Everything about Polio Vaccine totally explained
Two
polio vaccines are used throughout the world to combat
polio. The first was developed by
Jonas Salk, first tested in
1952, and announced to the world by Salk on
April 12,
1955. It consists of an injected dose of inactivated (dead)
poliovirus. The second was an oral vaccine developed by
Albert Sabin using
attenuated poliovirus that he'd received from
Hilary Koprowski.
Human trials of Sabin's vaccine began in
1957 and it was licensed in
1962. The two vaccines have
eradicated polio from most of the countries in the world and reduced the worldwide incidence from an estimated 350,000 cases in
1988 to just over 1000 cases in
2007.
The "great race"
In 1936 Maurice Brodie, a research assistant at
New York University, attempted to produce a
formaldehyde-killed polio vaccine from ground-up monkey spinal cords. His initial attempts were hampered by the difficulty of obtaining enough virus. Brodie first tested the vaccine on himself and several of his assistants. He then gave the vaccine to three thousand children: many developed allergic reactions, but none developed immunity to polio. Philadelphia pathologist John Kollmer also claimed to have developed a vaccine that same year, but it too produced no immunity and was blamed for causing a number of cases, some of them fatal.
A breakthrough came in
1948 when a research group headed by
John Enders at the
Children's Hospital Boston successfully cultivated the
poliovirus in human tissue in the laboratory. This development greatly facilitated vaccine research and ultimately allowed for the development of vaccines against polio. Enders and his colleagues,
Thomas H. Weller and
Frederick C. Robbins, were recognized for their labors with a
Nobel Prize in Physiology or Medicine in 1954. Other important advancements that lead to the development of polio vaccines were: the identification of three poliovirus serotypes (Poliovirus type 1 (PV1 or Mahoney), PV2 (Lansing), and PV3 (Leon)), the finding that preceding paralysis, the virus must be present in the blood, and the demonstration that administration of antibodies in the form of gamma-globulin protects against paralytic polio.
In 1952 and 1953, the U.S. experienced an outbreak of 58,000 and 35,000 polio cases, respectively, up from a typical number of some 20,000 cases a year. Amid this U.S. polio epidemic, millions of dollars were invested in finding and marketing a polio vaccine by commercial interests, including Lederle Laboratories in New York under the direction of
H. R. Cox.
Polish-born virologist and immunologist
Hilary Koprowski, who also worked at Lederle, claims to have created the first successful polio vaccine (in 1950) but his vaccine, a live attenuated virus taken orally, was still in the research stage and wouldn't be ready for use until five years after Jonas Salk's polio vaccine (a dead injectable vaccine) reached the market.
The samples of difficult-to-manufacture attenuated virus that
Albert Sabin used to develop his oral polio vaccine were given to him by
Hilary Koprowski. "Koprowski would later complain that the polio vaccine he'd discovered became known as the Sabin vaccine." Koprowski's own vaccine was ultimately tested, but the outcome was a failure. After the attenuated live virus entered the body, it sometimes reverted to a
virulent state. Nevertheless, from 1957 to 1960, large-scale tests were carried out in the
Congo. The results have been controversial, and
accusations in the 1990s arose that the vaccine created the conditions necessary for the transmission of
SIV from
chimpanzees to humans, causing
HIV/AIDS. This hypothesis has, however,
been refuted.
The development of two polio vaccines led to the first modern mass
inoculations. The last cases of paralytic poliomyelitis caused by endemic transmission of
wild virus in the United States were in 1979, when an outbreak occurred among the
Amish in several
Midwest states. The disease was entirely eradicated in
the Americas by 1994.
Salk's "inactivated polio vaccine"
The first effective polio vaccine was developed in 1952 by
Jonas Salk at the
University of Pittsburgh. The Salk vaccine, or
inactivated poliovirus vaccine (IPV), is based on three wild,
virulent reference strains, Mahoney (type 1 poliovirus), MEF-1 (type 2 poliovirus), and Saukett (type 3 poliovirus), grown in a type of monkey
kidney tissue culture (
Vero cell line), which are then inactivated with
formalin. By the conclusion of the study, roughly 440,000 received one or more injections of the vaccine, about 210,000 children received a
placebo, consisting of harmless
culture media, and 1.2 million children received no vaccination and served as a control group, who would then be observed to see if any contracted polio. Soon after Salk's vaccine was licensed in 1955 children's vaccination campaigns were launched. In the U.S, following a mass immunization campaign promoted by the
March of Dimes, the annual number of polio cases fell to 5,600 by 1957. The IPV vaccine was used extensively in the U.S. until the early 1960s. An enhanced-
potency IPV was licensed in the United States in November 1987, and is currently the vaccine of choice in the United States. The OPV is a live-
attenuated vaccine, produced by the passage of the virus through non-human cells at a sub-
physiological temperature, which produces spontaneous mutations in the viral genome.
There are 57
nucleotide substitutions which distinguish the attenuated Sabin 1 strain from its virulent parent (the Mahoney serotype), two nucleotide substitutions attenuate the Sabin 2 strain, and 10 substitutions are involved in attenuating the Sabin 3 strain. which alters
stem-loop structures, and reduces the ability of poliovirus to translate its RNA template within the host cell.
The attenuated poliovirus in the Sabin vaccine replicates very efficiently in the gut, the primary site of infection and replication, but is unable to replicate efficiently within
nervous system tissue. The OPV proved to be superior in administration, and also provided longer lasting
immunity than the Salk vaccine.
