Sam I-Ching, Chan Yoke Fun, Chan Shie Yien, Loong Shih Keng, Chin Hock Khim, Hooi Poh Sim, Ganeswrie Rajasekaram, Abubakar Sazaly
Tropical Infectious Diseases Research and Education Centre, Department of Medical Microbiology, Faculty of Medicine, University Malaya, Kuala Lumpur, Malaysia.
J Clin Virol. 2009 Oct;46(2):180-3. doi: 10.1016/j.jcv.2009.07.016. Epub 2009 Aug 14.
Chikungunya virus (CHIKV) of the Central/East African genotype has caused large outbreaks worldwide in recent years. In Malaysia, limited CHIKV outbreaks of the endemic Asian and imported Central/East African genotypes were reported in 1998 and 2006. Since April 2008, an unprecedented nationwide outbreak has affected Malaysia.
To study the molecular epidemiology of the current Malaysian CHIKV outbreak, and to evaluate cross-neutralisation activity of serum from infected patients against isolates of Asian and Central/East African genotypes.
Serum samples were collected from 83 patients presenting in 2008, and tested with PCR for the E1 gene, virus isolation, and for IgM. Phylogenetic analysis was performed on partial E1 gene sequences of 837bp length. Convalescent serum from the current outbreak and Bagan Panchor outbreak (Asian genotype, 2006) were tested for cross-neutralising activity against representative strains from each outbreak.
CHIKV was confirmed in 34 patients (41.0%). The current outbreak strain has the A226V mutation in the E1 structural protein, and grouped with Central/East African isolates from recent global outbreaks. Serum cross-neutralisation activity against both Central/East African and Asian genotypes was observed at titres from 40 to 1280.
The CHIKV strain causing the largest Malaysian outbreak is of the Central/East African genotype. The presence of the A226V mutation, which enhances transmissibility of CHIKV by Aedes albopictus, may explain the extensive spread especially in rural areas. Serum cross-neutralisation of different genotypes may aid potential vaccines and limit the effect of future outbreaks.
近年来，中/东非基因型的基孔肯雅病毒（CHIKV）在全球引发了大规模疫情。1998年和2006年，马来西亚分别报告了有限的地方性亚洲基因型和输入性中/东非基因型CHIKV疫情。自2008年4月以来，马来西亚爆发了前所未有的全国性疫情。
研究当前马来西亚CHIKV疫情的分子流行病学，并评估感染患者血清对亚洲和中/东非基因型分离株的交叉中和活性。
收集了2008年就诊的83例患者的血清样本，采用PCR检测E1基因、病毒分离及IgM。对837bp长度的部分E1基因序列进行系统发育分析。检测了本次疫情恢复期血清和巴干榜鹅疫情（2006年，亚洲基因型）血清对各疫情代表性毒株的交叉中和活性。
34例患者（41.0%）确诊感染CHIKV。本次疫情毒株的E1结构蛋白存在A226V突变，与近期全球疫情中的中/东非分离株归为一类。观察到血清对中/东非和亚洲基因型的交叉中和活性滴度为40至1280。
导致马来西亚最大规模疫情的CHIKV毒株为中/东非基因型。A226V突变的存在增强了白纹伊蚊对CHIKV的传播能力，这可能解释了疫情尤其是在农村地区的广泛传播。不同基因型血清的交叉中和作用可能有助于研发潜在疫苗并限制未来疫情的影响。
