Picornaviruses are small, naked (nonenveloped), icosahedral viruses (Figure 1), which contain a single-stranded, nonsegmented RNA genome and four structural proteins. Picornaviridae are divided into five genera: enteroviruses, rhinoviruses, cardioviruses, aphthoviruses, and hepatoviruses. Cardiovirus species cause encephalitis and myocarditis in mice, whereas Aphthovirus species is represented by “foot-and mouth” disease virus, which infects cattle. Enterovirus, Rhinovirus, and Hepatovirus species cause a wide variety of clinical syndromes in humans. Although the most intensively studied picornavirus is poliovirus, what has been learned about the structure and replication of poliovirus also applies in large measure to the other viruses in this family.

Fig1. Poliovirus, a type of Picornavirus, is one of the simplest and smallest viruses.

A. Enterovirus

More than seventy enteroviruses have been identified. Currently, as new enteroviruses are identified, they are not assigned to one of these groups but are simply given numerical designations (for example, enterovirus 68, enterovirus 69, and so forth).

1. Epidemiology: Individuals are infected with enteroviruses by ingestion of contaminated food or water. Enteroviruses are stable at the low pH of the stomach, replicate in the gastrointestinal (GI) tract, and are excreted in the stool. Thus, these viruses are said to be transmitted by the fecal–oral route. The virus can replicate in a variety of tissues. For example, after replicating in the oropharynx and intestinal tract lymphoid tissue, enteroviruses can enter the bloodstream and, thereby, spread to various target organs (for example, poliovirus spreads to the central nervous system [CNS]). Although the great majority of infections are asymptomatic, infection, whether clinical or subclinical, usually results in protective immunity. Enteroviruses account for an estimated 10 to 15 million symptomatic infections per year in the United States.

2. Viral replication: Enteroviruses bind to specific receptors on host cell surfaces. For example, poliovirus binds to a receptor that is a member of the immunoglobulin (Ig) supergene family of proteins. Cells lacking these specific receptors are not susceptible to infection.

a. Mechanism of genome replication: This is the same process as described for Type I RNA viruses : Namely, the incoming parental RNA serves as the template for a genome size, negative-strand RNA, and this, in turn, serves as a template for multiple copies of progeny positive-strand RNA.

b. Translation: Enterovirus RNA contains a single, long, open reading frame. Translation of this message results in the syn thesis of a single, long polyprotein, which is processed by viral proteases into structural proteins and nonstructural proteins, including the viral RNA polymerase needed to synthesize additional copies of the viral genome.

3. General clinical significance of enterovirus infections: All enteroviruses can cause CNS disease. For example, enteroviruses are currently the major recognizable cause of acute aseptic meningitis syndrome, which refers to any meningitis (infectious or noninfectious) for which the cause is not clear after initial examination plus routine stains and cultures of the cerebrospinal fluid (CSF). Viral meningitis is a common infection in the United States, with an estimated 75,000 cases each year. Viral meningitis can usually be distinguished from bacterial meningitis because: 1) the viral disease is milder; 2) there is an elevation of lymphocytes in the CSF, rather than the elevated neutrophils seen in bacterial meningitis; and 3) the glucose concentration in the CSF is not decreased. Viral meningitis occurs mainly in the summer and fall, affecting both children and adults. The treatment is symptomatic, and the course of the illness is usually benign. Viruses can be isolated from the stool or from various target organs (CNS in meningitis cases and from conjunctival fluid in conjunctivitis cases). Evidence of infection can also be obtained by demonstration of a rise in antibody titer against a specific enterovirus. No antiviral drugs are available for treatment of infections caused by Enterovirus species.

4. Clinical significance of poliovirus infection: Poliomyelitis is an acute illness in which the poliovirus selectively destroys the lower motor neurons of the spinal cord and brainstem, resulting in flaccid, asymmetric weakness or paralysis. In the United States, no cases of paralytic poliomyelitis caused by wild-type poliovirus have occurred in more than 20 years. The few cases of polio that occur (less than 10 per year) are all caused by the reversion to virulence of the virus in the live-attenuated Sabin polio vaccine (see below). In countries with low immunization rates, paralytic polio continues to occur. There are only three countries that remain polio endemic: Afganistan, Pakistan, and Nigeria. The number of countries is down significantly from 125 in 1988. Notably, India was polio free for the first time in 2011. Although this represents significant progress toward the goal of eradicating polio from the world, in 2009–2010, 23 previously polio-free countries were reinfected due to importation of the virus.

a. Transmission and pathogenesis: Poliovirus infections may follow one of several courses: 1) asymptomatic infection, which occurs in 90 to 95 percent of cases and causes no disease and no sequelae; 2) abortive infection; 3) nonparalytic infection; or 4) paralytic poliomyelitis (Figure 2). The classic presentation of paralytic poliomyelitis is flaccid paralysis, most often affecting the lower limbs. This is a result of viral replication in, and destruction of, the lower motor neurons in the anterior horn of the spinal cord (Figure 3). Respiratory paralysis may also occur, following infection of the brainstem. Poliomyelitis should be considered in any unimmunized person with the combination of fever, headache, neck and back pain, asymmetric flaccid paralysis without sensory loss, and lymphocytic pleocytosis (an increase in the number of lymphocytes in the spinal fluid).

