Christian Griot

Genetics, infectivity and virulence of California serogroup viruses

The California serogroup of viruses includes 14 viruses which take their name from California encephalitis virus, the prototype of the serogroup, which was isolated in California in the 1950s (Hammon and Reeves, 1952). This serogroup is part of the Bunyauirus genus within the family Bunyaviridae (Gonzalez-Scarano and Nathanson, 1990; Kolakofsky, 1991; Whitman and Shope, 1962). La Crosse virus, the most medically significant member of the California serogroup, was isolated in 1964 from a fatal case of encephalitis diagnosed in La Crosse, Wisconsin (Thompson et al., 1965). Although California encephalitis virus was initially reported in association with a few cases of encephalitis, it is not an important human pathogen. On the other hand, La Crosse virus is a common cause of encephalitis in the pediatric age group, with an average of about 75 reported cases of encephalitis each year (Kappus et al., 1983). In years when other arboviruses are not epidemic, La Crosse virus is the most important cause of arbovirus encephalitis in the United States. The virus is estimated to cause more than 100,000 inapparent infections annually which are concentrated in the midwest (Grimstad et al., 1984), which is the principal habitat of Aedes triseriatus, its major mosquito vector. Bunyavirions are roughly spherical particles about 100 nm in diameter consisting of a lipid envelope containing nucleocapsids representing the three different RNA species (L segment, 6.8 kb; M segment, 4.5 kb; and S segment, 0.9 kb) which comprise the negative-sense genome (Elliott, 1990; Gonzalez-Scarano and Nathanson, 1990). The viral envelope contains two glycoproteins, Gl and G2, and

11 Bovine Spongiform Encephalopathy and Related Diseases

In Great Britain, a previously unrecognized neurologic disease in cattle was first defined in 1986, on the basis of a constellation of clinical signs associated with characteristic pathologic changes in the brain (Wells et al. 1987). There was the insidious onset of altered behavior (either fear or sometimes aggressive responses), ataxia (incoordinated gait with falling), and dysesthia or reflex hyperesthesia (abnormal responses to touch and sound). The relentless progression of these symptoms made it impossible to handle animals, requiring slaughter within 1–6 months (Wilesmith et al. 1988). Histologically, the brain exhibited spongiform lesions and astrogliosis (Wells et al. 1987). It was immediately recognized (Wells et al. 1987) that the lesions were similar to those characteristic of transmissible spongiform encephalopathies (TSEs) or prion diseases in other species, specifically scrapie of sheep, the prototype of the TSEs. In retrospect, cases of BSE had been seen in England as early as 1985, but probably not before that year. This new disease was made statutorily notifiable (Anonymous 1996a; Wilesmith 1996a) and the numbers of cases continued to increase each month, indicating the onset of a major epidemic (Fig. 1). EPIDEMIOLOGY OF BSE The United Kingdom The advent of a new prion disease in epidemic form led to a detailed investigation of its possible cause. An important clue was offered by mapping of the cases occurring within the first 18 months of the outbreak (Wilesmith 1991), which showed that they were widely distributed throughout much of England. The same pattern is reflected in Figure...