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    • Outer membrane proteins porins A and

    2018-10-30

    Outer membrane proteins, porins A and B (PorA, PorB) (Russell et al., 2004; Tanabe et al., 2010) and iron-regulated enterobactin (FetA) (Thompson et al., 2003) are used for “fine typing” of meningococcal isolates while factor H binding protein (FHbp) (Seib et al., 2015), Neisserial adhesion A (NadA) (Capecchi et al., 2005) and Neisserial heparin binding antigen (Nhba) (Serruto et al., 2010) are components of capsule-independent vaccines developed for prevention of serogroup B disease (Granoff, 2010). Meningococci have a very plastic genome as a result of frequent acquisition of genetic material from other Neisseria or more distant bacterial species through recombination (Kong et al., 2013; Holmes et al., 1999). Recombination involving major outer membrane antigen genes — “antigenic shift” has been linked to increased incidence of meningococcal disease (Harrison et al., 2006). Capsular switching – acquisition of novel caffeic acid specific genes through recombination has also facilitates the emergence and persistence of virulent meningococcal lineages (Swartley et al., 1997; Harrison et al., 2010). Through capsular switching, defined as presence of different capsular phenotypes within the same clonal complex, meningococcal strains belonging to virulent lineages may escape vaccine induced immunity. In the 1970s to 1990s, serogroup W was a rare cause of meningococcal disease. In 2000, the first recorded serogroup W meningococcal disease outbreak occurred during the annual Hajj pilgrimage in Mecca, Saudi Arabia (Taha et al., 2000; Aguilera et al., 2002). The Hajj outbreak strain, referred to as the Hajj clone, was characterized as belonging to the hypervirulent sequence type (ST)-11 genetic lineage and having the PorA antigen-encoding gene type P1.5,2 (Mayer et al., 2002). Since 2000, W ST-11 strains that are genetically similar to the Hajj clone have caused large epidemics in the African meningitis belt (Decosas and Koama, 2002; Collard et al., 2010; MacNeil et al., 2014) and have caused case clusters and smaller outbreaks in South Africa (von Gottberg et al., 2008), China (Zhou et al., 2013), Taiwan (Chiou et al., 2006), Brazil (Lemos et al., 2010), and most recently in Argentina (Efron et al., 2009), Chile (Barra et al., 2013) and the United Kingdom (Ladhani et al., 2015). A majority of ST-11 strains isolated in 1960–1999 expressed serogroup C capsule (http://pubmlst.org/neisseria/). As a result, W ST-11 is thought to have emerged from serogroup C ST-11 lineage through capsular switching though the direction of capsular switching has not been established (Kelly and Pollard, 2003). The Hajj clone was highly similar by most molecular typing techniques including pulsed field gel electrophoresis (PFGE), PorA and FetA genotyping to historical rare sporadic group W ST-11 strains isolated globally from 1970 to 1999 (Mayer et al., 2002; Fonkoua et al., 2002; Taha et al., 2004). These “pre-Hajj” strains were distinguished by 16S ribosomal RNA (rRNA) genotyping as 16S type 13 and type 14 compared to type 31 associated with the Hajj clone (Mayer et al., 2002). The high genetic and antigenic similarity between the Hajj clone and pre-Hajj W ST-11 strains by traditional molecular techniques markedly contrasts with the abrupt and dramatic changes in the epidemiology of W ST-11 that began with the Hajj outbreak in 2000 (Kelly and Pollard, 2003). In a recent study, we compared capsular gene sequences from the Hajj clone and 24 other invasive W ST-11 strains isolated from 1970 to 2012 (Mustapha et al., 2014). Phylogenetic and BLAST analyses against a database of over 2300 genome sequences demonstrated that the Hajj clone and 24 other invasive W ST-11 strains shared identical capsular recombination events, with a sporadic group W strain and Y ST-23 as the most likely donor lineages into a serogroup C ST-11 strain (Mustapha et al., 2014). Taken together, these studies suggest that historical sporadic W ST-11 strains and the Hajj clone have a common origin and likely emerged from a capsular switching event in a single ancestral C ST-11 strain. Furthermore, these studies suggested that genetic differences outside the capsule region may be responsible for increased virulence seen in the Hajj clone when compared to historical sporadic W ST-11 strains.