Yellow fever is a
viral hemorrhagic fever, which
affects people living in
Africa and
South America and is caused by the
yellow fever virus, the prototype species in the
Flavivirus genus (
Flaviviridae family).
Yellow fever virus infection can produce a wide spectrum of symptoms, ranging from
asymptomatic infection or oligosymptomatic illness to severe
disease with a high fatality rate. In this
review, we focus in the mechanisms associated with the
physiopathology of
yellow fever in
humans and
animal models. It has been demonstrated that several factors
play a
role in the pathological outcome of the severe form of the
disease including direct
viral cytopathic effect,
necrosis and
apoptosis of
hepatocyte cells in the midzone, and a minimal inflammatory response as well as low-flow
hypoxia and
cytokine overproduction. New information has filled several gaps in the
understanding of
yellow fever pathogenesis and helped comprehend the
course of illness. Finally, we discuss prospects for an immune
therapy in the
light of new immunologic, viral, and pathologic tools. (AU)