Inactivated vaccine
The first effective polio vaccine was developed in 1952 by Jonas Salk at the University of Pittsburgh. But it needed years of testing. To encourage patience, Salk went on CBS radio to report a successful test on a small group of adults and children on March 26, 1953; two days later the results were published in JAMA.[22]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.[6] The injected Salk vaccine confers IgG-mediated immunity in the bloodstream, which prevents polio infection from progressing to viremia and protects the motor neurons, thus eliminating the risk of bulbar polio and post-polio syndrome.
Beginning February 23, 1954, the vaccine was tested at Arsenal Elementary School and the Watson Home for Children in Pittsburgh, Pennsylvania.[23] Salk's vaccine was then used in a test called the Francis Field Trial, led by Thomas Francis; the largest medical experiment in history. The test began with some 4,000 children at Franklin Sherman Elementary School in McLean, Virginia,[24] and would eventually involve 1.8 million children, in 44 states from Maine to California.[25] 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.[13] The results of the field trial were announced April 12, 1955 (the tenth anniversary of the death of Franklin D. Roosevelt; see Franklin D. Roosevelt's paralytic illness). The Salk vaccine had been 60 - 70% effective against PV1 (poliovirus type 1), over 90% effective against PV2 and PV3, and 94% effective against the development of bulbar polio.[26] 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 from 35,000 in 1953 to 5,600 by 1957.[27] By 1961 only 161 cases were recorded in the United States.[28]
An enhanced-potency IPV was licensed in the United States in November 1987, and is currently the vaccine of choice in the United States.[16] 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.[16] The timing of the third dose depends on the vaccine formulation but should be given between 6–18 months of age.[29] A booster vaccination is given at 4 to 6 years of age, for a total of four doses at or before school entry.[30] In some countries, a fifth vaccination is given during adolescence.[29] Routine vaccination of adults (18 years of age and older) in developed countries is neither necessary nor recommended because most adults are already immune and have a very small risk of exposure to wild poliovirus in their home countries.[16]
In 2002, a pentavalent (5-component) combination vaccine (called Pediarix) containing IPV was approved for use in the United States. The vaccine also contains combined diphtheria, tetanus, and acellular pertussis vaccines (DTaP) and a pediatric dose of hepatitis B vaccine.[16] In the UK, IPV is combined with tetanus, diphtheria, pertussis and Haemophilus influenzae type b vaccines.[29] When the current formulation of IPV is used, 90% or more of individuals develop protective antibody to all three serotypes of poliovirus after two doses of inactivated polio vaccine (IPV), and at least 99% are immune to poliovirus following three doses. The duration of immunity induced by IPV is not known with certainty, although a complete series is thought to provide protection for many years.[31]
Oral vaccine
Oral polio vaccine (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.[32] Oral polio vaccines were developed by several groups, one of which was led by Albert Sabin. Other groups, led by Hilary Koprowski and H.R. Cox, developed their own attenuated vaccine strains. In 1958, the National Institutes of Health created a special committee on live polio vaccines. The various vaccines were carefully evaluated for their ability to induce immunity to polio, while retaining a low incidence of neuropathogenicity in monkeys. Based on these results, the Sabin strains were chosen for worldwide distribution.[13]
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.[6] The primary attenuating factor common to all three Sabin vaccines is a mutation located in the virus's internal ribosome entry site (IRES)[33] which alters stem-loop structures, and reduces the ability of poliovirus to translate its RNA template within the host cell.[34] 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. OPV also proved to be superior in administration, eliminating the need for sterile syringes and making the vaccine more suitable for mass vaccination campaigns. OPV also provided longer lasting immunity than the Salk vaccine.
In 1961, type 1 and 2 monovalent oral poliovirus vaccine (MOPV) was licensed, and in 1962, type 3 MOPV was licensed. In 1963, trivalent OPV (TOPV) was licensed, and became the vaccine of choice in the United States and most other countries of the world, largely replacing the inactivated polio vaccine.[8] A second wave of mass immunizations led to a further dramatic decline in the number of polio cases. Between 1962 and 1965 about 100 million Americans (roughly 56% of the population at that time) received the Sabin vaccine. The result was a substantial reduction in the number of poliomyelitis cases, even from the much reduced levels following the introduction of the Salk vaccine.[35]
OPV is usually provided in vials containing 10-20 doses of vaccine. A single dose of oral polio vaccine (usually two drops) contains 1,000,000 infectious units of Sabin 1 (effective against PV1), 100,000 infectious units of the Sabin 2 strain, and 600,000 infectious units of Sabin 3. The vaccine contains small traces of antibiotics— neomycin and streptomycin—but does not contain preservatives.[36] One dose of OPV produces immunity to all three poliovirus serotypes in approximately 50% of recipients.[16] Three doses of live-attenuated OPV produce protective antibody to all three poliovirus types in more than 95% of recipients. OPV produces excellent immunity in the intestine, the primary site of wild poliovirus entry, which helps prevent infection with wild virus in areas where the virus is endemic.[30] The live virus used in the vaccine is shed in the stool and can be spread to others within a community, resulting in protection against poliomyelitis even in individuals who have not been directly vaccinated. IPV produces less gastrointestinal immunity than does OPV, and primarily acts by preventing the virus from entering the nervous system. In regions without wild poliovirus, inactivated polio vaccine is the vaccine of choice.[30] In regions with higher incidence of polio, and thus a different relative risk between efficacy and reversion of the vaccine to a virulent form, live vaccine is still used. The live virus also has stringent requirements for transport and storage, which are a problem in some hot or remote areas. As with other live-virus vaccines, immunity initiated by OPV is probably lifelong.[31]
(Source from en.Wikipedia.org/wiki/Polio_vaccine)
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