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Gantavirus causes severe and sometimes death-related respiratory infections, but it is the secret that they transmit lung cells. Today's release NatureAlbert Einstein suggests entering the lung cells by "unlocking" the cell surface receptor, called the Hantavirus Producer-1 (PCDH1), including researchers at the Medical College. Removal of this receptor was very resistant to infection of laboratory animals. Studies have shown that PCDH1 can cause death (HPS).
The research was led by PhD Dr. Kardyk Chandran. Candidate of Pharmacy in the Netherlands Cancer Institute Thijn R. Brummelkamp; John M. Dye, Ph.D., USAMRIID at the US Army Corps of Infectious Diseases Research Institute; and John D. Wang, PhD, at the Jund University State University.
The danger it produces
The HPP was first discovered in 1993. In the United States, there are 728 cases in western countries, mostly in rural areas. "If Xantovirus infections rarely occur, climate change will increase over the next decade, as the temperature rises worldwide," said Dr. Chandran, a professor of microbiology and immunology. A scholar at the Harold and Maryle Block faculty in Einstein's virology.
Hantavirus is administered to persons who are inhaled by urine, stool or saliva of infected rodents. Early symptoms of gypsum include weakness, fever, and muscle aches, which are followed by coughing and breathing in a week. According to the Centers for Disease Control and Prevention, GTS mortality rate is about 40%. No treatment or vaccine. "Our results provide us with new insights on how these infections develop and how they can be prevented or treated," wrote Dr. Chandran.
Defining a viral access point
In the search for host factors that enable the infection of Hantavirus, researchers have created a "non-functional" genetic screen to see if the Hantavirus penetration of the stem cell gene can stop. The PCDH1 gene has been detected on the screen, which encodes the PCDH1 protein receptor found in the cell membranes. More precisely, PCDH1 has previously been related to respiratory and lung diseases, but can not play a role in infection with xanthuvirus or other viruses.
Researchers have confirmed that they have lost their pulmonary endothelial cells (ie cell lungs) for confirming the role of PCDH1 in Hantavirus's infection. These cells were endemic to the transmission of two major HPS-generating gangrene found in North and South America: the Sin Nombre virus and the Andes virus. Most importantly, Syria's golden hamsters (Hantavirus researcher's main rodent model) developed for the lack of PCDH1 receptors were resistant to infections and pulmonary damage caused by the Andes virus. In contrast, many of the control animals that have receptor have been infected with the virus. "Our research plays an important role in PCDH1 in lung infections caused by hantovirus-based animals, which are key features of HPS," said Dai, senior researcher at the USAMRIID Viral Immunology Department.
Researchers also point to a certain part of the PCDH1 protein that is directly recognized by xanthaviruses, making the protein region a prospective goal for the drug to develop. Indeed, the teams form monoclonal antibodies with a high degree of proximity to the PCDH1 region, which are associated with the endothelial cells of the lung and protect the And and Sin Nombri virus infection. Current studies evaluate the antibodies against the xenovirus infection and disease of animals.
Interestingly, another group of Hantavirus, causing severe kidney disease in Europe and Asia, and sometimes even the United States PCDH1 infection receptor is not needed. "There are other ways to print the cells that continue to detect these viruses," said Rohit Jangra, Einstein's researcher and co-author of the study.
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The materials are presented Albert Einstein Medical College. Note: The content can be edited for style and length.
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