vaccinated children or vaccine virus strains pose the same risk of virus mutations as wild viruses the big difference is that while an unvaccinated child may or may not get a specific virus all the vaccinated ones (live virus vaccines- MMR, chicken pox, oral polio,flu etc) have the same potential to contribute to virus mutations and they have.
read this
http://www.cdc.gov/mmwr/preview/mmwrhtml/mm54d1014a1.htm
you can also find articles about measles vaccine virus shading for more then 4 weeks after MMR shot or also search atipical measels
You need to read the article. That is EXACTLY the opposite of what it says.
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).