The switch from trivalent to bivalent oral poliovirus vaccine: Will it lead to polio?

bivalent OPVIn four months, 155 countries will together switch from using trivalent to bivalent oral poliovirus vaccine. Will this change lead to more cases of poliomyelitis?

There are three serotypes of poliovirus, each of which can cause paralytic poliomyelitis. The Sabin oral poliovirus vaccine (OPV), which has been used globally by WHO in the eradication effort, is a trivalent vaccine that contains all three serotypes.

In September 2015 WHO declared that wild poliovirus type 2 has been eradicated from the planet – no cases caused by this serotype had been detected since November 1999. However, in 2015, there were 9 cases of poliomyelitis caused by the type 2 vaccine. For these reasons WHO decided to remove the type 2 Sabin strain from OPV, and switch from trivalent to bivalent vaccine in April 2016.

After OPV is ingested, the viruses replicate in the intestinal tract, providing immunity to subsequent infection. During replication in the intestine, the vaccine viruses lose the mutations that prevent them from causing paralysis. Everyone who receives OPV sheds these revertant viruses in the feces. In rare cases (about one in 1.5 million) the revertant viruses cause poliomyelitis in the vaccine recipient (these cases are called VAPP for vaccine-associated paralytic poliomyelitis). Vaccine-derived polioviruses can also circulate in the human population, and in under-vaccinated populations, they can cause poliomyelitis.

There were 26 reported cases of poliomyelitis caused by the type 1 or type 2 vaccine viruses in 2015. Nine cases of type 2 vaccine-associated polio were detected in four countries: Pakistan, Guinea, Lao People’s Democratic Republic, and Myanmar. Removing the type 2 strain from OPV will eliminate vaccine-associated poliomyelitis in recipients caused by this serotype. When the US switched from OPV to the inactivated poliovaccine (IPV) in 2000, VAPP was eliminated.

The problem with the trivalent to bivalent switch is that vaccine-derived type 2 poliovirus is likely still circulating somewhere on Earth. The last two reported cases of type 2 vaccine-associated polio in 2015 were reported in Myanmar in October. The viruses isolated from these cases were genetically related to strains that had been circulating in the same village in April of the that year. In other words, type 2 vaccine-derived strains have been circulating for an extended period of time in Myanmar; they have been known to persist for years elsewhere. If these viruses continue to circulate past the time that immunization against type 2 virus stops, they could pose a threat to the growing numbers of infants and children who have not been immunized against this serotype.

Eventually as type 3, and then type 1 polioviruses are eradicated, it will also be necessary to stop immunizing with the respective Sabin vaccine strains. The switch from trivalent to bivalent vaccine in April 2016 is essentially an experiment to determine if it is possible to stop immunizing with OPV without placing newborns at risk from circulating vaccine-derived strains.

Over 18 years ago Alan Dove and I argued that the presence of circulating vaccine-derived polioviruses made stopping immunization with OPV a bad idea. We suggested instead a switch from OPV to IPV until circulating vaccine-derived viruses disappeared. At the time, WHO disagreeed, but now they recommend that all countries deliver at least one dose of IPV as part of their immunization program. Instead of simply removing the Sabin type 2 strain from the immunization programs of 155 countries, it should be replaced with the inactivated type 2 vaccine. This change would maintain immunity to this virus in children born after April 2016. Such a synchronized replacement is currently not in the WHO’s polio eradication plans. I hope that their strategy is the right one.

TWiV 371: Sympathy for the devil

TWiVOn episode #371 of the science show This Week in Virology, the TWiVologists discuss the finding of a second transmissible cancer in Tasmanian devils, and development of new poliovirus strains for the production of inactivated vaccine in the post-eradication era.

You can find TWiV #371 at www.microbe.tv/twiv.

Virologists, start your poliovirus destruction!

I have worked on poliovirus for over thirty-six years, first as a posdoctoral fellow with David Baltimore in 1979, and then in my laboratory at Columbia University. The end of that research commences this year with the destruction of my stocks of polioviruses.

