History of polio vaccination

Poliomyelitis is an acute paralytic disease caused by three poliovirus(PV)serotypes.Less than 1%of PV infections result in acute flaccid paralysis.The disease was controlled using the formalin-inactivated Salk polio vaccine(IPV)and the Sabin oral polio vaccine(OPV).Global poliomyelitis eradication was proposed in 1988by the World Health Organization to its member states.The strategic plan established the activities required for polio eradication,certification for regions,OPV cessation phase and post-OPV phase.OPV is the vaccine of choice for the poliomyelitis eradication program because it induces both a systemic and mucosal immune response.The major risks of OPV vaccination are the appearance of Vaccine-Associated Paralytic Poliomyelitis cases(VAPP)and the emergence of Vaccine Derived Polioviruses strains.The supplementary immunization with monovalent strains of OPV type 1 or type 3 or with a new bivalent oral polio vaccine b OPV(containing type1 and type 3 PV)has been introduced in those regions where the virus has been difficult to control.Most countries have switched the schedule of vaccination by using IPV instead of OPV because it poses no risk of vaccine-related disease.Until 2008,poliomyelitis was controlled in Romania,an Eastern European country,predominantly using OPV.The alternative vaccinationschedule(IPV/OPV)was implemented starting in September 2008,while beginning in 2009,the vaccination was IPV only.The risk of VAPP will disappear worldwide with the cessation of use of OPV.The immunization for polio must be maintained for at least 5 to 10 years using IPV.

Lipopolysaccharide Inhibits FI-RSV Vaccine-enhanced Inflammation Through Regulating Th Responses

Respiratory syncytial virus (RSV) infection is the primary cause of respiratory disease in infants. The formalin-inactivated RSV (FI-RSV) vaccine resulted in an enhanced respiratory disease (ERD) in infants upon natural RSV infection, which is a major obstacle for development of safe and efficacious vaccines. Excessive and uncontrolled Th immune responses could be involved in the ERD. Agonists of TLRs are used as adjuvants to guide the type of immune response induced by vaccines. We evaluated the impact of lipopolysaccharide (LPS), the agonist of TLR4, on ERD as the adjuvant of FI-RSV. The results showed that LPS remarkably inhibited FI-RSV-enhanced lung inflammation, mucus production, airway inflammatory cell infiltration, and inflammatory cytokines following RSV challenge. Interestingly, LPS inhibited both Th2 and Th17 type cytokines in lungs of FI-RSV-immunized mice following RSV challenge, without an increase in the Thl type cytokines, suggesting a controlled immune response. In contrast, Pam3Cys and Poly(I:C), the agonist of TLR1/2 or TLR3, partly inhibited FI-RSV-enhanced lung inflammation. Pam3Cys inhibited Th17 type cytokine IL-17, but promoted both Th1 and Th2 type cytokines. Poly(I:C) inhibited Th2 and Th 17 type cytokines, but promoted Th1 type cytokines. In addition, LPS promoted IgG and IgG2a antibody production, which might provide protection from RSV challenge. These results suggest that LPS inhibits ERD without impairment in antibody production and protection, and the mechanism appears to be related with regulation of Th responses induced by FI-RSV.