The influenza virus that caused the Spanish flu pandemic that killed 50 million people worldwide in 1918 was lethal because the virus attacked the immune system in the early stages of infection, a team of researchers led by University of Tokyo Prof. Yoshihiro Kawaoka has reported.
The finding may lead to the development of a treatment for a new human flu virus that could arise from a sudden mutation of the H5 type of avian influenza virus currently circulating around the globe.
According to a report published online in the British scientific journal Nature, Kawaoka and his Canadian, U.S. and Japanese colleagues constructed the genes of the 1918 Spanish flu virus from published sequences and generated the complete virus using a plasmid- based reverse genetics method.
The research team then infected cynomolgus macaques, selected as model nonhuman primates, with the virus.
They reported that in the infected monkeys, the number of interferons, which are proteins produced by the cells of the immune system to inhibit viral replication within other cells, did not increase in the early stages of infection, unlike macaques infected with a harmless human virus.
The abnormality in the immune reaction led to inflammation in the lungs, they said.
"Lungs of the 1918-virus-infected macaques were the only tissue to exhibit macroscopic pathologic changes as severe lesions, with 60 pct to 90 pct of the lung tissue affected by day 6-8 (from the infection)," the team said in the report.
"The ability of influenza viruses to modulate host immune responses, such as that demonstrated for the avian H5N1 influenza virus, may be a feature shared by the virulent influenza viruses," they said.
"Better understanding of the virus-host interaction will aid development of interventions that can interfere with the virus' ability to modulate host innate immune responses and thus alter outcome of severe infections due to viruses such as the H5N1 viruses circulating at present," they said.END
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