Research Roundup: Emerging Viral Diseases and More
Every week there are numerous scientific studies published. Here’s a look at some of the more interesting ones.
More Worries About Emerging Viral Diseases
If the current COVID-19 pandemic is teaching the world anything, it’s that viral diseases can be extremely dangerous and disruptive. Researchers with the University of Colorado Anschutz Medical Campus released a new study calling attention to the emergence of mosquito-borne viral outbreaks in West Africa, including dengue (DNV), chikungunya (CHIKV) and Zika (ZIKV) viruses. They published their research in Acta Tropica.
The study reviewed 50 years of literature on arboviruses in West Africa. The goal was to define evidence of DENV, ZIKV and CHIKV and the distribution of their Aedes mosquito vectors in the region. They found strong evidence that transmission of these diseases is occurring in urban areas of West Africa, which is distinct from the rural transmission of yellow fever virus that has been historically present in the region. They found evidence that the epidemiology of arboviral disease in West Africa has shifted and that rapid urbanization and climate change could increase risk of outbreaks in the future.
“Large arboviral outbreaks will occur around the world,” said Elizabeth Carlton, assistant professor of environmental and occupational health at the Colorado School of Public Health and co-author of the study. “Building awareness and surveillance capacity before the outbreaks occur can help detect outbreaks early and enable prompt and effective response to reduce health impacts.”
Research lead Andrea Buchwald, a postdoctoral fellow, said, “Emerging viruses are at the forefront of everyone’s attention due to the COVID-19 pandemic. It has underscored the importance of preparing for and preventing large viral outbreaks that can have massive public health and economic consequences. We hope our research will prompt the development of early warning systems and adoption of control measures to prevent infectious outbreaks in West Africa. This will greatly impact the spread and severity of future outbreaks.”
Vaccine Design Leveraging Artificial Proteins
Investigators at Ecole Polytechnique Federale de Lausanne in France developed a computational approach to create artificial proteins, which they believe could be used to create safer and more effective vaccines. They note that when vaccines don’t work, there’s a tendency to think it’s because the antibodies produced aren’t protective, but usually it’s because the immune system is making the wrong type of antibodies. The new method was able to design artificial proteins that could precisely instruct the body’s immune system which antibodies to produce.
New Genetic Link for NASH Identified
Non-alcoholic steatohepatitis is a fatty liver disease similar to cirrhosis of the liver but in people who drink little or no alcohol. Researchers at German Diabetes Center, German Institute of Human Nutrition Potsdam-Rehbrucke (DlfE), and Helmholtz Zentrum Munchen, discovered new genes that play a role in fatty liver disease. The genes are IRGM, Ifgga2 and Ifgga4. They are responsible for the production of regulatory proteins of the family of immunity-related GTPases that counteract fat accumulation in the liver. A genetic variation causes formation of fewer of these proteins.
University of Waterloo researchers studying the 3D structure of the COVID-19 protein believe a specific class of diabetes drugs could potentially be used to treat COVID-19. The study has not yet been peer-reviewed, but they found evidence that dipeptidyl peptidase 4 inhibitors (DPP4 inhibitors) could bind to the protein. They are continuing research and hope to scale up to clinical trials. Common DPP4 inhibitors include AstraZeneca’s Onglyza (saxagliptin), Merck’s Januvia (sitagliptin), Takeda’s Nesina (alogliptin) and Boehringer Ingelheim’s Tradjenta (linagliptin).
How Triglyceride is Made
Triglycerides are a type of dietary fat that are associated with increased risk of heart disease, diabetes, obesity and fatty liver disease. Researchers at Baylor College of Medicine identified a 3D structure and mode of action of an enzyme, acylglycerol O-acyltransferase-1 (DGAT1) that synthesizes triglycerides. It is also required for human dietary fat absorption and storage. DGAT1 is a known target for treating diabetes and metabolic diseases, so understanding the mechanism of action may lead to better interventions. The research was published in the journal Nature.
“DGAT1 is a particularly interesting enzyme because it synthesizes triglycerides, which are the main component of hard fat, the type of fat usually found in the belly or midsection in our body,” said co-corresponding author Ming Zhou, Ruth McLean Bowman Bowers Professor in Biochemistry in the Department of Biochemistry and Molecular Biology at Baylor. “Triglycerides also are part of the particles that transport cholesterol — high-density lipoproteins (HDL, or ‘good cholesterol’), and low-density and very-low-density lipoproteins (LDL and VLDLD, or ‘bad cholesterols’). Learning to regulate this enzyme can help regulate fat synthesis and potentially manage related conditions.”
Accumulated Neuron Damage as We Age
Researchers at Massachusetts Institute of Technology (MIT) identified an enzyme called HDAC1 that is critical for repairing age-related DNA damage in genes associated with memory and cognition. In Alzheimer’s patients, as well as in normally aging adults, HDAC1 is often found in lower amounts. Their research suggests that restoring the enzyme could have benefits for both groups. The research was published in the journal Nature Communications.
“It seems that HDAX1 is really an anti-aging molecule,” said Li-Huei Tsai, director of MIT’s Picower Institute for Learning and Memory, and senior author of the research. “I think this is a very broadly applicable basic biology finding, because nearly all of the human neurodegenerative diseases only happen during aging. I would speculate that activating HDAC1 is beneficial in many conditions.”
In 2013, the same group published two papers linking HDAC1 to DNA repair in brain cells. The new research studied what happens when HDAC1-mediated repair didn’t happen. They worked with mice engineered to not produce HDAC1 in neurons and another type of brain cell, astrocytes. At first there was no noticeable difference in DNA damage levels or behavior, but as the mice aged, DNA damage began to accumulate in the HDAC1-deficient mice and lost some of their brain plasticity and problems in memory and spatial navigation. The loss of HDAC1 was associated with a specific type of DNA damage called 8-oxo-guanine lesions.