Complement protein levels and MBL2 polymorphisms are associated with dengue and disease severity
Ngo Truong Giang1,2, Hoang van Tong3,4, Do Quyet5
1Department of Pathophysiology, Vietnam Military Medical University, 160 Phung Hung, Ha Dong, Hanoi, Vietnam.
Genetic variants in mannose-binding lectin (MBL2) are linked to dengue risk in Vietnam. Complement protein levels are altered during dengue infection, correlating with disease severity and liver function.
Area of Science:
- Immunology
- Genetics
- Infectious Diseases
Background:
- The complement system plays a potential role in dengue virus infection and severe dengue progression.
- Understanding genetic factors and complement protein alterations is crucial for dengue pathogenesis research.
Purpose of the Study:
- To investigate the association of MBL2 genetic variants and serum MBL levels with dengue in Vietnamese patients.
- To analyze the levels of various complement proteins in dengue patients and their correlation with clinical parameters.
Main Methods:
- Genotyping of MBL2 polymorphisms (e.g., -550L/H, codon 54) and diplotypes/haplotypes.
- Quantification of serum MBL and complement factors (C2, C5, C5a, C9, factor D, factor I, C4b).
- Statistical analysis to correlate genetic variants and protein levels with dengue status and clinical markers (AST, ALT, WBC, platelet counts).
Main Results:
- Specific MBL2 genotypes, diplotypes, and haplotypes were associated with dengue in the Vietnamese population.
- Elevated levels of complement factors C2, C5, and C5a, and decreased factor D were observed in dengue patients.
- Complement factor levels (C2, C5a, C9, factor D) showed significant correlations with liver enzymes (AST, ALT), WBC counts, and platelet counts.
Conclusions:
- MBL2 polymorphisms are significantly associated with dengue susceptibility in the Vietnamese population.
- Complement protein levels (C2, C4b, C5, C5a, C9, factor D, factor I) are modulated during the clinical course of dengue.
- These findings highlight the involvement of the complement system and MBL2 genetics in dengue pathogenesis and severity.
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