Viruses Can Steal Our Genetic Code to Form New Genes

Ho JSY et al. Hybrid Gene Origination Creates Human-Virus Chimeric Proteins during Infection. Cell, June 2020;

Viruses have the ability to inflict their hosts with a multitude of dreadful, and often deadly, diseases. Humans have dealt with deadly viral diseases for millennia ranging from smallpox to the Spanish flu and the recent COVID-19 pandemic. One of the most fascinating features of these tiny, deadly organisms is that they cannot even build their own proteins. They depend entirely on their host to build their proteins for them. When a virus infects a host cell, it uses the cell’s transcription and translation machinery in order to produce its proteins and to generate copies of itself. A new paper describes a previously unknown mechanism that can occur during this process wherein viruses steal genetic signals from their hosts to expand their own genomes. This allows viruses to make hybrids of host mRNAs with their own genes thereby producing novel hybrid proteins named “UFO” (Upstream Frankenstein Open reading frame) proteins. As a proof-of-principle, scientists showed that at least 10% of influenza A viruses had these hybrid UFO proteins. Furthermore, UFO proteins can be detected by our immune systems and may even modulate virulence. Further studies are still needed to understand this novel class of proteins and the implications of their pervasive expression by many of the RNA viruses that cause epidemics and pandemics. UFO proteins can potentially alter the course of viral infections and could very well be positively exploited for new, and more effective, vaccines.

Superhuman Antibodies Can Protect Against COVID-19

Rogers TF et al. Isolation of potent SARS-CoV-2 neutralizing antibodies and protection from disease in a small animal model. Science, June 2020.

Development of a treatment, or vaccine, for COVID-19 is currently the world’s top public health priority. Globally, about 8 million people have tested positive for SARS-CoV-2 infection, and more than 400,000 have died. The daily toll of new infections is still rising. Amid an international race to find a vaccine for COVID-19, researchers have discovered a subset of antibodies, in the blood of recovered COVID-19 patients, that provide powerful protection against SARS-CoV-2, the coronavirus that causes the disease. Researchers first took blood samples from patients who had recovered from mild-to-severe COVID-19. Then, they tested whether antibody-containing blood from these patients could bind to the virus and strongly block it from infecting test human cells that express ACE2, the receptor that SARS-CoV-2 uses to infect human cells. Initial experiments led to the isolation of 1000 distinct antibodies produced by immune cells, each of which showed a distinct anti-SARS-CoV-2 affinity. Among those antibodies, the team identified several antibodies that could successfully block the virus and protect hamsters against heavy viral exposure. These super-strength neutralizing antibodies are found to target spike proteins of the Coronavirus that are localized at the viral surface and are essential for the virus to attach itself to human cells. These antibodies effectively keep the virus from entering human cells and could essentially knock out the infection. Interestingly, while non-neutralizing Coronavirus antibodies are found in 75% of patients, neutralizing antibodies are only found in fewer than 5% of patients. The current strategy involves cloning the immune cells that produce these super antibodies in order to mass-produce them and reinject them into sick patients. Scientists predict that if further safety tests in animals and clinical trials in people go as expected, the antibodies could potentially be used in clinical settings as early as next January. This new study proposes a paradigm of swift reaction to an emergent and deadly viral pandemic and sets the stage for clinical trials and additional tests of the antibodies.

Living Environments Are the Key to Longevity

Bhardwaj R. et al. Environmental Correlates of Reaching a Centenarian Age: Analysis of 144,665 Deaths in Washington State for 2011−2015. International Journal of Environmental Research and Public Health. April, 2020.

Growing evidence indicates that while good genes can help us live longer, they do not tell the full story when it comes to what it takes to live a long and healthy life. A new study found that where you live has a substantial impact on the likelihood that you will reach centenarian (100+ years old) age. Researchers examined the data of 145,000 Washington residents who died at the age of 75 or older between 2011-2015. Survival analysis derived from these data showed that neighborhood walkability, higher socioeconomic status, and a high percentage of working age populations were found to be positively correlated with reaching 100 years of age. One important indication from this study is that mixed-age communities where streets are more conducive for walking makes exercise more accessible for older adults and thus makes it easier for them to access medical care and grocery stores. Moreover, older adults are less likely to experience isolation, and receive important community support in these settings. Past studies estimated that heritable factors only explain about roughly 20% to 35% of an individual’s chances of reaching centenarian age. This study supports the idea that you can modify your susceptibility to different genetic diseases through your behavior. In other words, if you live in environments that support healthy aging, it will likely impact your ability to beat your genetic odds through lifestyle changes.

