Latest research from the National Institute for Biological Standards and Control (NIBSC) in collaboration with Oxford University provides some insight as to why, in outbreaks of meningococcal disease, some people contract invasive disease whilst others escape with an asymptomatic infection. NIBSC scientists identified a protein called factor H binding protein (fHbp) found on the surface of meningococci to be associated with severe invasive meningococcal disease of a patient during the outbreak of meningococcal disease at the University of Southampton (UK) in 1997.
Scientists at NIBSC compared the complete set of proteins expressed by two closely related meningococcal strains (serogroup C) to understand why one strain (‘Case’) caused severe disease leading to death of a student while the other strain (‘Carrier’), which is genetically very similar to the first strain, did not cause disease. Most importantly, only the ‘Case’ produced the surface bound fHbp.
Factor H binding protein plays an important role in survival of the bacteria in human sera thus allowing the bacteria to proliferate and spread rapidly through the blood stream leading to a severe invasive disease. Using an assay which measures bacterial survival in sera we showed that the ‘Case’ is highly resistant to killing by human serum. On the contrary, the Carrier is unable to survive in human serum. Moreover, when the ‘Carrier’ strain was genetically modified to produce fHbp, these bacteria were found to be resistant to killing by human sera too. This suggests that fHbp protein produced by the ‘Case’ played a role in causing the death of the patient while the absence fHbp protein in the ‘Carrier’ meant that the bacteria could not survive in the blood and thus could not proliferate to cause disease.
This study identified the surface bound fHbp protein produced by the ‘Case’ to be a major contributor of virulence which resulted in contrasting clinical outcomes between the ‘Case’ and the ‘Carrier’.
Read the full article in Access Microbiology.