Division of Bacteriology, ICMR-National Institute of Cholera and Enteric Diseases, Kolkata, India.
Biomedical Informatics Center, ICMR-National Institute of Cholera and Enteric Diseases, Kolkata, India.
PLoS Negl Trop Dis. 2020 Apr 1;14(4):e0008128. doi: 10.1371/journal.pntd.0008128. eCollection 2020 Apr.
Cholera continues to be an important public health concern in developing countries where proper hygiene and sanitation are compromised. This severe diarrheal disease is caused by the Gram-negative pathogen Vibrio cholerae belonging to serogroups O1 and O139. Cholera toxin (CT) is the prime virulence factor and is directly responsible for the disease manifestation. The ctxB gene encodes cholera toxin B subunit (CTB) whereas the A subunit (CTA) is the product of ctxA gene. Enzymatic action of CT depends on binding of B pentamers to the lipid-based receptor ganglioside GM1. In recent years, emergence of V. cholerae Haitian variant strains with ctxB7 allele and their rapid spread throughout the globe has been linked to various cholera outbreaks in Africa and Asia. These strains produce classical type (WT) CTB except for an additional mutation in the signal sequence region where an asparagine (N) residue replaces a histidine (H) at the 20th amino acid position (H20N) of CTB precursor (pre-CTB). Here we report that Haitian variant V. cholerae O1 strains isolated in Kolkata produced higher amount of CT compared to contemporary O1 El Tor variant strains under in vitro virulence inducing conditions. We observed that the ctxB7 allele, itself plays a pivotal role in higher CT production. Based on our in silico analysis, we hypothesized that higher accumulation of toxin subunits from ctxB7 allele might be attributed to the structural alteration at the CTB signal peptide region of pre-H20N CTB. Overall, this study provides plausible explanation regarding the hypertoxigenic phenotype of the Haitian variant strains which have spread globally, possibly through positive selection for increased pathogenic traits.
霍乱仍然是发展中国家重要的公共卫生关注点,在这些国家,适当的卫生和环境卫生条件受到影响。这种严重的腹泻病是由革兰氏阴性病原体霍乱弧菌引起的,属于 O1 和 O139 血清群。霍乱毒素(CT)是主要的毒力因子,直接导致疾病的表现。ctxB 基因编码霍乱毒素 B 亚单位(CTB),而 A 亚单位(CTA)是 ctxA 基因的产物。CT 的酶促作用依赖于 B 五聚体与基于脂质的受体神经节苷脂 GM1 的结合。近年来,具有 ctxB7 等位基因的海地变异株霍乱弧菌的出现及其在全球的迅速传播,与非洲和亚洲的各种霍乱暴发有关。这些菌株产生经典型(WT)CTB,但在信号序列区域有一个额外的突变,即在 CTB 前体(pre-CTB)的第 20 个氨基酸位置(H20N)处,一个天冬酰胺(N)残基取代组氨酸(H)。在这里,我们报告说,在体外毒力诱导条件下,从加尔各答分离的海地变异 O1 株霍乱弧菌产生的 CT 量高于当代 O1 El Tor 变异株。我们观察到,ctxB7 等位基因本身在更高的 CT 产生中起着关键作用。根据我们的计算机分析,我们假设 ctxB7 等位基因更高的毒素亚单位积累可能归因于 pre-H20N CTB 的 CTB 信号肽区域的结构改变。总的来说,这项研究提供了关于海地变异株高毒力表型的合理解释,这些变异株已经在全球范围内传播,可能是通过对增加的致病特征的正选择。