A team of researchers at the University of California – Riverside recently determined that the yellow fever virus replicates primarily in the liver and other organ failures that often follow are due to secondary effects.
In the study, published in "PLOS Neglected Tropical Diseases," researchers found the virus replicates quickly in the liver where inflammatory cytokines proteins are made in massive amounts. The researchers said the proteins most likely damage other organs as they travel in the bloodstream.
The research team also discovered a clinical parameter that could help in treating yellow fever cases.
"Yellow fever causes severe loss of lymphocytes," Ilhem Messaoudi, an associate professor of biomedical sciences in the UC Riverside School of Medicine and lead researcher on the project, said. "This process, called lymphopenia, occurs before any measurable changes in liver enzymes can be detected -- that is, about a day or so before we see changes in the liver. It could provide an earlier clinical outcome measure of subsequent disease severity, giving doctors a good prognostic tool for offering more aggressive supportive care for these patients."
The research, performed on rhesus macaques at the Oregon National Primate Research Center, is the first study on yellow fever in primates in more than 20 years.
"Yellow fever is truly a neglected tropical disease," Messaoudi said. "Even though it continues to cause fatality, it remains understudied. While it is true there is a highly effective vaccine, it remains extremely challenging to get comprehensive vaccine coverage in sub-Saharan Africa and Latin America. Moreover, the vaccine works well if you are between 1 and 55 years old. It is not safe for babies or the elderly, who could develop yellow fever from the vaccine."
To further the research, Messaoudi and her team plan to study gene expression in animals that survive yellow fever and want to identify viral proteins responsible for compromising the immune system. This could lead to the creation of antiviral drugs.