The virion has a centrally located nucleic acid enclosed within a protein core or capsid. 'Naked' viruses are composed of this nucleocapsid only, while larger viruses have an envelope in addition. The nucleic acid is RNA or DNA, which is single- or double-stranded. If the RNA is infectious and functions as messenger RNA it is termed positive-stranded, otherwise minus-stranded (synonyms are positive- or negative-sense polarity). On the basis of the type of nucleic acid, the morphology of the capsid (cubical or helical) and the presence or absence of an envelope, a simplified scheme for classification can be constructed (see Chapter 1).
Since the cell cannot replicate RNA, viruses with an RNA genome furnish the cell with an RNA polymerase. The polymerase constitutes part of the core proteins of negative-stranded RNA viruses (e.g. influenzavirus), while positive-stranded RNA viruses (e.g. poliovirus) encode the production of the enzyme without incorporating it. Retroviruses have the enzyme reverse transcriptase which catalyses the formation of DNA from viral RNA; RNA is then synthesized from double-stranded DNA (provirus) by means of cellular enzymes. The viral envelope is a cell-derived lipid bilayer with inserted viral glycoproteins. The viral glycoproteins project from the surface of viruses and infected cells as spikes or peplomers and render the cell antigenically foreign, and as such a target for immune reactions.
The pathogenesis can in most cases be ascribed to degeneration and death of the infected cells. This may be mediated directly by the virus or by the immune clearance mechanisms. Denatured proteins elicit local inflammatory and systemic reactions. The local inflammatory response dominates the clinical picture in some infections, such as common colds, croup and bronchiolitis, while cell and organ failure or dysfunction is typical in poliomyelitis and hepatitis. Some infections are particularly dangerous to the fetus (CMV infection, rubella) or to the child in the perinatal period (herpes simplex, coxsackie B, varicella-zoster, hepatitis B and HIV infections). Bronchiolitis is seen only in the first 2 years of life, and croup mostly in children below school age. Otherwise the clinical course is not markedly different in children compared with adults.
The defence mechanisms involve phagocytosis, humoral and cellular immune responses and interferon production. In brief, interferon can arrest the local spread of the infection in the early phase; antibodies restrict further viraemic spread of the infection, mediate long-lasting immunity and sensitize infected cells for killing by macrophages and T-cells; while the cellular immune reactions include a series of events leading to the development of cytotoxic cells and release of lymphokines, including interferon. In the recovery from infection and protection against reinfection the various activities of the defence mechanisms are very interdependent.
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