Viruses are scary enough as small micro-organisms that we cannot see with the naked eye, but artist Luke Jerram takes these deadly microscopic agents, and blows them up, literally, as glass sculptures.
Instead of the usual cartoons found in textbooks, these viruses can be examined from various angles, to understand their structures better. Great detail is put into each piece, making the glass sculptures practically exact replicas. Aesthetically, the work is beautiful, and few would even know that what they are admiring are the structures of an HIV virus, E. coli or even Smallpox.
The sculptures allow viewers to better understand, or at least to finally see for themselves, what attacks their immune (or other) systems, and especially what causes them to be sick. Of course, this does not mean that it will be easier to fight a virus if you know what it looks like, but for science, the sculptures are a great learning tool to understand the virus’ structures, and possibly even to recognize them better when looking under a microscope.
Viruses can spread through the air in two ways: inside large droplets that fall quickly to the ground (red), or inside tiny droplets that float in the air (gray). In the first route, called droplet transmission, the virus can spread only about 3 to 6 feet from an infected person. In the second route, called airborne transmission, the virus can travel 30 feet or more.
“The discovery of more and more viruses of record-breaking size calls for a reclassification of life on Earth.”
The theory of evolution was first proposed based on visual observations of animals and plants. Then, in the latter half of the 19th century, the invention of the modern optical microscope helped scientists begin to systematically explore the vast world of previously invisible organisms, dubbed “microbes” by the late, great Louis Pasteur, and led to a rethinking of the classification of living things.
In the mid-1970s, based on the analysis of the ribosomal genes of these organisms, Carl Woese and others proposed a classification that divided living organisms into three domains: eukaryotes, bacteria, and archaea. (See “Discovering Archaea, 1977,” The Scientist, March 2014) Even though viruses were by that time visible using electron microscopes, they were left off the tree of life because they did not possess the ribosomal genes typically used in phylogenetic analyses. And viruses are still largely considered to be nonliving biomolecules—a characterization spurred, in part, by the work of 1946 Nobel laureate Wendell Meredith Stanley, who in 1935 succeeded in crystallizing the tobacco mosaic virus. Even after crystallization, the virus maintained its biological properties, such as its ability to infect cells, suggesting to Stanley that the virus could not be truly alive.
Recently, however, the discovery of numerous giant virus species—with dimensions and genome sizes that rival those of many microbes—has challenged these views. In 2003, my colleagues and I announced the discovery of Mimivirus, a parasite of amoebae that researchers had for years considered a bacterium. With a diameter of 0.4 micrometers (μm) and a 1.2-megabase-pair DNA genome, the virus defied the predominant notion that viruses could never exceed 0.2 μm. Since then, a number of other startlingly large viruses have been discovered, most recently two Pandoraviruses in July 2013, also inside amoebas. Those viruses harbor genomes of 1.9 million and 2.5 million bases, and for more than 15 years had been considered parasitic eukaryotes that infected amoebas.
Now, with the advent of whole-genome sequencing, researchers are beginning to realize that most organisms are in fact chimeras containing genes from many different sources—eukaryotic, prokaryotic, and viral alike—leading us to rethink evolution, especially the extent of gene flow between the visible and microscopic worlds. Genomic analysis has, for example, suggested that eukaryotes are the result of ancient interactions between bacteria and archaea. In this context, viruses are becoming more widely recognized as shuttles of genetic material, with metagenomic studies suggesting that the billions of viruses on Earth harbor more genetic information than the rest of the living world combined. These studies point to viruses being at least as critical in the evolution of life as all the other organisms on Earth.
Scientists have cracked the mystery of what has killed millions of sea stars in waters off the Pacific coast, from British Columbia to Mexico.
Microbiology Prof. Ian Hewson of Cornell University in Ithaca, N.Y., said the culprit is densovirus, commonly found in invertebrates.
He said the virus literally made what are commonly called star fish dissolve within two to 10 days after infection, leaving them in a pile of goo on the ocean floor.
Hewson is the lead author of a study along with Ben Miner of Western Washington University that was published Monday in the Proceedings of the National Academy of Sciences.
He said the wasting disease hit about 18 months ago, at a time when the number of sea stars inexplicably exploded.
Most viruses in nature are common and help keep dominant species in check, but he said divers reported seeing mountains of sea stars in the ocean around the time mass mortalities started occurring.
“This very high number of sea stars in the Pacific Northwest leading up to this disease epidemic probably is what exacerbated the virus and made the switch between something relatively benign into something that was totally virulent,” Hewson said.
This is what happened when I searched the word “nightmare” under “places” on Facebook after an anonymous tip. As of now, I’m guessing that this is just a mass emailing virus. Still, it’s pretty creepy. If any of you have had similar emails, or messages, please let me know.
Here’s a nice picture of some Myoviridae phage which infect Salmonella. Generally in the phage world, there are three more common families although others have been found:
Siphoviridae with long flexible tails. (P2 above)
Myoviridae with long contractile tails (T4 above)
Podoviridae with short non-contractile tails. (P22 above)
Phage are first classified based on their morphologies, but bioinformatic information shows the relationships between the families. Typically families of phage are grouped on their appearance as a large amount of the phage genome goes into making the structural proteins.
Myoviridae are quite interesting in the sense that when they bind their host, there are large visible structural changes in the tail region. The tail sheath contracts and the DNA is transported from the head into the bacterium. Other less visible mechanisms are present in the other two morphology types too.
Scientifically speaking, why can't viruses be cured?
This depends on your definition of cure.
Many viruses can be prevented. Rotavirus, Polio, HPV, Varicella, Measles, Mumps, Rubella, Influenza, Hepatitis A & B can all be prevented with immunizations. However, many vaccinations are not 100% effective in preventing infection for two reasons: your personal immune system’s response to the vaccine, and mutation of viruses.
