Complement alternative pathway genetic variation and Dengue infection in the Thai population
Version of Record online: 6 OCT 2013
© 2013 The Authors. Clinical and Experimental Immunology published by John Wiley & Sons Ltd on behalf of British Society. for Immunology.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Clinical & Experimental Immunology
Volume 174, Issue 2, pages 326–334, November 2013
How to Cite
Kraivong, R., Vasanawathana, S., Limpitikul, W., Malasit, P., Tangthawornchaikul, N., Botto, M., Screaton, G. R., Mongkolsapaya, J. and Pickering, M. C. (2013), Complement alternative pathway genetic variation and Dengue infection in the Thai population. Clinical & Experimental Immunology, 174: 326–334. doi: 10.1111/cei.12184
- Issue online: 6 OCT 2013
- Version of Record online: 6 OCT 2013
- Accepted manuscript online: 7 AUG 2013 05:06AM EST
- Manuscript Accepted: 30 JUL 2013
- Royal Thai Government
- alternative complement pathway;
- Dengue infection;
- genetic polymorphism
Dengue disease is a mosquito-borne infection caused by Dengue virus. Infection may be asymptomatic or variably manifest as mild Dengue fever (DF) to the most severe form, Dengue haemorrhagic fever (DHF). Mechanisms that influence disease severity are not understood. Complement, an integral component of the immune system, is activated during Dengue infection and the degree of activation increases with disease severity. Activation of the complement alternative pathway is influenced by polymorphisms within activation (factor B rs12614/rs641153, C3 rs2230199) and regulatory [complement factor H (CFH) rs800292] proteins, collectively termed a complotype. Here, we tested the hypothesis that the complotype influences disease severity during secondary Dengue infection. In addition to the complotype, we also assessed two other disease-associated CFH polymorphisms (rs1061170, rs3753394) and a structural polymorphism within the CFH protein family. We did not detect any significant association between the examined polymorphisms and Dengue infection severity in the Thai population. However, the minor allele frequencies of the factor B and C3 polymorphisms were less than 10%, so our study was not sufficiently powered to detect an association at these loci. We were also unable to detect a direct interaction between CFH and Dengue NS1 using both recombinant NS1 and DV2-infected culture supernatants. We conclude that the complotype does not influence secondary Dengue infection severity in the Thai population.