, and TB preventive treatment for HIV-infected patients if necessary[54].