Original article: Kim P. et al, ACS Nano (2012, online ahead of print)

Frost formation on aircrafts at high altitudes poses major safety threats and high-maintenance costs. Now, Joanna Aizenberg with her research team present a solution in their recent publication reporting on outstanding capabilities of a surface coating to prevent frost formation on metal surfaces. The technology called SLIPS (Slippery, Liquid-Infused Porous Surfaces) was inspired by the slippery surface of the carnivorous pitcher plant, which enables the plant to capture insects. “Some of the most extreme examples in biology can provide the most amazing and unexpected ideas…” says Aizenberg, who is a professor at the Wyss Institute for Biologically Inspired Engineering at Harvard University. Rendering surfaces slippery is not new to scientists, and the earlier inspirations also came from biology. Mimicking the surface of the leaf of another plant (Nelumbo nucifera, or commonly known as the Lotus plant), scientists have been successful in fabricating surface coatings that would repel water-based dirt, but Lotus-inspired coatings failed for oily substances. On the other hand, Aizenberg’s SLIPS technology offers a single solution for repelling any type of accumulated unwanted material. The pitcher plant thus offers a solution that virtually proves to be the “silver bullet” in generating non-sticky coatings as described again in Aizenberg’s own words: “In following its example, we should be able to develop a platform that works for almost any sticky problem, no matter how seemingly unrelated, whether it’s ice accumulation, bacterial attachment, environmental contamination, clogging of pipes, marine biofouling, or graffiti, rather than having to come up with a host of individual solutions.” Thanks to the wondrous design in the pitcher plant, it looks like doctors will be delivered from replacing bacteria-contaminated arterial stents, and we can all give a kiss goodbye to frosty freezers.

2- Airborne bird flu virus possesses a great risk

Original articles: Herfst S. et al, Science 336, 1534 & Russell C.A. et al, Science 336, 1541.

Science magazine recently published a special issue (June 22, 2012 issue) on the H5N1 infection (a.k.a. bird flu) with two reports revealing the pandemic (a disease prevalent throughout an entire country, continent, or the whole world, such as AIDS) potential of bird flu. Bird flu virus has so far killed millions of birds and many more millions of birds were culled to stop the propagation of the virus. Thankfully, this virus has not yet caused a pandemic in humans mainly because of its inability to spread easily among humans. One mechanism that makes viruses highly contagious is their ability to spread through air, such as through the nose and mouths of people when they cough and sneeze. Viruses that spread through air are called airborne viruses. One big difference between bird flu virus and the more recent swine flu virus (H1N1) was that swine flu is an airborne virus and bird flu is not, and therefore swine flu caused a mild pandemic in 2009. As reported in these studies, researchers identified several genetic mutations that will cause bird flu virus to become airborne. Viruses undergo mutations all the time and unfortunately some of these identified mutations have already started taking place in circulating virus strains. This poses a great risk. One important aspect of these reports is that they were written about a year ago but withheld since now, because of concerns about misuse of this information to pose a threat to humanity. Now that the information is public, our hope is that it will be used to monitor the virus closely and be prepared if bird flu virus transforms into an airborne virus.

3- Not all bacteria are the same after all

Original article: Chung H. et al, Cell 149, 1578 (2012)

The impact of our own bacteria on human life has been intensely researched in recent years. One of the common ground is that humans acquire many useful bacteria over their existence. However, this microbial flora constantly changes as the conditions do. Therefore, the real number of 500 to 1000 microbial species inhabiting mammals is anybody’s guess. Nonetheless, some scientists did not shy away predicting a connection between having a specific microbial flora to avoid certain diseases. A recent article by Chung et al presented an interesting clue why constant change in microbial flora, especially if that leads to a loss of important bacteria, may be linked to the increase in human autoimmune disorders. “For every cell in your body that is you, that contains your specific genetic information, there are approximately nine foreign bacterial cells, primarily in your digestive tract and even on your skin,” said Dennis Kasper, professor at Harvard Medical School and senior author on the paper. To address the question if microbial affects immune system development, authors compared two groups of mice, both of which had never had bacteria in their intestine before the experiment. One group of mice received mice microbial flora and the other received human microbial flora. Both groups had similar number of bacteria in their digestive tracks. However, authors observed a stark contrast between the two groups in terms of the level of immune cells in intestinal tissues. Mice that received human flora had surprisingly low number of immune cells compared to the mice that received mouse flora, which is native to mice. When this experiment was repeated with rat microbial flora, astonishingly, similar immune deficiency was observed. “I was very surprised to see that. I would have expected more of a half-way response,” Chung said, considering how closely rats and mice are related. The study points out that we really need to preserve our own microbial flora that has been tailored for us. Disrupting this balance by means of current antibiotics overuse may have detrimental effects in the future.

Original Article: Ichinohe T. et al., PNAS (published online before print 2011).

