Picornavirus
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Second millennium disease: Poliomyelitis is believed to be an ancient disease. It has been suggested that the depiction of a young man with an atrophic limb on an Egyptian stele from the second millennium BC represents a sequela of poliomyelitis.
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In the 8th century, a letter from Pope Zacharias to Archbishop St. Boniface of Mainz describes an outbreak of jaundice which is thought to be hepatitis A.
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In the 1800s, poliomyelitis was clinically described for the first time.
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Foot-and-mouth disease virus was the first animal virus to be discovered, by Loeffler and Frosch in 1898.
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Poliovirus was isolated in 1908 during an epidemic poliomyelitis outbreak in the early 20th century.
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In the period from 1900 to 1910, Wickman and others recognized the communicable nature of poliomyelitis, the importance of asymptomatic infected individuals in transmission of PV, and the role of enteric infection in disease pathogenesis.
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In 1912, Cockayne used the term infectious hepatitis to describe this epidemic form of jaundice.
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In 1914 Kruse showed that cell-free filtrates of nasal secretions from affected individuals could transmit colds.
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In 1930, Dochez et al.50 confirmed Kruse’s findings by transmitting colds to volunteers and apes using filtered nasal secretions that were free of bacteria. This indicated a viral etiology.
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During the 1930s, Trask , who formed the Polyomyelitis Study Unit at Yale, showed the role of the gastrointestinal tract in the initiation and spread of PV infection.
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During and after WWII, epidemiological studies and human volunteer experiments were conducted that confirmed the viral cause of hepatitis A, indicated its short incubation period and its fecal–oral mode of transmission. These studies also showed that Hep A was different from homologous serum jaundice, another form of hepatitis.
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In 1947, MacCallum introduced the terms hepatitis A and hepatitis B.
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In 1946, Common Cold Unit (CCU) by the UK Medical Research Council was established, thus accelerating progression of research that would lead to discovery of rhinoviruses.
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1947 Coxsackieviruses (group A) were first isolated during poliomyelitis outbreaks in 1947 from the feces of paralyzed children in Coxsackie, New York.
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In 1948, the first coxsackievirus (CV) group B was isolated from cases of aseptic meningitis.
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In 1949, scientists discovered that poliovirus could be propagated in cultured cells. The plaque assay, a method for quantification of viral infectivity, was developed with poliovirus.
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In 1951, echoviruses were first isolated from the stool of asymptomatic individuals.
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In 1952, the Polio epidemic in the US affected more than 50000 people and paralyzed more than 20000 people.
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In 1955, The Salk vaccine was licensed for Polio in the US.
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In 1956, Rhinoviruses were discovered by two groups working independently.
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In 1961, The Sabin vaccine for Polio was licensed in the US.
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In 1963, Franklin discoveredRNA-dependent RNA polymerase by studying mengovirus, a picornavirus.
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Between the mid-1950s and early 1970s, the studies of Murray and of Krugman et al at the Willowbrook State School for the mentally handicapped defined the seroepidemiologic relationships between hepatitis A and B.
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In 1967, Deinhardt et al provided the first evidence for propagation of Hepatitis A Virus(HAV) in small primates. This lead to the subsequent recovery of the CR326 strain of human HAV from an experimentally infected Saguinus mystax.
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In 1967, a collaborative program classified the known rhinoviruses into 55 different serotypes.
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In 1972, rhinovirus serotypes 56 through 89 were classified.
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In 1973, Feinstone identified Hepatitis A in feces of infected patients by using immune electron microscopy.
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In 1973, the WHO Expert Committee on Viral Hepatitis adopted the names Hepatitis A and B.
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In 1979, Provost and Hilleman successfully cultivated and serially passaged the CR326 Hepatitis A strain in cell culture for the first time.
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In 1981 the Poliovirus genome was published for the first time by David Baltimore and Vincent Racaniello.
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In 1981 Racaniello and Baltimore made the first infectious DNA clone of an animal RNA virus, which was poliovirus.
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In the 1980s, the synthesis of a precursor polyprotein from which viral proteins are derived by proteolytic processing was first identified in poliovirus-infected cells.
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In 1985 Bonneau showed that poliovirus lacked the 5’ cap structure. It was the first messenger RNA (mRNA) shown to lack a 5′ cap structure. This observation was subsequently explained by the finding that the genome RNA of poliovirus and other picornaviruses is translated by internal ribosome binding, a process now known to occur on cellular mRNA.
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In 1987, the remainder of the classical rhinovirus serotypes were added.
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In 1988, the WHO started a global polio eradication campaign.
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In 1989, Mendelsohn et al. identified the PV receptor, CD155, a finding that was followed by the generation of mice carrying CD155 as a transgene.
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In 1999, Type 2 Poliovirus was eradicated.
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In 2002, Eckert Wimmer’s group made the world’s first synthetic virus, a poliovirus.
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In 2012, the last case of Type 3 Poliovirus was reported.
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In the last 15 years, the introduction of molecular detection methods, and the last 15 years have seen a rapid expansion in the number of recognized enteroviruses.