In 2015 there were 70 reported cases of poliomyelitis caused by wild type 1 poliovirus, and 26 cases of poliomyelitis caused by circulating vaccine derived polioviruses (cVDPV) types 1 and 2. The last case of type 2 poliovirus occurred in India in 1999, and the virus was declared eradicated in 2015. Consequently the World Health Organization has decided that all remaining stocks of wild type 2 poliovirus should be destroyed by the end of 2015.

My laboratory has worked extensively with type 2 polioviruses. Before we produced transgenic mice susceptible to poliovirus, we had studied the Lansing strain of type 2 poliovirus because it had the unusual ability to infect wild type mice (polioviruses normally only infect certain primates). We determined the nucleotide sequence of the viral genome, identified the capsid as a determinant of the ability of the virus to infect wild type mice, and showed that swapping an eight amino acid sequence of capsid protein VP1 from a type 1 strain with that from Lansing conferred the ability to infect non-transgenic mice. These findings indicate that the ability of the Lansing strain of poliovirus to infect mice is likely due to recognition by the viral capsid of a receptor in the mouse central nervous system. In the past year we took advantage of the ability to produce mouse neurons from stem cells to attempt to identify the murine cellular receptor for Lansing virus.

To prevent further cases of poliomyelitis caused by cVDPVs, WHO has decided that there will be a synchronized, global switch from trivalent OPV to bivalent OPV in April 2016. By July of 2016 all remaining stocks of the Sabin type 2 poliovirus strains, which are used to produce OPV, will also be destroyed.

No wild type 3 poliovirus has been detected since November 2012, and it is likely that this virus will be declared eradicated within the next several years. At that time we will have to destroy our stocks of type 3 poliovirus. That leaves wild poliovirus type 1, which circulates only in Pakistan and Afghanistan. Given the small number of cases of paralysis caused by this type, it is reasonable to believe that eradication will occur within the next five years. If this timeline is correct, it means that I will be destroying my last vials of poliovirus around 2020.

It is of course necessary to destroy stocks of wild and vaccine polioviruses to prevent reintroduction of the virus and the disease that it causes. The 1978 release of smallpox virus from a laboratory in the United Kingdom, which caused one death, lead to requests for reducing the number of laboratories that retained the virus. Today there are just two official repositories of smallpox virus in the United States and Russia.

It is rare for an investigator to be told to destroy stocks of the virus that is the subject of his or her research. Over the years we have published 81 papers on poliovirus replication, vaccines, and pathogenesis. While I realize that it is absolutely essential to stop working on this virus, I do so with a certain amount of sadness. What other emotion could I have for a virus on which I have expended so much thought and effort?

Image: Poliovirus by Jason Roberts

Correction: The synchronized switch in April 2016 is from trivalent to bivalent OPV, not OPV to IPV. Consequently I have removed comments related to an OPV-IPV switch.

An unexpected benefit of inactivated poliovirus vaccine

Poliovirus by Jason Roberts

Poliovirus by Jason Roberts

The polio eradication and endgame strategic plan announced by the World Health Organization in 2014 includes at least one dose of inactivated poliovirus vaccine (IPV). Since 1988, when WHO announced the polio eradication plan, it had relied exclusively on the use of oral poliovirus vaccine (OPV). The rationale for including a dose of IPV was to avoid outbreaks of vaccine-derived type 2 poliovirus. This serotype had been eradicated in 1999 and had consequently been removed from OPV. However IPV, which is injected intramuscularly and induces highly protective humoral immunity, is less effective in producing intestinal immunity than OPV. This property was underscored by the finding that wild poliovirus circulated in Israel during 2013, a country which had high coverage with IPV. Furthermore, in countries that use only IPV, over 90% of immunized children shed poliovirus after oral challenge. I have always viewed this shortcoming of IPV as problematic, in view of the recommendation of the World Health Organization to gradually shift from OPV to IPV. Even if the shift to IPV occurs after eradication of wild type polioviruses, vaccine-derived polioviruses will continue to circulate because they cannot be eradicated by IPV. My concerns are now mitigated by new results from a study in India which indicate that IPV can boost intestinal immunity in individuals who have already received OPV.

