Paramyxoviruses have large genomes (approximately 15,000 bases) and their replication cycle is reminiscent of that described for rhabdoviruses. One notable exception is that several (including mumps) generate mRNA that has been edited by the addition of extra G nucleotides as the mRNAs for specific genes are expressed. The addition of these nucleotides is apparently accomplished by a stuttering step similar to that involved in the addition of polyA residues at the end of transcripts. This editing results in several variant mRNAs being expressed from a single viral gene.
Paramyxoviruses can be subdivided further into paramyxovirus proper, parainfluenza virus, mumps virus (Rubulavirus), measles virus (Morbillivirus), and pneumoviruses such as respiratory syncytial virus. The structure of Sendai virus, a typical paramyxovirus that causes respiratory disease in mice, and its genetic map are shown in Fig.15.4.
Mumps, measles, canine distemper, and rinderpest are all caused by paramyxoviruses. Mumps is classified as a relatively benign "childhood" disease; the infection usually occurs in children just when they begin to socialize in preschool or day-care facilities. The virus spreads rapidly, generally causes a mild inflammation of glandular tissue in the head and neck, and leads to lifelong immunity. Since the symptoms are generally forgotten and do not lead to any notable physiological consequences, the disease is considered mild.
Infection of postpubescent children or adults, however, can be a significantly different story. Here, the virus can infect gonadal tissue and lead to major discomfort, and occasionally, to permanent reproductive damage.
The pathology of respiratory syncytial virus also is quite different for infants and adults. This virus establishes a mild, cold-like infection in an adult's nasopharynx. Following recovery, the virus can persist in the throat as a relatively normal member of the microbe population that coexists in this moist, warm environment. Since it is not invasive, the persistent infection is usually asymptomatic unless there is a complicating environmental factor. Such a factor can be very dry air in heated buildings during winter in temperate zones throughout the world. This dry air can lead to chronic respiratory irritation and mild infections by respiratory syncytial virus, as well as other pathogens. Unfortunately, the virus can spread from adults to children and infants. In hospitals, an active infection in nursery health care workers can lead to fatal epidemics in newborns whose undeveloped immune systems cannot cope with the infection.
Measles, as described in Chapter 4, Part I, although often termed a childhood disease, can cause major neurological damage to infected children, and its introduction into unprotected populations has resulted in high mortality.
Measles and the closely related distemper and rinderpest viruses cause serious and often fatal diseases at all ages. Distemper infections cause high mortalities in domestic and wild animals, and the broad host range and easy transmission of canine distemper has resulted in its being a major infectious agent in marine mammals. Another related virus, rinderpest, is a serious disease of domestic cattle that has spread to wild ungulates in sub-Saharan Africa. Indeed, it is considered a greater threat than human habitat encroachment to the survival of much African wildlife, both because of its pathology and because of human efforts to stop the natural and necessary seasonal migration of wild ungulates that harbor the virus to prevent reinfection of domestic cattle. This is a prime example of human habitat disruption leading to ecological distress. Such disruption can be a major factor in evolution of viral disease as discussed in Chapters 1 and 22.
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