Iatrogenic (vaccine-induced) polio
A major concern attributable to the oral polio vaccine (OPV) is that it can revert to a virulent form. Clinical disease caused by vaccine-derived poliovirus (VDPV) is indistinguishable from that caused by wild polioviruses. This is believed to be a rare event, but outbreaks of vaccine-derived poliovirus (VDPV) have been reported, and tend to occur in areas of low coverage by OPV, presumably because the OPV is itself protective against the related outbreak strain. Reversion isn't possible in IPV vaccinations used in the U.S., and thus vaccine-induced polio isn't a concern.
The rate of vaccine-associated paralytic poliomyelitis (VAPP) varies by region but is generally about 1 case per 750,000 vaccine recipients. VAPP is more likely to occur in adults than in children. In
immunodeficient children, the risk of VAPP is almost 7,000 times higher, particularly for persons with
B-lymphocyte disorders (for example,
agammaglobulinemia and
hypogammaglobulinemia), which reduce the synthesis of protective
antibodies.
Outbreaks of VAPP occurred independently in
Belarus (1965–66),
Egypt (1983–1993),
Hispaniola (2000–2001),
Philippines (2001),
Madagascar (2001–2002), and in
Haiti (2002), where political strife and poverty have interfered with vaccination efforts. In 2006 an outbreak of vaccine-derived poliovirus occurred in
China. Cases have been reported from
Cambodia (2005-2006),
Myanmar (2006-2007), Iran (1995, 2005-2007), Syria, Kuwait and Egypt, while in northern Nigeria, 69 cases were reported in 2007.
Vaccination schedule
Following the widespread use of poliovirus vaccine in the mid-1950s, the incidence of poliomyelitis declined rapidly in many industrialized countries. As the incidence of wild polio diminishes, nations transition from use of the oral vaccine back to the injected vaccine because the risk of latrogenic polio outweighs the risk of subclinical transmission.
The use of OPV was discontinued in the United States in 2000, but it continues to be used around the globe.
The first dose of polio vaccine is given shortly after birth, usually between 1-2 months of age, a second dose is given at 4 months of age. In some countries a fifth vaccination is given during
adolescence.
The development of immunity to polio efficiently blocks person-to-person transmission of wild poliovirus, thereby protecting both individual vaccine recipients and the wider community. Because there's no long term
carrier state for poliovirus in immunocompetent individuals, polioviruses have no non-primate reservoir in nature, and survival of the virus in the environment for an extended period of times appears to be remote, interruption of person-to person transmission of the virus by vaccination is the critical step in global polio eradication.
Contamination concerns
In 1960, it was determined that the
rhesus monkey kidney cells used to prepare the poliovirus vaccines were infected with a virus called
SV40 (or Simian Virus-40). SV40, also discovered in 1960, is a naturally occurring
virus that infects monkeys. In 1961, SV40 was found to cause tumors in
rodents. More recently, the virus was found in certain forms of
cancer in humans, for instance
brain and
bone tumors,
mesotheliomas, and some types of
non-Hodgkin's lymphoma. However, it hasn't been determined that SV40 causes these cancers.
SV40 was found to be present in stocks of the injected form of the polio vaccine (IPV) in use between 1954 to 1962. It isn't found in the OPV form (which was licensed later). Over 98 million Americans received one or more doses of polio vaccine between 1955 to 1963 when a proportion of vaccine was contaminated with SV40; it has been estimated that 10 - 30 million Americans may have received a dose of vaccine contaminated with SV40.
In 1998, the
National Cancer Institute undertook a large study, using cancer case information from the Institutes SEER database. The published findings from the study revealed that there was no increased incidence of cancer in persons who may have received vaccine containing SV40. Another large study in Sweden examined cancer rates of 700,000 individuals who had received potentially contaminated polio vaccine as late as 1957; the study again revealed no increased cancer incidence between persons who received polio vaccines containing SV40 and those who did not. The question of whether SV40 causes cancer in humans remains controversial however, and the development of improved assays for detection of SV40 in human tissues, will be needed to resolve the controversy. If this long-term public-health goal is achieved, poliomyelitis would join
smallpox as only the second infectious disease of humans to be eradicated worldwide, and should make subsequent polio vaccinations unnecessary.
By 2004, cases of poliomyelitis in Africa had been reduced to just a small number in isolated regions of in the western portion of the continent, with sporadic cases elsewhere. However, recent opposition to vaccination campaigns have evolved, often relating to fears that the vaccine might induce
sterility. The disease has since resurged in
Nigeria and in several other African nations, which some
epidemiologists cite is due to refusals by certain local populations to allow their children to receive the polio vaccine. Some public-health workers argue that debates relating to the
OPV AIDS hypothesis have further fueled vaccination fears among contemporary Africans.
Polio is also endemic in areas of India and Pakistan, and has again spread into Bangladesh. Recent studies by the
Indian Medical Association suggest that some OPV preparations currently in use there are inducing vaccine-associated paralytic poliomyelitis (VAPP) among vaccine recipients at rates not before seen in prior vaccination campaigns, with at least 70 confirmed cases of vaccine-derived disease in Nigeria in 2006, and at least 1600 cases in India. Although the exact cause of this vaccine-derived outbreak hasn't been determined, at least some public-health authorities in India are recommending discontinuing use of live-virus OPV in favor of more costly IPV in future polio eradication efforts there.
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