To assess the ability of IPV to boost mucosal immunity, 954 children in three age groups (6-11 months, 5 and 10 years) were immunized with IPV, bivalent OPV (bOPV, containing types 1 and 3 only), or no vaccine. Four weeks later all children were challenged with bOPV, and virus shedding in the feces was determined 0, 3, 7, and 14 days later. The results show that 8.8, 9.1, and 13.5% of children in the 6-11 month, 5-year and 10-year old groups shed type 1 poliovirus in feces, compared with 14.4, 24.1, and 52.4% in the control group. Immunization with IPV reduced fecal shedding of poliovirus types 1 (39-74%) and 3 (53-76%). The reduction of shedding was greater after immunization with IPV compared with bOPV.

This study shows that a dose of IPV is more effective than OPV at boosting intestinal immunity in children who have previously been immunized with OPV. Both IPV and OPV should be used together in the polio eradication program. WHO therefore recommends the following vaccine regimens:

  • In all countries using OPV only, at least 1 dose of type 2 IPV should be added to the schedule.
  • In polio-endemic countries and in countries with a high risk for wild poliovirus importation and spread: one OPV birth dose, followed by 3 OPV and at least 1 IPV doses.
  • In countries with high immunization coverage (90-95%) and low wild poliovirus importation risk: an IPV-OPV sequential schedule when VAPP is a concern, comprising 1-2 doses of IPV followed by 2 or mores doses of OPV.
  • In countries with both sustained high immunization coverage and low risk of wild poliovirus importation and transmission: an IPV only schedule.

Type 2 OPV will be gradually removed from the global immunization schedules. There have been no reported cases of type 3 poliovirus since November 2012. If this wild type virus is declared eradicated later this year, presumably WHO will recommend withdrawal of type 3 OPV and replacement with type 3 IPV.

All 342 confirmed cases of poliomyelitis in 2014 were caused by type 1 poliovirus in 9 countries, mainly Pakistan and Afghanistan. Given the social and political barriers to immunization, it will likely take many years to eradicate this serotype.

Poliovirus escapes antibodies

Antibodies bound to poliovirus.

Antibodies (purple) bound to poliovirus. Image credit: Jason Roberts

Antigenic variation is a hallmark of influenza virus that allows the virus to evade host defenses. Consequently influenza vaccines need to be reformulated frequently to keep up with changing viruses. In contrast, antigenic variation is not a hallmark of poliovirus – the same poliovirus vaccines have been used for nearly 60 years to control infections by this virus. An exception is a poliovirus type 1 that caused a 2010 outbreak in the Republic of Congo.

The 2010 outbreak (445 paralytic cases) was unusual because the case fatality ratio of 47% was higher than typically observed (usually less than 10% of patients with confirmed disease die). The first clue that something was different in this outbreak was the finding that sera from some of the fatal cases failed to effectively block (neutralize) infection of cells by the strain of poliovirus isolated during this outbreak (the strain is called PV-RC2010). The same sera effectively neutralized the three Sabin vaccine viruses as well as wild type 1 polioviruses isolated from previous outbreaks. Therefore gaps in vaccination coverage were solely not responsible for this outbreak.

Examination of the nucleotide sequence of the genome of type I polioviruses isolated from 12 fatal cases revealed two amino acid changes within a site on surface of the viral capsid that is bound by neutralizing antibodies (illustration). The sequence of this site, called 2a, was changed from ser-ala-ala-leu to pro-ala-asp-leu. This particular combination of amino acid substitutions has never been seen before in poliovirus. Virus PV-RC2010, which also contains these two amino acid mutations, is completely resistant to neutralization with monoclonal antibodies that recognize antigenic site 2 (monoclonal antibodies recognize a single epitope, as opposed polyclonal antibodies which is a mixture of antibodies that recognize many epitopes. The antibodies in serum are typically polyclonal).

Poliovirus neutralization titers were determined using sera from Gabonese and German individuals who had been immunized with Sabin vaccine. These sera effectively neutralized the type I strain of Sabin poliovirus, as well as type 1 polioviruses isolated from recent outbreaks. However the sera had substantially lower neutralization activity against PV-RC2010. From 15-29% of these individuals would be considered not to be protected from infection with this strain.

Nucleotide sequence analysis of PV-RC2010 reveals that it is related to a poliovirus strain isolated in Angola in 2009, the year before the Republic of Congo outbreak. The Angolan virus had just one of the two amino acid changes in antigenic site 2a found in PV-RC2010.

