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    • br Introduction Although the incidence of

    2018-10-23


    Introduction Although the incidence of HIV has peaked in much of sub-Saharan Africa, the tuberculosis (TB) epidemic continues unabated with TB remaining the leading cause of death in those living with HIV (World Health Organization, 2014). While many studies have investigated the impact of HIV infection on anti-TB immunity, the interaction between Mycobacterium tuberculosis (M. tb) infection and HIV disease progression is less well understood. Previous work suggests that in the absence of combination antiretroviral therapy (cART), the progression of HIV infection to AIDS and mortality among HIV-infected people in sub-Saharan Africa may be higher than in Western populations (Morgan et al., 1997). While this is likely multifactorial, the different burdens of chronic co-infections in these settings may play a role. Recent studies have demonstrated that elevated levels of certain soluble markers of inflammation or hyperactivation of the innate immune system can independently predict progression to AIDS, immune reconstitution inflammatory syndrome (IRIS), and death in HIV-infected patients (Boulware et al., 2011; Sandler et al., 2011; Marchetti et al., 2013). Specifically, soluble markers of monocyte turnover, inflammation, and fibrosis, including soluble CD14 (sCD14), lipopolysaccharide, interleukin (IL)-6, IL-8, interferon gamma-induced protein 10 (IP-10), hyaluronic acid, and C-reactive protein (CRP) have been shown to be associated with increased risk of progression to AIDS and death (Boulware et al., 2011; Hasegawa et al., 2009; Neuhaus et al., 2010; French et al., 2009). Markers of lymphocyte activation have also been shown to predict disease progression in HIV-infected patients. Immune activation, as measured by the elevated pitavastatin of CD38 or co-expression of CD38 and HLA-DR on T-cells has been shown to be associated with shorter survival, transient low level viremia, drop in CD4+ T-cell count, and mortality upon initiation of cART (Giorgi et al., 1993, 1999; Hunt et al., 2003, 2011a; Deeks et al., 2004; Sousa et al., 2002; Vujkovic-Cvijin et al., 2013; Zhang et al., 2013; Taiwo et al., 2013; Dillon et al., 2014). Certain co-infections such as cytomegalovirus (CMV), hepatitis C virus (HCV), and hepatitis B virus (HBV) have been shown to contribute to immune activation in HIV-infected individuals (Hunt et al., 2011b; Beltran et al., 2014; Crane et al., 2014; Marchetti et al., 2014). The impact of M. tb co-infection on immune activation during HIV infection has not been fully characterized. Active TB has been shown to contribute to immune activation and inflammation in the absence of HIV infection (Bloom et al., 2012, 2013). Additionally, active TB has been implicated in elevated plasma sCD14 and increased T-cell activation in HIV co-infected individuals (Toossi et al., 2013; Lawn et al., 2000; Mahan et al., 2010). However, the impact of latent TB infection, which affects an estimated 1/3 of people worldwide and an estimated 77–88% of adults in South Africa (Barry et al., 2009; Hanifa et al., 2009; Wood et al., 2010), on either soluble markers of inflammation or lymphocyte activation in HIV-patients has not been assessed.
    Materials and Methods
    Results
    Discussion We have shown that in HIV-infected individuals, both active and latent TB co-infections are associated with biomarkers of immune activation that are known to correlate with more rapid HIV disease progression and mortality pitavastatin (Giorgi et al., 1993, 1999; Hunt et al., 2003, 2011a; Deeks et al., 2004; Sousa et al., 2002; Vujkovic-Cvijin et al., 2013; Zhang et al., 2013; Taiwo et al., 2013; Dillon et al., 2014). Soluble markers of inflammation were elevated only in those with active TB. In contrast, T-cell activation, as measured by CD38 and HLA-DR expression on CD4+ and CD8+ T-lymphocytes, was elevated in both latent and active TB. Though other studies have shown that active TB contributes to systemic inflammation in HIV-infected and uninfected individuals, the finding that individuals latently co-infected with TB also display elevated T-cell activation has not been previously described, and may be important for understanding the interplay between HIV and TB in individuals and in populations.