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ABSTRACT: Genetic diversity in invasive meningococcal isolates

PROVIDER: PRJNA853880 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19893900_1.fastq.gz	Fastqsanger.gz
	SRR19893900_2.fastq.gz	Fastqsanger.gz
	SRR19894000_1.fastq.gz	Fastqsanger.gz
	SRR19894000_2.fastq.gz	Fastqsanger.gz
	SRR19894100_1.fastq.gz	Fastqsanger.gz

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Project description:Genetic diversity in invasive meningococcal isolates

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Evolution of an outbreak of meningococcal disease among men who have sex with men

Project description:Neisseria meningitidis (meningococcus) is usually transmitted via respiratory droplets, whereas its close relative, the gonococcus is sexually transmitted. Invasive meningococcal disease due to isolates of serogroup C increased in Europe and the United States among men who have sex with men (MSM). These isolates were also recovered from cases of urethritis suggesting sexual transmission. Genome sequencing of representative strains revealed that isolates from MSM and urethritis cases belonged to a unique clade within clonal complex11. Proteome analysis showed expression of nitrite reductase by these isolates, enabling anaerobic growth as in gonococci. Invasive isolates from MSM, but not urethritis isolates expressed functional human factor H (hfH) binding protein associated with enhanced survival in transgenic mice expressing hfH, a complement regulatory protein. Our data provide a unique example of meningococcal evolution with adaptation to sexual transmissibility, initially associated with low virulence but with subsequent fHbp-associated invasiveness. Implications for vaccination strategies are discussed.

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Project description:Although usually a harmless colonizer of the human nasopharynx, Neisseria meningitidis (meningococcus) can spread to the blood stream and cause invasive disease. For survival in blood, N. meningitidis evades the complement system by expression of a polysaccharide capsule and surface proteins sequestering the complement regulator fH. Meningococcal strains are highly diverse and are categorized by their serogroup and multilocus sequence typing. The sequence type 41/44 clonal complex makes up a major proportion of serogroup B meningococcal disease worldwide, but it is also common in asymptomatic carriers. Proteome analysis of a serum resistant isolate from invasive meningococcal disease and two less resistant isolates from healthy carriers identified NspA as the sole protein consistently expressed more abundantly in the invasive isolate. Knock-out of nspA reduced serum resistance, accompanied by stronger deposition of membrane attack complex (C5b9). High or low expression of NspA was associated with sequence variation within a homopolymeric tract located in the -10/-35 region of the nspA promotor: A tract with 5 adenosines dictated low NspA expression, whereas a 6-adenosine motif led to high NspA expression. High levels of NspA correlated with high factor H sequestration onto the bacteria. We could not link the homopolymeric tract length to phase variation, unlike described for other N. meningitidis surface proteins with similar sequence motifs. Epidemiological evidence from carriage and disease isolates indicates that NspA contributes to serum resistance, but is not a prerequisite for invasive disease. Thus, the lineage ST-41/44 meningococcal strains are heterogenous in their NspA expression.

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