It is possible that the relative resistance of the polioviruses to antibody neutralization might have been an important contributor to the high virulence observed during the Republic of Congo outbreak. The reduced ability of serum antibodies to neutralize virus would have lead to higher virus in the blood and a greater chance of entering the central nervous system. Another factor could also be that many of the cases of poliomyelitis were in adults, in which the disease is known to be more severe.

An important question is whether poliovirus strains such as PV-RC2010 pose a global threat. Typically the fitness of antigenically variant viruses is not the same as wild type, and therefore such viruses are not likely to spread in well immunized populations. Today some parts of the world have incomplete poliovirus immunization coverage, which together with the reduced circulation of wild type polioviruses leads to reduced population immunity. Such a situation could lead to the evolution of antigenic variants. This situation occurred in Finland in 1984, when an outbreak caused by type 3 poliovirus took place. The responsible strains were antigenic variants that evolved due to use of a sub-optimal poliovirus vaccine in that country.

The poliovirus outbreaks in the Republic of Congo and Finland were stopped by immunization with poliovirus vaccines, which boosted the population immunity. These experiences show that poliovirus antigenic variants such as PV-RC2010 will not cause outbreaks as long as we continue extensive immunization with poliovirus vaccines, coupled with environmental and clinical testing for the presence of such viruses.

Implications of finding poliovirus in sewers of Brazil and Israel

Poliovirus by Jason RobertsWild poliovirus has been detected in the sewers of Brazil and Israel. Fortunately, no cases of poliomyelitis have been reported in either country. Why is poliovirus present in these countries and what are the implications for the eradication effort?

Wild type poliovirus (e.g. not vaccine-derived virus) was detected in sewage samples that had been collected in March 2014 at Viracopos International Airport in the State of Sao Paulo. Wild type poliovirus had not been detected in Brazil since 1989 when the last case of poliomyelitis was reported in that country, and has not been found since March 2014.

Sequence analysis of the RNA genome of the wild type poliovirus found in the Brazilian sewer indicates that it is closely related to an isolate from a case of poliomyelitis in Equatorial Guinea. It seems likely that this virus was carried to Brazil in the intestine of an infected person who did not have symptoms of paralytic disease (only 1 in 100 poliovirus infections lead to paralysis). This individual might have traveled from Equatorial Guinea to the Brazilian airport where use of the bathroom lead to introduction of poliovirus into the sewer.

There have been 8 reported cases of poliomyelitis in Equatorial Guinea in 2014, from which we can extrapolate that there have been approximately 800 infected individuals. Given the number of cases of poliomyelitis that have been reported globally over the past 20 years, it is surprising that virus has not been detected previously in Brazilian sewage, especially at the airport. I suspect that wild type poliovirus would be detected in sewage in the US, given the number of individuals who enter that country each day. However the US does not conduct routine surveillance for poliovirus in sewage.

Brazil utilizes the Sabin vaccine to control poliomyelitis, and in the past 8 years over 95% immunization coverage has been achieved. The Sabin vaccine is taken orally and replicates in the intestine where it induces mucosal immunity. The intestine of Brazilians do not support the replication of wild type poliovirus, which is why the presence of wild type virus in sewage is not a threat – it is unlikely to spread in the population.

The isolation* of wild type poliovirus from sewage and from stool samples in Israel is a far more serious matter. As with Brazil, there have been no reported cases of poliomyelitis in Israel since 1989. Yet ten different sites in central and south Israel have been persistently positive for wild type poliovirus since February 2013. Wild type poliovirus has been found intermittently at 8 of 47 different sampled sites in southern and central Israel, and in stool from healthy persons collected in July 2013.

Two major lineages of wild type polioviruses currently circulate in endemic countries: the South Asian (SOAS) lineage in Pakistan and Afghanistan, andthe West African lineage in Nigeria. Nucleotide sequence analysis of the wild type poliovirus isolates from Israel indicate that they are closely related to the South Asian lineage, and in particular to polioviruses that circulated in Pakistan in 2012 and in Egypt in 2012. Molecular clock analysis of the sequences indicate that poliovirus was probably transmitted in 2012 from Pakistan into Egypt and Israel, and then spread in the latter country.

