Viruses Can Steal Our Genetic Code to Create New Human-Virus Genes

AHA Publisher — Wed, 24 Jun 2020 07:00:58 +0000

Mount Sinai Health System via Newswise – Like a scene out of “Invasion of the Body Snatchers,” a virus infects a host and converts it into a factory for making more copies of itself. Now researchers have shown that a large group of viruses, including the influenza viruses and other serious pathogens, steal genetic signals from their hosts to expand their own genomes. This finding is presented in a study published online today and in print June 25 in Cell. The cross-disciplinary collaborative study was led by researchers at the Global Health and Emerging Pathogens Institute at Icahn School of Medicine at Mount Sinai in New York, and at the MRC-University of Glasgow Centre for Virus Research in the UK. The cross-disciplinary team of virologists looked at a large group of viruses known as segmented negative-strand RNA viruses (sNSVs), which include widespread and serious pathogens of humans, domesticated animals and plants, including the influenza viruses and Lassa virus (the cause of Lassa fever). They showed that, by stealing genetic signals from their hosts, viruses can produce a wealth of previously undetected proteins. The researchers labeled them as UFO (Upstream Frankenstein Open reading frame) proteins, as they are encoded by stitching together the host and viral sequences. There was no knowledge of the existence of these kinds of proteins prior to this study. These UFO proteins can alter the course of viral infection and could be exploited for vaccine purposes. “The capacity of a pathogen to overcome host barriers and establish infection is based on the expression of pathogen-derived proteins,” said Ivan Marazzi, PhD, Associate Professor of Microbiology at Icahn School of Medicine and corresponding author on the study. “To understand how a pathogen antagonizes the host and establishes infection, we need to have a clear understanding of what proteins a pathogen encodes, how they function, and the manner in which they contribute to virulence.” Viruses cannot build their own proteins, so they need to feed suitable instructions to the machinery that builds proteins in their host’s cells. Viruses are known to do this through a process called “cap-snatching,” in which they cut the end from one of the cell’s own protein-encoding messages (a messenger RNA, or mRNA) and then extend that sequence with a copy of one of their own genes. This gives a hybrid message to be read. “For decades we thought that by the time the body encounters the signal to start translating that message into protein (a ‘start codon’) it is reading a message provided to it solely by the virus. Our work shows that the host sequence is not silent,” said Dr. Marazzi. The researchers show that, because they make hybrids of host mRNAs with their own genes, viruses (sNSVs) can produce messages with extra, host-derived start codons, a process they called “start snatching.” This makes it possible to translate previously unsuspected proteins from the hybrid host-virus sequences. They further show that these novel genes are expressed by influenza viruses and potentially a vast number of other viruses. The product of these hybrid genes can be visible to the immune system, and they can modulate virulence. Further studies are needed to understand this new class of proteins and what the implications are of their pervasive expression by many of the RNA viruses that cause epidemics and pandemics. Ed Hutchinson, PhD, corresponding author and a research fellow at MRC-University of Glasgow Centre for Virus Research, said, “Viruses take over their host at the molecular level, and this work identifies a new way in which some viruses can wring every last bit of potential out of the molecular machinery they are exploiting. While the work done here focusses on influenza viruses, it implies that a huge number of viral species can make previously unsuspected genes.” Researchers say the next part of their work is to understand the distinct roles the unsuspected genes play. “Now we know they exist, we can study them and use the knowledge to help disease eradication,” said Dr. Marazzi. “A large global effort is required to stop viral epidemics and pandemics, and these new insights may lead to identifying novel ways to stop infection.” This study was supported by funders including the National Institute of Allergy and Infectious Diseases and the UK Medical Research Council. To read the original article click here.

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Study Reveals Birth Defects Caused by Flame Retardant

AHA Publisher — Fri, 19 Jun 2020 07:00:01 +0000

University of Georgia via Newswise – *Research focuses on man’s exposure prior to conception. A new study from the University of Georgia has shown that exposure to a now-banned flame retardant can alter the genetic code in sperm, leading to major health defects in children of exposed parents. Published recently in Scientific Reports, the study is the first to investigate how polybrominated biphenyl-153 (PBB153), the primary chemical component of the flame retardant FireMaster, impacts paternal reproduction. In 1973, an estimated 6.5 million Michigan residents were exposed to PBB153 when FireMaster was accidentally sent to state grain mills where it made its way into the food supply. In the decades since, a range of health problems including skin discoloration, headache, dizziness, joint pain and even some cancers have been linked to the exposure. More striking, the children of those who were exposed seemed to experience a host of health issues as well, including reports of hernia or buildup in the scrotum for newborn sons and a higher chance of stillbirth or miscarriage among adult daughters. Yet, little work has been done to understand how the chemical exposure could have impacted genes passed from an exposed father, said study author Katherine Greeson. Relatively new idea “It is still a relatively new idea that a man’s exposures prior to conception can impact the health of his children,” said Greeson, an environmental health science doctoral student in Charles Easley’s lab at UGA’s College of Public Health and Regenerative Bioscience Center. “Most studies where a toxic effect is observed in children look only to the mothers and the same has been true of studies conducted on PBB153,” she said. Greeson and a team of researchers from UGA and Emory University used a unique combination of observational and laboratory approaches to demonstrate how PBB153 acted on sperm cells. “Typically, scientific studies are either epidemiological in nature and inherently observational or focus on bench science, but in this study, we did both,” said Greeson. This approach allowed the researchers to mimic the known blood exposure levels of PBB153 in a lab environment. “We were uniquely able to recreate this effect using our previously characterized human stem cell model for spermatogenesis,” she said, “which allowed us to study the mechanism that causes this effect in humans.” The team looked at the expression of different genes in their human spermatogenesis model after dosing with PBB153 and found marked alterations in gene expression between dosed and undosed cells, specifically at genes important to development, such as embryonic organ, limb, muscle, and nervous system development. Changes to the DNA “PBB153 causes changes to the DNA in sperm in a way that changes how the genes are turned on and off,” said Greeson. “PBB153 seems to turn on these genes in sperm which should be turned off,” said Greeson, which may explain some of the endocrine-related health issues observed in the children of exposed parents. Though the study used this model to directly replicate exposure to PBB153, Greeson says this approach could be used to better understand the impact of other environmental exposures on reproduction, including large-scale accidental exposures to toxic chemicals or everyday exposures. More studies combining epidemiology “Hopefully this work will lead to more studies combining epidemiology and bench science in the future, which will tell us more about why we’re seeing an effect from an environmental exposure in human populations and encourage experimental studies to more closely mimic human exposures,” she said. To read the original article click here.

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Viruses Can Steal Our Genetic Code to Create New Human-Virus Genes

Study Reveals Birth Defects Caused by Flame Retardant