Every year or two, another potentially deadly virus hits the U.S. A few years ago, it was Zika virus, which is transmitted by the Aedes mosquitoes. Symptoms include fever, rash, conjunctivitis, muscle and joint pain, and headache. In pregnant women, Zika infection has been associated with microcephaly in the children. It has also been associated with Guillain-Barre syndrome, which can lead to muscle paralysis.
Zika was first observed in humans in 1952 in Uganda and Tanzania, then seen in the U.S. and other parts of the world in 2015.
Researchers with Temple University Health System have found that the Zika virus responds to an HIV drug called rilpivirine, which is marketed by Janssen, a Johnson & Johnson company, as Edurant. In addition, the enzymes targeted by rilpivirine are also found in other viruses similar to Zika, including the viruses that cause dengue fever, yellow fever, West Nile fever, and hepatitis C.
The researchers published their research in the journal Molecular Therapy.
“HIV and Zika virus are distinct types of RNA viruses,” said Kamel Khalili, the Laura H. Carnell Professor and chair of the Department of Neuroscience, director of the Center for Neurovirology, and director of the Comprehensive NeuroAIDS Center at the Lewis Katz School of Medicine at Temple University (LKSOM).
He went on to say, “By discovering that rilpivirine blocks Zika virus replication by binding to an RNA polymerase enzyme common to a family of RNA viruses, we’ve opened the way to potentially being able to treat multiple RNA virus infections using the same strategy.”
The Zika virus requires an enzyme known as non-structural protein 5 RNA-dependent RNA polymerase (NS5 RdRp). The researchers showed that rilpivirine prevents viral replication by binding to the NS5 domain. They carried out experiments in mice that were infected with Zika virus. Usually Zika-infected mice become very sick within a week and eventually die.
“We found, however, that when treated with rilpivirine, the animals survived,” said Jennifer Gordon, associate professor of Neuroscience at Temple’s Center for Neurovirology. “Our conclusion is that rilpivirine disrupted the virus’s usual course of infection.”
Rilpivirine is a non-nucleoside reverses transcriptase inhibitor (NNRTI). The researchers tested two other NNRTIs in Zika-infected cells and found similar effects.
“We now have a clear path forward,” said Khalilli. “We have a starting point from which we can find ways to make these drugs even more potent and more effective against flaviviruses.”
According to the U.S. Centers for Disease Control and Prevention (CDC), the biggest outbreaks of Zika virus in the Americas, particularly Puerto Rico, the U.S. Virgin Islands, and Florida and Texas, occurred in 2015 and 2016. The U.S. reported cases declined in 2017 and in 2018 and 2019 there were no reports of Zika virus transmission in the continental United States.
In 2015, 62 symptomatic cases of Zika virus were reported in the U.S., with all cases in travelers returning from affected areas. In U.S. territories, there were 10 symptomatic Zika virus case reported, with one in a traveler and nine acquired via mosquito bite. The following year, in 2016, there were 5,168 symptomatic Zika virus cases reported in the U.S., with 36,512 cases reported in U.S. territories. In 2017, that dropped significantly to 452 in the U.S. and 666 in the U.S. territories.
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