This article has been reviewed according to Science X's editorial process and policies. Editors have highlighted the following attributes while ensuring the content's credibility: Earlier this year, an outbreak of Andes hantavirus on a cruise ship, which killed three passengers and sickened 13, highlighted the lack of approved vaccines or treatments for the virus. In a study published in Nature, scientists at Albert Einstein College of Medicine and collaborators from Institut Pasteur and LSU Health Shreveport show how the virus recognizes its target on a human cell, a finding that could lead to effective therapies against Andes virus and other hantaviruses.
"Eight years ago, we discovered that Andes virus infects human cells by using a particular protein on the cell's surface, called a receptor, but we couldn't figure out exactly how the virus recognized it," said co-corresponding author Kartik Chandran, Ph.D., professor of microbiology and immunology at Einstein. "Our latest work solves this puzzle: We reveal a new way in which a virus can capture its receptor during infection and also suggest how we can fight back with therapies targeted to exploit the resulting viral vulnerability." Chandran is also the Gertrude and David Feinson Chair in Medicine and the Harold and Muriel Block Faculty Scholar in Virology at Einstein, and a member of Montefiore Einstein Comprehensive Cancer Center. Hantaviruses are a large family of viruses carried mainly by rodents.
They can cause serious and sometimes fatal diseases, including hantavirus pulmonary syndrome, a severe respiratory illness that can rapidly lead to breathing failure. Human infections are mainly caused by inhaling airborne virus particles from infected rodents' urine, droppings or saliva. Of the more than 20 hantaviruses known to sicken humans, Andes virus is the only one known to spread from person to person, typically through close and prolonged contact.
This year's cruise ship outbreak provided a dramatic example of that capability. The research team had previously shown that, to infect a human cell, the spike protein on the Andes virus surface must latch onto a particular protein, a receptor called PCDH1 on the cell's surface. This receptor essentially serves as a doorway for the virus to enter the cell and then multiply inside it.
But an important question remained unanswered: How does the virus's spike protein latch onto PCDH1? Following the discovery of PCDH1 as the Andes virus receptor, the researchers became aware that hantaviruses behave in an unusual way compared to most viruses. For example, the spike protein of SARS-CoV-2, the virus that causes COVID-19, has three identical protein units that come together in a triangle shape.
Each unit has a separate part called the receptor-binding domain (RBD) that latches onto its receptor, ACE2. In contrast, the Andes virus spike is an arrangement of four identical protein units locked together into a square. Unlike with SARS-CoV-2 and ACE2, a single protein unit from the Andes virus cannot bind to its receptor; instead, the entire square-shaped spike is needed to capture PCDH1.
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