Variation in Genes of β-glucan Recognition Pathway and Susceptibility to Opportunistic Infections in HIV-Positive Patients

• Published in: Immunological investigations Vol. 40; no. 7-8; pp. 735 - 750
• Main Authors: Rosentul, Diana C., Plantinga, Theo S., Papadopoulos, Antonios, Joosten, Leo A. B., Antoniadou, Anastasia, Venselaar, Hanka, Kullberg, Bart-Jan, van der Meer, Jos W. M., Giamarellos-Bourboulis, Evangelos J., Netea, Mihai G.
• Format: Journal Article
• Language: English
• Published: England Informa Healthcare 2011; Taylor & Francis
• Subjects: Adult; AIDS-Related Opportunistic Infections - epidemiology; AIDS-Related Opportunistic Infections - genetics; AIDS-Related Opportunistic Infections - microbiology; Candidiasis, Oral - epidemiology; Candidiasis, Oral - genetics; Candidiasis, Oral - microbiology; CARD Signaling Adaptor Proteins - genetics; Cohort Studies; Female; Genetic Predisposition to Disease; Genetic Variation; HIV; HIV Seropositivity - complications; HIV Seropositivity - epidemiology; HIV Seropositivity - genetics; Humans; Immunity, Innate; Incidence; Innate immunity; Lectins, C-Type - genetics; Male; Middle Aged; Opportunistic infections; Polymorphism, Single Nucleotide - genetics
• ISSN: 0882-0139; 1532-4311
• DOI: 10.3109/08820139.2011.599088

Opportunistic infections are the main cause of morbidity and death among HIV-positive patients. Most of these infections are linked to the immunodeficiency due to low CD4+ counts. However, not all patients with low CD4+ counts are equally susceptible to infections, and we hypothesize that variability in genes of innate immunity may also play an important role. The dectin-1/CARD9 pathway is crucial for recognition of both fungal and bacterial pathogens. The aim of this study was to assess the possible association between the occurrence of opportunistic infections and single nucleotide polymorphisms in DECTIN-1 and CARD9 in a cohort of 187 HIV-infected patients. The incidence of oropharyngeal candidiasis and other opportunistic infections was not influenced by either the Y238X DECTIN-1 or the S12N CARD9 polymorphism. Surprisingly however, the prevalence of pneumonia was significantly higher in patients bearing the defective variant DECTIN-1 allele. These results suggest a role of dectin-1 in the host defense against respiratory bacterial infections, and future studies are warranted to confirm this association.