Mannose-binding Lectin and the Risk of HIV Transmission and Disease Progression in Children

Israëls, Joël; Scherpbier, Henriëtte J.; Frakking, Florine N. J.; Wetering, Marianne D. van de; Kremer, Leontien C. M.; Kuijpers, Taco W.

doi:10.1097/inf.0b013e3182678bc4

Cited by 12 publications

(8 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, the frequency of low-MBL genotypes was observed to be especially high (46.2%) in younger children with IPD caused by opportunistic serotypes. A recent systematic review has reported a probable association between HIV disease progression and MBL deficiency, and this association was especially high in children <2 years of age [24]. Interestingly, when rates of low-MBL genotypes among patients with IPD caused by serotypes with high invasiveness (high-attack-rate serotypes) were analyzed, we did not find a significantly high proportion of low-MBL genotypes either in young children aged <2 years or in other patients.…”

Section: Discussioncontrasting

confidence: 64%

High prevalence of genetically-determined mannose binding lectin deficiency in young children with invasive pneumococcal disease

Muñoz-Almagro¹,

Bautista

Arias

et al. 2014

Clinical Microbiology and Infection

View full text Add to dashboard Cite

Susceptibility to invasive pneumococcal disease (IPD) correlates with age, younger children being the group with the highest burden of disease. The relevance of the innate immune response and particularly the role of mannose-binding lectin (MBL) in combating IPD is not well known. This is a 2-year prospective study (February 2011 to March 2013) including patients with IPD who attended two hospitals from Catalonia, Spain. Variables including attack rate of pneumococcal serotype (high or low invasive potential serotypes) and genotypes associated with low serum MBL levels were recorded. One hundred and forty-seven patients were included in the study. One hundred and two (69.4%) patients were children or adolescents <18 years and 45 (30.6%) were adults. Overall, low-MBL genotypes (O/O; XA/O) were detected in 23 (15.6%) patients. Children <2 years showed a higher frequency of low-MBL genotypes compared with other patients (31.0% vs. 11.9%; p = 0.031). Further sub-analysis revealed a higher proportion of low-MBL genotypes in children <2 years with IPD caused by opportunistic or low-attack-rate serotypes when compared with older patients (46.2% vs. 13.2%; p = 0.02). However, no statistically significant differences between the two groups were observed when including patients infected with invasive or high-attack-rate serotypes (18.8% vs. 10.0%; p = 0.59). Our data suggest that young children with a genetically determined low-MBL production are at a higher risk of developing IPD, particularly that caused by opportunistic or low-attack-rate pneumococcal serotypes.

show abstract

Section: Discussioncontrasting

confidence: 64%

High prevalence of genetically-determined mannose binding lectin deficiency in young children with invasive pneumococcal disease

Muñoz-Almagro¹,

Bautista

Arias

et al. 2014

Clinical Microbiology and Infection

View full text Add to dashboard Cite

show abstract

“…It has been suggested that MBL is involved in the recognition of HIV due to interaction with the highly glycosylated envelope protein gp120 (Ying et al, 2004). This could explain the fact that MBLdeficiency was reported to be a risk factor for HIV infection (Garred et al, 1997;Nielsen et al, 1995), which was recently confirmed in a meta-analysis by Israels et al (2012).…”

Section: Mbl and (Bacterial) Infectionmentioning

confidence: 86%

Restoration of MBL-deficiency: Redefining the safety, efficacy and viability of MBL-substitution therapy

Keizer

Wouters

Schlapbach

et al. 2014

Molecular Immunology

View full text Add to dashboard Cite

“…In support of this notion, recent genetic evidence indicates that MBL deficiency is associated with an increased risk of vertical HIV-1 transmission (Mangano et al, 2008) and the association between HIV-1 disease progression and MBL deficiency is most pronounced in children less than 2 years of age, probably due to immaturity of their adaptive immunity (Israels et al, 2012). Three genetic studies of Chinese populations have demonstrated that MBL deficiencies are associated with increased susceptibility to HIV-1 infection and disease progression (Sheng et al, 2010) (Tan et al, 2009) (Li et al, 2013) and serum circulating levels of normal MBL in HIV-1-infected patients could be an important auxiliary biological marker in association with CD4(+) T cell counts in the evaluation of HIV-1 disease progression (Tan et al, 2009).…”

Section: Complement Activation In Hiv-infectionmentioning

confidence: 96%

Complement and HIV-I infection/HIV-associated neurocognitive disorders

et al. 2014

View full text Add to dashboard Cite

The various neurological complications associated with HIV-1 infection, specifically HIV-associated neurocognitive disorders (HAND) persist as a major public health burden worldwide. Despite the widespread use of anti-retroviral therapy, the prevalence of HAND is significantly high. HAND results from the direct effects of an HIV-1 infection as well as secondary effects of HIV-1-induced immune reaction and inflammatory response. Complement, a critical mediator of innate and acquired immunity, plays important roles in defeating many viral infections by the formation of a lytic pore or indirectly by opsonization and recruitment of phagocytes. While the role of complement in the pathogenesis of HIV-1 infection and HAND has been previously recognized for over fifteen years, it has been largely underestimated thus far. Complement can be activated through HIV-1 envelope proteins, mannose binding lectins (MBL) and anti-HIV-1 antibodies. Complement not only fights against HIV-1 infection but also enhances HIV-1 infection. Also, HIV-1 can hijack complement regulators such as CD59 and CD55 and can utilize these regulators and factor H to escape from complement attack. Normally, complement levels in brain are much lower than plasma levels and there is no or little complement deposition in brain cells. Interestingly, local production and deposition of complement are dramatically increased in HIV-1-infected brain, indicating that complement may contribute to the pathogenesis of HAND. Here, we review the current understanding of the role of complement in HIV-1 infection and HAND as well as potential therapeutic approaches targeting to the complement system for the treatment and eradications of HIV-1 infection.

show abstract

Mannose-binding Lectin and the Risk of HIV Transmission and Disease Progression in Children

Cited by 12 publications

References 25 publications

High prevalence of genetically-determined mannose binding lectin deficiency in young children with invasive pneumococcal disease

High prevalence of genetically-determined mannose binding lectin deficiency in young children with invasive pneumococcal disease

Restoration of MBL-deficiency: Redefining the safety, efficacy and viability of MBL-substitution therapy

Complement and HIV-I infection/HIV-associated neurocognitive disorders

Contact Info

Product

Resources

About