Hypocomplementaemia in children with Plasmodium falciparum malaria

Williamson, W.A.; Damisah, M.; Greenwood, Brian; Gilles, H. M.

doi:10.1016/0035-9203(78)90042-1

Cited by 3 publications

(3 citation statements)

References 2 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…They concluded that by 7 days after the onset of illness, serum C3 and C4 titers had returned to normal levels. Our titers for children with P. falciparum gametocytemia (72% [145.4 mg/100 ml] for C3 and 149% [60.5 mg/100 ml] for C4) did not show any statistical differences as compared with those of Williamson et al (16). None of the children in this study had been taking any anti-malarial drug when examined; hence, it may be conjectured that the fall in C3 VOL.…”

Section: Discussioncontrasting

confidence: 62%

See 1 more Smart Citation

Correlation of Plasmodium falciparum gametocytemia with complement component titers in rural Nigerian school children

Ade-Serrano¹,

Ejezie²,

Kassim³

1981

J Clin Microbiol

View full text Add to dashboard Cite

The relationship between Plasmodium falciparum gametocytemia and the complement components C3, C4, and C3b was investigated in 141 ambulant rural Nigerian school children. Three groups were studied. Group 1 included 42 children with circulating P. falciparum gametocytemia in which the mean titers of C3, C4, and C3b were 145.4 +/- 22.6 mg/100 ml (72%), 60.5 +/- 0.2 mg/100 ml (149%), and 64.0 +/- 5.9 mg/liter (65%), respectively. These findings indicated marked C3b hypocomplementemia. Group 2 included 50 children who were used as controls and lacked malaria parasitemia. C3, C4, and C3b mean titers were 161.6 +/- 28.9 mg/100 ml (80%), 56.8 +/- 2.07 mg/100 ml (140%), and 84.8 +/- 11.4 mg/liter (86%), respectively. Group 3 included 49 children with other blood stages of P. falciparum parasitemia but no gametocytes. C3, C4, and C3b mean titers in this group were 103.0 mg/100 ml (51%), 18.3 +/- 1.2 mg/100 ml (45%), and 90.7 mg/liter (92%), respectively. Our findings suggest that C3b hypocomplementemia may be related to the advent of circulating P. falciparum gametocytes in children. We also confirmed C3 and C4 hypocomplementemia in acute human malaria. The implication of our findings in relation to neat in vitro culture of P. falciparum gametocytes or total inhibition of gametocytogenesis in malaria control is still speculative.

show abstract

Section: Discussioncontrasting

confidence: 62%

“…Williamson et al (16) obtained titers of 84 + 15% and 180 ± 43% for C3 and C4, respectively, on day 7. On day 14, titers were 81 ± 19% and 150 ± 52%.…”

Section: Discussionmentioning

confidence: 97%

Correlation of Plasmodium falciparum gametocytemia with complement component titers in rural Nigerian school children

Ade-Serrano¹,

Ejezie²,

Kassim³

1981

J Clin Microbiol

View full text Add to dashboard Cite

show abstract

“…In addition, certain infectious diseases may modulate complement levels e.g. acute malaria is a pervasive ancient infectious disease that can cause hypocomplementemia [97,98]. Furthermore, complement may be reduced to varying extents by certain auto-immune conditions that drive immune complex formation, although these events are relatively rare.…”

Section: Discussionmentioning

confidence: 99%

Lectin-Dependent Enhancement of Ebola Virus Infection via Soluble and Transmembrane C-type Lectin Receptors

et al. 2013

View full text Add to dashboard Cite

Mannose-binding lectin (MBL) is a key soluble effector of the innate immune system that recognizes pathogen-specific surface glycans. Surprisingly, low-producing MBL genetic variants that may predispose children and immunocompromised individuals to infectious diseases are more common than would be expected in human populations. Since certain immune defense molecules, such as immunoglobulins, can be exploited by invasive pathogens, we hypothesized that MBL might also enhance infections in some circumstances. Consequently, the low and intermediate MBL levels commonly found in human populations might be the result of balancing selection. Using model infection systems with pseudotyped and authentic glycosylated viruses, we demonstrated that MBL indeed enhances infection of Ebola, Hendra, Nipah and West Nile viruses in low complement conditions. Mechanistic studies with Ebola virus (EBOV) glycoprotein pseudotyped lentiviruses confirmed that MBL binds to N-linked glycan epitopes on viral surfaces in a specific manner via the MBL carbohydrate recognition domain, which is necessary for enhanced infection. MBL mediates lipid-raft-dependent macropinocytosis of EBOV via a pathway that appears to require less actin or early endosomal processing compared with the filovirus canonical endocytic pathway. Using a validated RNA interference screen, we identified C1QBP (gC1qR) as a candidate surface receptor that mediates MBL-dependent enhancement of EBOV infection. We also identified dectin-2 (CLEC6A) as a potentially novel candidate attachment factor for EBOV. Our findings support the concept of an innate immune haplotype that represents critical interactions between MBL and complement component C4 genes and that may modify susceptibility or resistance to certain glycosylated pathogens. Therefore, higher levels of native or exogenous MBL could be deleterious in the setting of relative hypocomplementemia which can occur genetically or because of immunodepletion during active infections. Our findings confirm our hypothesis that the pressure of infectious diseases may have contributed in part to evolutionary selection of MBL mutant haplotypes.

show abstract