The central point of poliovirus circulation is within Bedouin communities in the south of Israel. The main virus reservoir within this community is children less than 9 years of age who had been immunized with inactivated poliovirus vaccine (IPV). This vaccine has been exclusively used in Israel since 2005, with overall vaccination coverage between 92-95%, and 81-100% within individual districts. The last nine birth cohorts in this country have been immunized solely with IPV.

The response to isolation of wild type poliovirus in Israeli sewers was to complete IPV immunization of all children in the south, raising coverage to above 99%. Then from August 2013 onwards, all children up to the age of nine years old were given a dose of bivalent oral poliovirus vaccine (OPV) containing types 1 and 3 poliovirus. All children who received OPV had previously been immunized with IPV, a strategy that prevents vaccine-associated poliomyelitis.

The finding of sustained circulation of wild type poliovirus in Israel shows that the virus can circulate silently in a population that has been well immunized with IPV. Such circulation occurs because IPV does not sufficiently protect the intestinal tract against poliovirus infection. However poliomyelitis does not occur in such populations because IPV-induced antibodies in the blood prevent virus invasion into the central nervous system. The US now exclusively uses IPV and it is likely that wild polioviruses are present in US sewage, although as mentioned above the US does not search for poliovirus in sewage. Silent circulation of wild type poliovirus in countries that use IPV poses a threat to other countries where immunization coverage is low.

These findings indicate that immunization with IPV will not lead to eradication of wild type poliovirus. This observation is problematic because the World Health Organization has recommended a gradual shift from OPV to IPV. In the past I have also supported such a transition, but I have also remained cautious about the ability of IPV to immunize the human gut. The experience in Israel confirms my suspicions.

The US shifted from using OPV to IPV because the associated vaccine-associated poliomyelitis was not acceptable in a country with no paralytic disease caused by wild type poliovirus. Now it seems that eradication cannot be achieved with IPV. What can be done about this conundrum? OPV should be used to eradicate remaining pools of wild type poliovirus in endemic countries (Nigeria, Afghanistan, Pakistan). At the same time environmental surveillance must be done in all countries that exclusively use IPV. If wild type poliovirus is found in the sewage of such countries, then introduction of OPV, in children previously immunized with IPV, should be considered to eliminate the reservoir of will type virus. It will be important to observe the effect of the distribution of OPV in Israel on the circulation of wild type poliovirus.

*Infectious poliovirus was isolated by adding sewer and stool filtrates to monolayers of L20B cells, which are mouse fibroblasts that produce the cellular receptor for poliovirus. These cells were produced in my laboratory, and are useful for isolating polioviruses because they are not susceptible to infection with non-polio enteroviruses. I am pleased to be able to contribute to efforts to control poliomyelitis.

TWiV 286: Boston TWiV party

On episode #286 of the science show This Week in Virology, Vincent and Alan meet up with Julie and Paul at the General Meeting of the American Society for Microbiology in Boston, to talk about their work on the pathogenesis of poliovirus and measles virus.

You can find TWiV #286 at www.microbe.tv/twiv.

Should variola virus, the agent of smallpox, be destroyed?

variola virusLater this month (May 2014) the World Health Assembly will decide whether to destroy the remaining stocks of variola virus – the agent of smallpox – or to allow continued research on the virus at WHO-approved laboratories.

After the eradication of smallpox in 1980, the World Health Organization called for destruction of known remaining stocks of variola virus. The known remaining stocks of the virus are closely guarded in the United States and Russia. These consist not of a single vial of the virus, but of hundreds of different strains, many of which have not been fully characterized, nor has their genome sequence been determined.

It can be argued that there still remains a good deal of work to be done on variola virus, including development of newer diagnostic tests, and identification of additional countermeasures (antivirals and vaccines have been stockpiled in the US). Damon, Damaso, and McFadden have written a summary of the research on variola virus that should be done. We also discussed whether the remaining variola virus stocks should be destroyed on episode #284 of This Week in Virology.

We are interested in what readers of this blog think about this issue – please fill out the poll below.

Should all known remaining stocks of variola virus, agent of smallpox, be destroyed?

