that it is most likely that an antiviral drug would be used as a supplement to vaccination in order to prevent infection.

In the first 2-3 years after OPV cessation, response to outbreaks of cVDPV is expected to consist of comprehensive, regional mOPV distribution (Aylward and Cochi 2004). Because the immune response to a live vaccine depends on replication of the vaccine virus in the gastrointestinal tract, concomitant administration of a potent antiviral drug would interfere with the induction of immunity. Therefore, when OPV is used for outbreak control, the role of an antiviral drug might be quite limited. If sufficiently safe and inexpensive, such a drug might be used by public health authorities to control spread of live polioviruses—both the virulent outbreak virus and OPV viruses—in unaffected areas that surround the outbreak zone. The drug supply would need to be very large and the logistics of distributing the drug would be complex, potentially draining resources from the areas affected by the outbreak.

The risk of an outbreak of cVDPV more than 3 years after OPV cessation is thought to be low (Duintjer Tebbens et al. 2005), but the consequences could be severe, in that the number of susceptible children would by then be substantial. It is during the period more than 3 years after OPV cessation that the committee concludes that an antiviral drug may be most useful. If such an outbreak occurs and it is undesirable to reintroduce live poliovirus to control it, IPV could be used as an alternative. IPV is safe and carries no risk either of VAPP or of initiating a cVDPV chain of transmission. However IPV does not induce a mucosal immune response and thus is less effective in interrupting transmission of polioviruses. By itself, IPV may not induce immunity quickly enough to stop an outbreak. Use of an antiviral drug in conjunction with IPV would protect vaccine recipients from poliovirus infection until IPV-induced immunity can be assured. Virtually all studies with the currently available IPV vaccines confirm that at least two doses are required to achieve seroconversion in more than half the vaccinees. Actual seroconversion rates vary, not only with the number of doses, but also with the interval between doses and with age (Sormunen et al. 2004; Simoes et al. 1985). Simoes et al. showed that IPV containing 40, 8, and 30 D antigen units for serotypes 1, 2, and 3, respectively, induced seroconversion rates of 96%, 80%, and 96% 4 weeks after the second dose, if two IPV doses were administered a month apart (Simoes et al. 1985). These rates are slightly lower than rates observed after a 2-month dose interval but it is likely that the shortest effective interval between IPV doses would be chosen for purposes of outbreak control.

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