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- Knowles, N J, et al.
(författare)
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Family - Picornaviridae
- 2012
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Ingår i: Virus Taxonomy. - San Diego - London : Elsevier. - 9780123846846 ; , s. 855-881
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Bokkapitel (refereegranskat)abstract
- This chapter focuses on Picornaviridae family whose member genuses includeEnterovirus, Cardiovirus, Aphthovirus, Hepatovirus, and Parechovirus. The virions of this family consist of a capsid with no envelope and surrounds a core of ssRNA. Hydrated native particles are 30 nm in diameter, but vary from 22 to 30 nm in electron micrographs due to drying and flattening during preparation. The virions contain one molecule of positive sense, ssRNA, and possess a single long ORF. The UTRs at both termini contain regions of secondary structure, which are essential to genome function. In addition to the major CPs, 1A, 1B, 1C and 1D, and 3B (VPg), small amounts of 1AB (VP0) are commonly seen in lieu of one or more copies of 1A and 1B. Protein 1A is small in hepatoviruses, and 1AB is uncleaved in avihepatoviruses, kobuviruses, parechoviruses, and a number of unclassified picornaviruses. Some picornaviruses carry a sphingosine-like molecule in a cavity located inside 1D, and protein 1A generally has a molecule of myristic acid covalently attached to the amino terminal glycine. The virion RNA is infectious and serves as both the genome and the viral mRNA. Infection is generally cytolytic, but persistent infections are common with some species and reported with others. Poliovirus infected cells undergo extensive vacuolation as membranes are reorganized into viral replication complexes.
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| 3. |
- Fohlman, Jan, et al.
(författare)
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Antiviral treatment with WIN 54954 reduces mortality in murine Coxsackie virus B3 myocarditis
- 1996
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Ingår i: Circulation. - 0009-7322 .- 1524-4539. ; 94:9, s. 2254-2259
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Coxsackieviruses B (CBVs) are dominant causative agents in myocarditis and are associated with pathogenesis is some cases of dilated cardiomyopathy, a clinical entity with a poor survival without heart transplantation. METHODS AND RESULTS: In vitro, the antiviral agent WIN 54 954 was shown to inhibit replication of CBV3 at a minimal inhibitory concentration value of 0.02 mg/L. Administration of WIN 54 954, 100 mg/kg BID PO, beginning on the day of infection resulted in complete protection from enteroviral mortality (P < .01). WIN 54 954 treatment did not abrogate the inflammatory reaction in the myocardium. No difference was found in the expression of surface lymphocyte subset markers. At 3 weeks, macrophages seemed to dominate the inflammatory reaction, regardless of treatment. There was no difference in CBV3 antibody titers, indicating that WIN 54 954 does not interfere with the development of protective immunity. Complement factors C3 and B were synthesized at a higher level during infection and correlated well with the degree of inflammatory reaction. CONCLUSIONS: The results show that WIN 54 954 is a potent antiviral agent with a highly significant effect on survival in CBV-induced myocarditis in the A/J mouse if treatment is started early. It is suggested that the reduction in mortality seen with WIN 54 954 administration is due to an inhibitory effect on virus replication in affected organs that does not interfere with cellular or humoral immunity.
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