India has been free of polio for three years

Poliovirus cutaway

Image credit: Jason Roberts

Three years ago today, on 13 January 2011, the last case of poliomyelitis was reported in India. This achievement represents a remarkable turnaround for a country where control of the disease had for years been extremely difficult. As recently as 2009 there were 741 confirmed cases of polio caused by wild-type virus in India. Being polio-free for three years is certainly a cause for celebration, but not for becoming complacent. Immunization efforts in India must not decline, because wild-type and vaccine-derived polioviruses continue to circulate and pose a threat to any unimmunized individual.

Wild polioviruses – those that have always been circulating in nature – continue to cause disease in Afghanistan and Pakistan, two countries close to India. Pakistan reported 58 polio cases in 2012, and 85 so far in 2013; for Afghanistan the numbers are 37 and 12. But distant countries can also transmit polio: recent outbreaks in the Horn of Africa and in Syria originated in Nigeria and Pakistan, respectively.

Perhaps a greater threat are vaccine-derived polioviruses. The Sabin poliovirus vaccines, which have so far been the mainstay of the polio eradication effort, comprise infectious viruses that are taken orally. Upon replication in the intestinal tract, the vaccine strains confer immunity to infection, but they also revert and become capable of causing paralysis. Such vaccine-derived polioviruses circulate and can cause outbreaks of polio. Because India has been using Sabin poliovirus vaccines intensely for many years, there is no doubt that vaccine-derived polioviruses are circulating in that country. If polio vaccine coverage drops, there will be outbreaks of polio caused by vaccine-derived strains. Even if wild polioviruses disappeared from the globe, as long as Sabin vaccines are used, vaccine-derived polioviruses will circulate. The solution to this conundrum is to switch to Salk’s inactivated poliovirus vaccine and wait for the Sabin-derived strains to disappear. This switch is now part of the WHO’s eradication plan (it wasn’t always), but it will not be easy: Salk vaccine must be injected, and therefore requires trained health care personnel; administering Sabin vaccine requires no special skills. But we cannot simply stop immunizing with Sabin vaccine – that is a recipe for outbreaks of polio.

According to the World Health Organization, being free of wild polio for three years means that the virus is probably no longer endemic in India. However, WHO does not certify individual countries as polio-free; rather it declares a WHO region polio-free when all countries in the Region have not reported a case of wild polio for 3 years in the face of highly active surveillance. The Americas, the Western Pacific, and European regions have been declared polio-free by WHO. India is part of the South-East Asia region, which also includes Bangladesh, Bhutan, Democratic People’s Republic of Korea, Indonesia, Maldives, Myanmar, Nepal, Sri Lanka, Thailand, and Timor-Leste, none of which have reported a case of polio for 3 years. WHO will decide in March whether to declare this region polio-free. That would leave the regions of Africa and the Eastern Mediterranean as the last known reservoirs of wild poliovirus.

World Polio Day

gold poliovirus

Image credit: Jason Roberts

As a virologist who has worked on poliovirus since 1979, I would be remiss if I did not note that today, 24 October, is World Polio Day. World Polio Day was established by Rotary International over a decade ago to commemorate the birth of Jonas Salk, who led the first team to develop a vaccine against poliomyelitis.

The polio eradication effort has made impressive progress towards eliminating polio from the planet. In 1988 it was estimated that there were a total of 350,000 cases of poliomyelitis (probably an underestimate); as of this writing there have been 301 cases in 2013, which is unfortunately already more than in all of 2012 (223). Some setbacks to the program include an outbreak in the Horn of Africa, the finding of wild poliovirus (but no paralytic cases) in Israel, and two suspected cases in Syria. Transmission of wild poliovirus has never been interrupted in three countries: Afghanistan, Nigeria, and Pakistan. The good news is that India remains polio-free, a remarkable achievement.

Currently the eradication effort mainly utilizes the Sabin oral poliovirus vaccine strains (OPV). These vaccines are taken orally and replicate in the intestine, followed by entry into the bloodstream. They induce antiviral immunity in both the intestine and the blood. However, a drawback to using the Sabin vaccines is that the viruses revert to neurovirulence during replication in the intestine. As a consequence, virulent polioviruses are shed in the feces. These can cause poliomyelitis, either in the vaccine recipient or in unimmunized contacts. As wild polioviruses are eliminated, vaccine-derived polioviruses will continue to circulate, necessitating ‘vaccinating against the vaccine’. As a consequence, WHO has proposed a switch to the inactivated poliovirus vaccine, IPV, which if prepared properly cannot cause poliomyelitis.

