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Pradeep Reddy Marri led a comparative whole-genome sequencing study of commensal and pathogenic Neisseria. The 2010 paper found that commensal species carry many virulence alleles and have extensive genetic exchange with other Neisseria. A harmless colonizer can therefore be a reservoir of genetic variants relevant to a pathogenic relative.^[ref]

This connects horizontal gene transfer to the evolution of disease-associated traits. Possessing a particular allele does not by itself establish pathogenicity: its genomic context, regulation and host interaction also matter.

Virulence is the degree to which a pathogen causes damage or disease in a specified host and setting. It is a quantitative aspect of pathogenic behaviour, not simply a label meaning that an organism can cause an infection.^[ref]

A comparison needs an endpoint and controlled conditions. One experiment might compare tissue damage after equal exposure; another might compare survival across a range of doses. If two strains differ in the dose required to produce an outcome, that result concerns the tested host, route and conditions. It is not automatically a universal ordering for every species or exposure route.

This also separates damage from transmission. A pathogen can spread efficiently without causing the most severe disease, while a damaging infection need not transmit efficiently. Keeping the outcomes separate makes evolutionary and experimental claims about virulence testable.