Your immune system, once exposed to a virus through infection or immunization, will create antibodies against a part of that virus (usually the envelope or shell of the virus). Over time, your antibodies may wane and you may be more susceptible to infection again. This is why we give booster vaccines, so that your immune system can “see” the invader again and bolster its defenses against it. For example, vaccination with one MMR shot offers 93% protection against measles, whereas protection goes to 97% with 2 shots.
Viruses also mutate (much like bacteria do when they become resistant to antibiotics) so that the body does not recognize them and attack with antibodies. They may also come in several common mutations or “strains,” so while you have immunity to one, you may be vulnerable to another. Some viruses mutate rapidly, like the flu, so we need repeat immunization against new strains and new mutations to keep up.
We tend to only vaccinate against the most common strains of a virus too, which is why you can get the Gardasil shot for HPV (which covers types 6,11,16, and 18) and still contract a less virulent strain of the virus. These multiple strains and mutations are also why it’s very hard to make a medication for viral illnesses (and why Tamiflu’s efficacy is modest at best for treating the flu). By the time a drug is made, the virus has mutated and it doesn’t work anymore.
Today’s #TBT is both a throwback and and a current news item: The measles, one of the most infectious viruses on the planet, is making a comeback in the United States. This comeback has kickstarted a nationwide discussion (and, in some cases, debate) - another comeback, one might say - on the importance of vaccination.
As anybody with a newspaper subscription, television, or even Facebook account is aware, the current measles outbreak started in California (at the happiest place on Earth, adding insult to injury!) and continues to spread, with the CDC adding 18 new cases a day to their official outbreak tally. As of just three days ago (!), 102 people in 14 states were infected with the virus.
According to an article, “Of the 34 people for whom the California Department of Public Health had vaccination records, only five had received both doses of the measles vaccine, according to the department. One received just the first dose. Nationally, officials are seeing the same trend, Schuchat said last week. ‘This is not a problem with the measles vaccine not working,” she said. “This is a problem of the measles vaccine not being used.’”
Vaccine denial may have been an easy conclusion to come to before, but following this outbreak, it’s become apparent just how dangerous this conclusion can be. However, a new study shows trying to convince those few remaining deniers might make things worse. From the article: “The paper tested the effectiveness of four separate pro-vaccine messages, three of which were based very closely on how the Centers for Disease Control and Prevention (CDC) itself talks about vaccines. The results can only be called grim: Not a single one of the messages was successful when it came to increasing parents’ professed intent to vaccinate their children. And in several cases the messages actually backfired, either increasing the ill-founded belief that vaccines cause autism or even, in one case, apparently reducing parents’ intent to vaccinate.”
Click the links interspersed above for further reading, and stay tuned for a (very belated, and long overdue) Disease Spotlight of the Week on…you guessed it: Measles.
When researcher Eric Delwart read about the many things that could be preserved in ice cores, he told NPR he realized he might be able to find buried treasure: caribou poop.
Now, the work has paid off. The well-preserved, 700-year-old remains of, yes, caribou poop that Delwart found contained DNA that he and some colleagues were able to extract. Eventually, they used it to reconstitute an entire plant virus.
“I mean we’re constantly shoving viruses down our throat and if you look at poo samples from humans and from animals you will find a lot of viruses,” Delwart, a researcher at Blood Systems Research Institute in San Francisco, told NPR.
The news, published in Proceedings of the National Academy of Sciences, is both exciting and scary: The virus “time capsules” found in Canada will undoubtedly help inform research on the evolution of viruses. But it also raises the possibility of unleashing ancient viruses as ice melts or Arctic regions are drilled.
“The find confirms that virus particles are very good ‘time capsules’ that preserve their core genomic material, making it likely that many prehistoric viruses are still infectious to plants, animals or humans,” Jean-Michel Claverie, of the Aix-Marseille University School of Medicine in France, told New Scientist. “This again calls for some caution before starting to drill and mine Arctic regions at industrial scales.”
Although Delwart’s team was able to get the buried virus to infect a type of tobacco plant, he told NPR that this particular virus isn’t dangerous.
“There’s a theoretical risk of this, and we know that the nucleic acid of the virus was in great shape in our sample,” Delwart told New Scientist. “But old viruses could only re-emerge if they have significant advantages over the countless perfect viruses we have at present.”
If you live in the US, you might have heard that the flu vaccine released this year is not a “good match” for the viruses going around. How could this have happened?
Influenza viruses have proteins on their surfaces that the immune system can recognize. Two of these proteins are called hemagglutinin (HA, shown in the graphic above) and neuraminidase (NA), which are the “H” and “N” found in the virus names. One of the reasons why flu viruses are so successful is because they can easily mutate and change the structure of these proteins. Here are two ways in which these mutations can happen:
Antigenetic drift: Errors occur in genes when they are being copied to make new viruses. This is common for flu virus genes because they are made of RNA, not DNA. The virus’ host cells have mechanisms to fix errors in DNA but they cannot fix RNA.
Antigenetic shift: Different subtypes of the same virus infect the same host cell and mix and match their genes to make a new virus. This happens often with flu viruses because of their ability to jump species. A flu virus that mostly infects birds may be able to infect a human cell and mix its genetic information with a flu virus that mostly infects humans, producing a new subtype of virus.
So should you still get the flu vaccine?Yes! Even though the H3N2 viruses’ surface proteins have changed, there is still a good chance that the H3N2 virus parts in the vaccine are similar enough to them that the vaccine can help teach the immune system to respond to them. There are also other two other viruses included in the vaccine that it can help protect you from.
The CDC has a nifty little vaccination pledge you can fill out if you have gotten the vaccine or are ready to get it.
You can read more about the flu vaccine, its safety and why it’s so important here.