vaccine could increase suddenly. Modern cell culture techniques could greatly improve the speed and economy of vaccine production.

Yellow fever virus is an arthropod-borne virus in the Flavivirus genus of the family Togaviridae. It shares group-specific antigens with other members of the genus (former group B viruses, e.g., in Africa: Zika, West Nile, Wesselsbron, dengue, Uganda S, Spondweni, Banzi, and other viruses) (Wildy, 1971).

Yellow fever and other flaviviruses contain a single-stranded, positive-polarity RNA genome. Viral particles are 43 nm in size; they contain a ribonucleoprotein core and a lipoprotein envelope. The virus is inactivated by deoxycholate, ether, proteases, and lipases. The envelope contains a single glycoprotein with type- and group-specific antigens.

The morphogenesis of YF virus is similar to that observed for other flaviviruses; that is, viral synthesis and maturation appear to be predominant in the rough endoplasmic reticulum. The formation of the surrounding envelope of the virion remains unclear. Mature virus particles accumulate within the cisternae of membranous organelles and are released extracellularly by exocytosis or by plasma membrane rupture.

The virus is pathogenic for adult mice by intracerebral inoculation, and for suckling mice by intracerebral, subcutaneous, and intraperitoneal inoculation. The rhesus monkey is highly susceptible to YF virus, and this animal may be used as a model to define the pathogenesis of the disease (Monath et al., 1981).

Yellow fever virus replicates in cell cultures of different origin, but the cell cultures are variously sensitive. Cell lines of mosquito, monkey kidney, and hamster kidney are useful for propagation and assay. The 17D attenuated strain can be grown in several cell substrates, such as primary or subcultured chick embryo fibroblast and monkey kidney cells; virus titers observed in these systems are comparable to those obtained in embryonated eggs (Pan American Health Organization, 1981).

Wild strains of YF virus vary in their pathogenicity for hosts, but the molecular basis for virulence is poorly understood. Host factors, including genetic and immunological parameters, probably affect susceptibility.

Neutralizing antibodies usually are detectable on the sixth or seventh day after onset of primary infection and are responsible for immune elimination of the virus. It is not unusual to find both infectious virus and antibody in serum, but the role of immune complexes in the pathogenesis of the disease remains uncertain. Antibody responses may be accelerated and broadened in individuals with prior flaviviral immunity. Yellow fever virus infection also may alter the