VDPVs emerge from OPV viruses as a result of 1) their continuous replication in immunodeficient persons (immunodeficiency-associated or iVDPVs) such as the index patient in this investigation or 2) their circulation in populations with low vaccination coverage (circulating or cVDPVs) (1). During community circulation, cVDPVs often recombine with other species C enteroviruses, which is not characteristic for iVDPVs (1). Because polioviruses accumulate nucleotide changes at a constant rate of mutation (approximately 1% per year), the time of replication can be inferred from the degree of divergence (1). Because cVDPVs commonly revert to a wild poliovirus phenotype, they can have increased transmissibility and high risk for paralytic disease; cVDPVs have caused outbreaks of poliomyelitis in several countries (1). VDPVs in highly immunized populations are rare. Before the VDPV identification in Minnesota, the most recent known VDPV excreter in the United States was a child with SCID (now deceased) who developed vaccine-associated paralytic poliomyelitis in 1995 (4).
lets see what low vaccination coverage means
a mix of vaccinated and vaccinated persons on whatever ratio you like
BUT
Unvaccinated ones need to get the VACCINE STRAIN VIRUS (mutated or not) from a vaccinated person as first source of infection .....but according to them only a immunodeficient (”and vaccinated in at least the first case” they don't add that) person propagate the virus mutated or not...
so the entire sentence about low coverage areas is pointless and meaningless unless not only immunodeficient persons can propagate the vaccine virus mutated or not....and in that case the first sentence is useless