Abstract
Mannose-binding lectin (MBL) plays a pivotal role in innate immunity; however, its impact on susceptibility to opportunistic infections (OIs) has not yet been examined in a natural history cohort of people living with HIV/AIDS. We used archived samples to analyze the association between MBL expression types and risk of major OIs including Pneumocystis jirovecii pneumonia (PCP), cryptococcosis, talaromycosis, toxoplasmosis, and tuberculosis in a prospective cohort in Northern Thailand conducted from 1 July 2000 to 15 October 2002 before the national antiretroviral treatment programme was launched. Of 632 patients, PCP was diagnosed in 96 (15.2%) patients, including 45 patients with new episodes during the follow-up period (1006.5 person-years). The total history of PCP was significantly associated with low MBL expression type: high/intermediate (81/587, 13.8%), low (10/33, 30.3%) and deficient (5/12, 41.7%) (p = 0.001), whereas the history of other OIs showed no relation with any MBL expression type. Kaplan-Meier analysis (n = 569; log-rank p = 0.011) and Cox's proportional hazards model revealed that deficient genotype dramatically increased the risk of PCP, which is independent upon sex, age, CD4 count, HIV-1 viral load and hepatitis B and C status (adjusted hazard ratio 7.93, 95% confidence interval 2.19-28.67, p = 0.002). Deficiency of MBL expression is a strong risk factor determining the incidence of PCP but not other major OIs.
Highlights
Among people living with human immunodeficiency virus (HIV) in Asia, Pneumocystis jirovecii pneumonia (PCP) is one of the most frequent opportunistic infections (OIs) in acquired immunodeficiency syndrome (AIDS)-defining diseases [1,2,3,4]
The total history of PCP was significantly associated with low Mannose-binding lectin (MBL) expression type: high/intermediate (81/587, 13.8%), low (10/33, 30.3%) and deficient (5/12, 41.7%) (p = 0.001), whereas the history of other OIs showed no relation with any MBL expression type
Kaplan–Meier analysis (n = 569; log-rank p = 0.011) and Cox’s proportional hazards model revealed that deficient genotype dramatically increased the risk of PCP, which is independent upon sex, age, CD4 count, HIV-1 viral
Summary
Among people living with human immunodeficiency virus (HIV) in Asia, Pneumocystis jirovecii pneumonia (PCP) is one of the most frequent opportunistic infections (OIs) in acquired immunodeficiency syndrome (AIDS)-defining diseases [1,2,3,4]. The incidence of PCP differs in various populations, such as a lower incidence in patients originating from sub-Saharan Africa compared with patients from Western origin [7], and CD4 cell counts in HIV patients are broadly distributed at the onset of PCP in the real world [8] This variability raises the possibility that risk factors, e.g., host factors and/or causative pathogens, other than CD4 cell counts contribute to the development of PCP. The P. jirovecii cell wall contains abundant glycoproteins including β-D glucan and mannose [6], and host pattern recognition receptors (PRRs) bind these glycoproteins via carbohydrates containing a C-type lectin-like domain, so-called C-type lectin receptors (CLRs) [9, 10]. Mannose-binding lectin (MBL) plays a pivotal role in innate immunity; its impact on susceptibility to opportunistic infections (OIs) has not yet been examined in a natural history cohort of people living with HIV/AIDS
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