Fig2. Clinical outcomes of infection with poliovirus.

Fig3. Central nervous system invasion by poliovirus.

b. Prognosis: Permanent weakness is observed in approximately two thirds of patients with paralytic poliomyelitis. Complete recovery is less likely when acute paralysis is severe, and patients requiring mechanical ventilation because of respiratory paralysis rarely recover without some permanent disability.

c. Postpoliomyelitis syndrome: Approximately 20 to 30 percent of patients who partially or fully recover from paralytic poliomyelitis experience a new onset of muscle weakness, pain, atrophy, and fatigue 25 to 35 years after the acute illness.

d. Treatment and prevention: Specific antiviral agents for the treatment of poliomyelitis are not available. Management, therefore, is supportive and symptomatic. Vaccination is the only effective method of preventing poliomyelitis. Poliomyelitis can be prevented by either live-attenuated (Sabin) or killed (Salk) polio vaccines. These vaccines have led to the elimination of wild-type polio from Western Europe, Japan, and the Americas. Killed polio vaccine has no adverse effects, whereas live polio vaccine may undergo reversion to a virulent form while it multiplies in the human intestinal tract and cause vaccine-associated paralytic poliomyelitis in those receiving the vaccine. Because the small numbers of cases of paralytic poliomyelitis in the United States since 1979 were due to vaccine-derived strains, the CDC changed its recommendation for routine polio vaccination to killed (inactivated) polio vaccine (IPV) in 2000.

5. Clinical significance of coxsackievirus and echovirus infections: These give rise to a large variety of clinical syndromes, including meningitis, upper respiratory infections, gastroenteritis, herpangina (severe sore throat with vesiculoulcerative lesions), pleurisy, pericarditis, myocarditis, and myositis.

6. Clinical significance of enteroviruses 70 and 71 infections: These have been associated with severe CNS disease. A particularly acute form of extremely contagious hemorrhagic conjunctivitis has also been associated with enterovirus 70.

B. Rhinovirus

Rhinoviruses cause the common-cold syndrome (Figure 4). They differ in two important respects from enteroviruses. First, whereas enteroviruses are acid stable (they must survive the acid environment of the stomach), rhinoviruses are acid labile. Second, rhinoviruses, which replicate in the nasal passages, have an optimal temperature for replication that is lower than that of enteroviruses. This permits rhinoviruses to replicate efficiently at temperatures several degrees below body temperature. Rhinovirus replication is simi lar to that of the poliovirus. Because there are more than 100 serotypes of rhinoviruses, development of a vaccine is impractical. Studies have shown that in addition to being spread by respiratory droplets, rhinoviruses can also be spread by hand-to hand contact. Therefore, hand washing at appropriate intervals can be a useful preventive measure.

Fig4. Pathogenesis of the common cold showing stages from infection to recovery.

C. Hepatovirus

The sole member of this genus is hepatitis A virus (HAV). Although at one time HAV was also known as enterovirus 72, sufficient differences have been found between HAV and the enteroviruses to war rant placing HAV in a genus by itself. HAV, of which there is only one serotype, causes viral hepatitis. As with the enteroviruses, transmission is by the fecal–oral route, and the virus is shed in the feces. For example, a common mode of transmission of the virus is through eating uncooked shellfish harvested from sewage-contaminated water. The main site of replication is the hepatocyte. Viral replication results in severe cytopathology, and liver function is significantly impaired (Figure 5). In contrast to most other picornaviruses, HAV grows poorly in tissue culture. The prognosis for patients with acute hepatitis A is generally favorable, and the development of persistent infection and chronic hepatitis is uncommon. HAV infection is most common in developing countries with poor sanitation (Figure 6). Prevention depends on taking measures to avoid fecal contamination of food and water. Immune globulin has been used for many years, mainly as postexposure prophylaxis. Vaccines prepared from whole virus inactivated with formalin are now available. HAV vaccination is recommended for children over age 1 year and for persons traveling to developing countries. A combination vaccine (Twinrix) is available to protect against both hepatitis A and hepatitis B virus infection.

Fig5. Time course of hepatitis A infection.

Fig6. Distribution of hepatitis A virus infection worldwide.

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الآخبار الصحية

تحذير من "عدوى بكتيرية" تسبب نوبات قلبية

ماذا يحصل لجسمك عند التوقف عن استخدام الزيت في الطهي؟

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الآخبار التكنلوجية

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المزيد

مواضيع ذات صلة

Pathogenesis and clinical significance of HIV

Transmission of HIV

HIV replication

Hepatitis D

Prevention and Treatment of hepatitis B

Differentiating Acute and Chronic Hepatitis and the Chronic Carrier State

Flaviviridae

Togaviridae

Caliciviridae

Laboratory Assays of Hepatitis B

Epidemiology of Hepatitis B

Hepatitis A