Influenza, also known as seasonal flu, affects up to 5 million people annually. Flu viruses infect and damage the animal respiratory tract, especially the lungs. Upon flu virus infection, a life or death battle between an animal’s immune system and the flu virus begins. To defeat the flu virus, the animal’s immune system synthesizes important flu-fighting molecules. Researchers at Yale University discovered that mice on the antibiotic regimen, a treatment that wipes out certain bacteria which normally live in the guts of the animal hosts, showed deficiency in immune responses against flu virus in the lungs compared to mice that had not been treated. This finding suggests an unexpected link that the bacteria living in the animals seem to control the production of these flu-fighting molecules. These commensal bacteria, or good bacteria, prime the immune system in making flu-fighting molecules even before infection, and this priming is important for subsequent flu-fighting strategies. The exact bacterial species that helps fight the flu are yet to be identified. It is interesting to contemplate why the immune system trusts bacteria with such an important job. Whatever that reason might be this finding warns against misuse or abuse of antibiotics. We don’t want to kill the good bacteria that might just protect us in the next flu season.

2- Less talking with longer words

Original Article: Piantadosi S.T. et al., PNAS 108, 3526 (2011).

What factors affect the length of a word? Do we prefer to use short words or long words while we are talking? For many years, researchers believed that the most frequently used words tend to be short in order to make the language more efficient. It is intuitive when we think of words such as “a,” “the,” “but” and their popularity in our everyday life. However, according to a recent study done by Piandatosi and coworkers in the Department of Brain and Cognitive Sciences at MIT, the length of a word reflects the amount of information it contains. They observed that people use many words in predictable sequences along with other words in their daily life. Most of the time a short word may not contain information per se, but carry information as a collection with other familiar words. This observation led the researchers to look at the problem from an ‘information content’ perspective. A word is said to have more information if it is less predictable in a sequence. An analysis was done on the Google text database in 11 different languages. The results show that word length closely correlates to information content. Once again, it is not important how much you talk. It is important how much you mean.

3- Ups and downs of sleep with alpha waves

Original Article: McKinney S.M. et al., PLoS One 6, e17351 (2011).

Why do we randomly wake up in the middle of the night? Searching for an answer for this question, researchers at the Massachusetts General Hospital (MGH) discovered a brain rhythm that determines one’s susceptibility to disturbance by the outside world while asleep. Scott McKinney and his colleagues conducted a study where they analyzed the electroencephalographs (EEGs) of 13 volunteers, who spent 3 nights in MGH’s Sleep laboratory. EEG devices use electrodes on the scalp to detect electrical activity in the brain. There are four major brain waves that can be detected by EEG: alpha, beta, delta and theta waves. Alpha waves usually emanate from the back of the head during relaxed wakefulness, particularly when your eyes are closed, and they are thought to gradually disappear when a person goes to sleep. Researchers developed a special computational method that can probe EEGs in much deeper data resolutions. Their analyses revealed that alpha waves never disappear during sleep; they just go below conventional detection levels. Moreover, when alpha wave activity spikes just before an obnoxious auditory stimuli (e.g., loud talking or traffic noise) is played, volunteers seems to wake up more easily than when alpha wave activity was low. These findings suggest that maybe the alpha wave activity is the brain’s way of keeping us aware of our surroundings during sleep, and perhaps it enables us to wake up quickly in case of danger. Of course, too much alpha activity might also have a downside: it can make you a light sleeper and give you restless nights.

4- Killer whales imitate enemies and friends

Original Article: Wei B.M. et al., Marine Mammal Science (published online before print 2011).

In marine mammals, as individuals frequently cannot see each other, sound is particularly important for communication. Killer whales live in groups or clans, and these different clans have their own dialects. A recent study showed that whales can do more than just talk in their own language: they can mimic calls from other groups with a different dialect. While analyzing the social behavior of wild orcas living near Vancouver Island in British Colombia, a group of researchers from the University of Vienna discovered that resident whales occasionally produce call types from the repertoires of other vocal clans. The calls resemble the calls of foreign groups that the original group interacted with before. When different clans are in close proximity, it is quite challenging to reliably distinguish original calls from resembling calls. For this reason, researchers recorded calls that resemble call types of a different clan in the absence of that clan and compared them to the originals of the respective call types by analyzing their sonograms. Sonograms reveal distinctive information about the structure of the sound waves, i.e. the spectral density of these signals, and this information can be used to classify animal sounds. The comparative analysis clearly shows that killer whales can imitate calls from other groups even when members of that group are not around. Researchers suggest that this could be a way of labeling outsiders or keeping tabs on their location. Maybe by impersonating the calls of a group, they are conveying a message about that group to their own family members. It is exciting to see that vocal mimicry is not limited to songbirds and dolphins, and that killer whales have more complex social lives than we previously thought.