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Picornaviruses are small (20–30 nm) nonenveloped viruses composed of an icosahedral nucleocapsid and a single-stranded RNA genome. The genome RNA has positive polarity (i.e., on entering the cell, it functions as the viral mRNA). There is no polymerase within the virion. Picornaviruses replicate in the cytoplasm of cells. They are not inactivated by lipid solvents, such as ether, because they do not have an envelope. The picornavirus family includes two groups of medical importance: the enteroviruses and the rhinoviruses. Among the major enteroviruses are poliovirus, coxsackie viruses, echoviruses, and hepatitis A virus. Enteroviruses infect primarily the enteric tract, whereas rhinoviruses are found in the nose and throat (rhino = nose). Enteroviruses replicate optimally at 37°C, whereas rhinoviruses grow better at 33°C, in accordance with the lower temperature of the nose. Enteroviruses are stable under acid conditions (pH 3–5), which enables them to survive exposure to gastric acid, whereas rhinoviruses are acid-labile. This explains why rhinovirus infections are restricted to the nose and throat.
This virus causes poliomyelitis. The host range is limited to primates (i.e., humans and non-human primates such as apes and monkeys). The virion interacts with specific cell receptors on the cell membrane and then enters the cell. Poliovirus is transmitted by the fecal–oral route. It replicates in the oropharynx and intestinal tract. Humans are the only natural hosts. After replicating in the oropharynx and small intestine, especially in lymphoid tissue, the virus spreads through the bloodstream to the central nervous system. It can also spread retrograde along nerve axons. In the central nervous system, poliovirus preferentially replicates in the motor neurons located in the anterior horn of the spinal cord. Death of these cells results in paralysis of the muscles innervated by those neurons. The range of responses to poliovirus infection includes (1) inapparent, asymptomatic infection; (2) abortive poliomyelitis; (3) nonparalytic poliomyelitis; and (4) paralytic poliomyelitis. Asymptomatic infection is quite common. Roughly 1% of infections are clinically apparent. The incubation period is usually 10 to 14 days. The most common clinical form is abortive poliomyelitis, which is a mild, febrile illness characterized by headache, sore throat, nausea, and vomiting. Most patients recover spontaneously. Nonparalytic poliomyelitis manifests as aseptic meningitis with fever, headache, and a stiff neck.
The diagnosis is made either by isolation of the virus or by a rise in antibody titer. Virus can be recovered from the throat, stool, or spinal fluid by inoculation of cell cultures. The virus causes a cytopathic effect (CPE) and can be identified by neutralization of the CPE with specific antisera. There is no antiviral therapy. Treatment is limited to symptomatic relief and respiratory support, if needed. Physiotherapy for the affected muscles is important. Poliomyelitis can be prevented by both the killed vaccine (Salk vaccine, inactivated vaccine, IPV) and the live, attenuated vaccine (Sabin vaccine, oral vaccine, OPV). The current version of the inactivated vaccine is called enhanced polio vaccine, or eIPV. Live vaccine has four disadvantages: (1) Rarely, reversion of the attenuated virus to virulence will occur, and disease may ensue (especially for the type 3 virus). (2) It can cause disease in immunodeficient persons and therefore should not be given to them. (3) Infection of the gastrointestinal tract by other enteroviruses can limit replication of the vaccine virus and reduce protection. (4) It must be kept refrigerated to prevent heat inactivation of the live virus.
Coxsackie viruses are named for the town of Coxsackie, NY, where they were first isolated. Coxsackie viruses cause a variety of diseases. Group A virus’s cause, for example, herpangina, acute hemorrhagic conjunctivitis, and hand-foot-and-mouth disease, whereas group B viruses cause pleurodynia, myocarditis, and pericarditis. The size and structure of the virion and the nature of the genome RNA are similar to those of poliovirus. The classification of Coxsackie viruses into group A or B is based on pathogenicity in mice. Coxsackie viruses are transmitted primarily by the fecal–oral route, but respiratory aerosols also play a role. Group A viruses have a predilection for skin and mucous membranes, whereas group B viruses cause disease in various organs such as the heart, pleura, pancreas, and liver. Both group A and B viruses can affect the meninges and the motor neurons (anterior horn cells) to cause paralysis. Both groups of viruses can cause aseptic meningitis, mild paresis, and acute flaccid paralysis similar to poliomyelitis. Upper respiratory infections, pharyngitis, and minor febrile illnesses with or without rash can occur also. The diagnosis is made either by isolating the virus in cell culture or suckling mice or by observing a rise in titer of neutralizing antibodies. A rapid (2.5-hour) polymerase chain reaction (PCR)–based test for enteroviral RNA in the spinal fluid is useful for making a prompt diagnosis of viral meningitis because culture techniques typically take days to obtain a result. There is neither antiviral drug therapy nor a vaccine available against these viruses. No passive immunization is recommended.
The prefix ECHO is an acronym for enteric cytopathic human orphan. Although called “orphans” because they were not initially associated with any disease, they are now known to cause a variety of diseases such as aseptic meningitis, upper respiratory tract infection, febrile illness with and without rash, infantile diarrhea, and hemorrhagic conjunctivitis. The structure of echoviruses is similar to that of other enteroviruses. More than 30 serotypes have been isolated. In contrast to Coxsackie viruses, they are not pathogenic for mice. Unlike polioviruses, they do not cause disease in monkeys. They are transmitted by the fecal–oral route and occur worldwide. Pathogenesis is similar to that of the other enteroviruses. Along with Coxsackie viruses, echoviruses are one of the leading causes of aseptic (viral) meningitis. The diagnosis is made by isolation of the virus in cell culture. Serologic tests are of little value, because there are a large number of serotypes and no common antigen. There is no antiviral therapy or vaccine available. In view of the difficulty in classifying many enteroviruses, all new isolates have been given a simple numerical designation since 1969. Enterovirus 70 is the main cause of acute hemorrhagic conjunctivitis, characterized by petechial hemorrhages on the bulbar conjunctivas. Complete recovery usually occurs, and there is no therapy. Enterovirus 71 is one of the leading causes of viral central nervous system disease, including meningitis, encephalitis, and paralysis. It also causes diarrhea, pulmonary hemorrhages, hand-foot-and-mouth disease, and herpangina.