A very good question is whether the use of IPV can lead to elimination of poliovirus from the planet. Consider the following scenario: at some point in the future the use of Sabin vaccines is discontinued, and all polio immunizations are done with IPV. Vaccine-derived polioviruses will still be present, and possibly also wild polioviruses. As shown by the recent detection of poliovirus in Israel, poliovirus can replicate in the intestines of individuals who have been immunized with IPV. Therefore, in a post-OPV world, immunization with IPV will still allow circulation of vaccine-derived polioviruses. As long as immunization continues at a high rate, there should be no cases of paralytic disease – but we already know that high immunization coverage is difficult to maintain. How long will we need to immunize with IPV before circulation of vaccine-derived polioviruses will stop?

Below are links to resources on polio, provided by David Gold at Global Health Strategies:

  • An expert panel including Dr. Bruce Aylward, WHO’s Assistant Director-General for Polio, will discuss the status of eradication today at Rotary International’s ‘Making History‘ event. Help share and watch live at 6:30 PM ET.
  • Look out for A Shot to Save the World, a documentary about Jonas Salk’s vaccine discovery, airing on the Smithsonian Channel today at 8:00 pm ET/PT.
  • President-elect of the Asia Pacific Pediatric Association Naveen Thacker wrote an opinion piece on India’s incredible achievements against polio, and the benefits and lessons India’s experience offers. Help share his piece.
  • Check out a video by footballer Leo Messi (tweet), a blog post by Paralympian polio-survivor Dennis Ogbe (tweet), a Vaccines Today blog post by Ramesh Ferris (tweet) and an Impatient Optimists post on other ways to get involved today.
  • Pakistan: Thanks to the work of heroic vaccinators, Pakistan has eliminated polio from much of the country. This year, 74% of cases, and 93% during the high season, have occurred in one region: the Federally Administered Tribal Areas (FATA) of northern Pakistan. North Waziristan, in FATA, has been inaccessible since June 2012, and has reported 14 wild polio cases this year in an increasingly severe outbreak. The program is intensifying immunizations in neighboring areas to prevent spread, but continued inaccessibility in this region poses a serious risk to the global effort.
  • Nigeria: Challenges persist in northern Nigeria, particularly in Borno and Kano, but other traditional reservoir areas appear to be largely polio-free — reminders that success is possible. Of particular importance, the northwest of the country, from which polio has historically spread into West Africa, has not had any cases this year. Read and help share a recent Science article (available with free registration) that takes an in-depth look at Nigeria’s eradication efforts.
  • Afghanistan: Afghanistan’s traditionally endemic Southern Region remains polio-free, with all cases this year linked to cross-border transmission with Pakistan. Next month will mark one year since the last case was recorded in the Southern Region.
  • Horn of Africa: GPEI partners responded rapidly to the outbreak, and we’re seeing signs of progress: there have been no confirmed cases in the Banadir region of Somalia, the epicenter of the outbreak, or in Kenya, since August. The number of unimmunized individuals in the region still poses a major risk for further spread. Outbreak response will continue aggressively into 2014.
  • Possible Polio Cases Detected in Syria: Syria reported a cluster of possible polio cases on 17 October that is currently being investigated. The country has been polio-free since 1999, but is considered at high risk for polio due to declining immunization rates. Syria’s Ministry of Health is preparing an urgent response across the country, aiming to conduct the first campaign by the end of October. Supplementary immunization activities are being planned in neighboring countries, including Lebanon, Jordan, Egypt, southern Turkey and western Iraq. The GPEI has a history of eliminating polio in areas of insecurity. Drawing from past successful efforts in insecure areas, including El Salvador and Angola, the Strategic Plan outlines approaches to eliminating polio in areas of conflict that are informing Syria’s response.
  • IMB Report: The International Monitoring Board (IMB), tasked with assessing the GPEI effort each quarter, met earlier this month to review the program’s progress, challenges and risks in endemic countries, the Horn of Africa and Israel. The IMB’s report from this meeting will be available here on Friday, 25 October