ABSTRACT
In 1964, Mackenzie et al. described a new hemorrhagic fever in the Beni region in northeastern Bolivia (Figure 19.1) (Mackenzie et al. 1964). The disease, by then named Bolivian hemorrhagic fever (BHF), had been rst recognized in 1959 on the Bolivian island of Orobayaya. There, 470 cases were reported in the years up to 1962. Another series of localized outbreaks then occurred between 1962 and 1964, which involved more than 1000 patients, of which 180 died. After 20 years of no reported cases, mainly as a result of rodent control measures (Kuns 1965), an outbreak of 19 cases was reported in 1994. Eight more cases were described in 1999, 18 cases in 2000, and 20 suspected cases between 2007 and 2008 (Aguilar et al. 2009). The latest BHF outbreak occurred at the end of 2011, again in the Beni region. At the time of writing, case numbers were still unclear. Machupo virus (MACV), named after a river close to the outbreak area, was isolated in 1963 from the spleen of a fatal human case studied in the town of San Joaquín and identied as the etiological agent of BHF (Johnson et al. 1965b). Similarly to Argentinian hemorrhagic fever (AHF), the BHF outbreak frequency peaks during the annual harvest (April-July). The case-fatality rate of BHF is approximately 5%–30%. Humans become infected with MACV through contact with infected rodents or inhalation of aerosolized virus from contaminated rodent blood, excreta or secreta (Charrel and de Lamballerie 2003). Direct human-to-human transmission, though possible, is probably not the
19.1 Introduction: History and Epidemiology of Bolivian Hemorrhagic Fever ........................... 339 19.2 Clinical Course of Bolivian Hemorrhagic Fever .................................................................. 341 19.3 Taxonomy and Phylogenetic Relationships .......................................................................... 341 19.4 Virus Structure and Life Cycle ............................................................................................. 342
19.4.1 Virus Properties ........................................................................................................ 342 19.4.2 Genomic Organization.............................................................................................. 342 19.4.3 Virus Life Cycle........................................................................................................ 343
19.4.3.1 Virus Entry ................................................................................................ 343 19.4.3.2 Virus Transcription and Protein Expression .............................................. 345 19.4.3.3 Virus Replication ....................................................................................... 345 19.4.3.4 Virus Assembly and Budding .................................................................... 345
19.5 Pathology and Pathogenesis of Bolivian Hemorrhagic Fever ...............................................346 19.6 Treatment and Vaccines ........................................................................................................348
