Where Do “New” Viruses Come From?

Every year there seems to be a new virus that just popped up out of nowhere to cause us a great deal of pain and suffering. Is it the work of a mad scientist vying for global domination? Are these viruses coming back to life after being frozen for millennia? Are they hitching a ride to Earth via meteorites?

The truth is many of these viruses are not so new – but we are creating new opportunities for them to infect us. Many viruses jump from other animals into people – a process known as “zoonotic transmission” – and some of our actions roll out the red carpet for the virus. Let’s take a closer look at where some of these “new” viruses may have originated and how they spiral out of control.

Zika

Microcephaly is a term used to describe babies born with much smaller head size than normal, which is indicative of incomplete brain development. In Brazil, this birth defect occurs about 150 times per year. However, in the past 4 months, nearly 4,000 babies have been born with microcephaly - a dramatic spike that has set off alarm bells.

Photo of a child born with microcephaly, which has been linked to the Zika virus.

While evidence is still circumstantial, the primary culprit is a previously obscure virus called Zika, named after the forest in Uganda where it was first identified in a rhesus monkey back in 1947. Zika is transmitted through mosquitoes, which basically operate like flying dirty syringes. If they fed on an infected person, they can transmit the virus to the next person they bite.

Global warming and increased travel have conspired to create excellent opportunities for viruses like Zika to spread. It only takes one infected person to attend a major spectacle (for example, the 2014 FIFA World Cup in Brazil) to start a chain reaction of viral transmission. Viruses need no passports and can jet set around the world in unprecedented time. Global warming is an issue because it has allowed the species of mosquito that carries these viruses to thrive in areas that used to be too cold. Even El Niño has been catching some of the blame for helping to spread Zika.

Ebola

While Zika jumped to humans from other primates, the African filovirus Ebola is thought to have originated in fruit bats. Bats can transmit a number of other deadly viruses, including rabies. Bats happen to be a source of food in several of the areas where Ebola outbreaks have occurred, consistent with the idea that bats are the culprits. Once Ebola infects a human, it can spread quite easily to other people through bodily fluids.

Bats like this one are now considered to be a major carrier capable of spreading the Ebola virus to people.

Ebola first appeared in humans in 1976 in the Sudan and the Democratic Republic of Congo. The initial outbreak killed an estimated 600 people, but the latest outbreak that began in 2014 in West Africa has been the worst in history, killing over 11,000 people. This wasn’t due to an enormous fruit bat invasion, but rather human-to-human transmission. Genetic studies indicated that the entire epidemic likely stemmed from just a single infected child in Guinea, the so-called “Patient Zero”. A catastrophic mix of poor health facilities and unsanitary practices ignited to spread the virus like wildfire.




The 2014 Ebola outbreak started with a toddler who fell sick in Meliandou village in Guinea. Source.
Credit: Live Science

MERS

MERS, Middle East Respiratory Syndrome, first made headlines in 2012. This life-threatening respiratory virus reared its ugly head in Saudi Arabia first, but has since been reported in 25 other countries, including those not in the Middle East (due to unwitting travelers carrying more than their luggage). MERS is caused by a coronavirus, so the causative agent is typically referred to as MERS-CoV. Like many other respiratory viruses, coughing in close proximity can spread MERS-CoV between people.

But how did MERS-CoV get into people in the first place? According to the World Health Organization:  “It is believed that humans can be infected through direct or indirect contact with infected dromedary camels in the Middle East. Strains of MERS-CoV have been identified in camels in several countries, including Egypt, Oman, Qatar and Saudi Arabia.”

It is easy to understand the respect and admiration one can have for a noble creature like the camel. But getting a little too intimate with a camel may literally leave you breathless.

So stay away from coughing camels! In some areas, camels are butchered for food and their milk and urine (yes, urine) is consumed. These practices provide additional avenues for possible transmission of MERS-CoV to humans.


UPDATE (3/1/16): A new study suggests that we have bats to thank once again for spreading MERS-CoV to camels.

HIV

Human Immunodeficiency Virus (HIV), which causes AIDS, wasn’t on anyone’s radar until an unusually large number of people starting suffering from rare diseases with strange names like Kaposi’s sarcoma, toxoplasmosis, and pneumocystis. These diseases are hardly ever seen in people with normal, healthy immune systems. Turns out they were secondary infections – the primary infection was HIV, which was destroying the very immune cells that are needed to keep those other illnesses at bay.

Historical records have placed the earliest cases of HIV infection to the 1950s, which suggests it has been moving through humans slowly through the decades prior to its explosion in the early 1980s. An increase in international travel, unsafe sexual practices, and intravenous drug use are all factors that have contributed to accelerating the epidemic.

HIV (yellow particles) is a cunning foe that destroys the immune cells (blue) designed to protect us from foreign invaders.

We still don’t know how HIV leapt into the fabric of human DNA, but the evidence is very strong that it came from other primates. SIV, or simian immunodeficiency virus, has been found in African primates and is highly similar to HIV; it is easy to imagine that blood from infected primates, some of which are butchered for food or kept as pets, found its way into a person's open wound. Once in humans SIV evolved into HIV, transmissible to others through bodily fluids. HIV likely spread around Africa in its early days through the use of shared needles in impoverished hospitals.

It’s a virus world after all

As you can see from these examples, many “new” viruses were actually pre-existing in other animals and just made a “species jump” into humans. But how did these viruses get into the other animals in the first place? That question is a lot harder to answer.

Viruses are little more than a fragment of DNA or RNA, perhaps rogue genes that escaped a cell and became independent, infecting other cells in order to replicate and spread. Richard Dawkins coined the term, “the selfish gene”, and that is a very accurate description of viral DNA/RNA. What we do know is that viruses have been around a long, long time, perhaps before the dawn of life itself. There are even viruses that infect bacteria.

Once inside host cells, viruses replicate quickly, which means they are very adaptable. Their ability to evolve quickly is likely to be a key factor explaining why these selfish genes can make a reproductive factory out of a wide variety of different hosts…and why “new” viruses can appear to spring out of nowhere.

While viruses are a nuisance to us now, they may have been important drivers of evolutionary change in the past. It has been proposed that RNA viruses may have led to the formation of DNA and DNA replication mechanisms, without which we would not even be here to complain about them!

Contributed by:  Bill Sullivan, Ph.D.

Follow Bill on Twitter.

Simpson, D. (1964). Zika virus infection in man Transactions of the Royal Society of Tropical Medicine and Hygiene, 58 (4), 339-348 DOI: 10.1016/0035-9203(64)90201-9


Forterre P (2006). The origin of viruses and their possible roles in major evolutionary transitions. Virus research, 117 (1), 5-16 PMID: 16476498


Koonin EV, Senkevich TG, & Dolja VV (2006). The ancient Virus World and evolution of cells. Biology direct, 1 PMID: 16984643


Baize, S., Pannetier, D., Oestereich, L., Rieger, T., Koivogui, L., Magassouba, N., Soropogui, B., Sow, M., Keïta, S., De Clerck, H., Tiffany, A., Dominguez, G., Loua, M., Traoré, A., Kolié, M., Malano, E., Heleze, E., Bocquin, A., Mély, S., Raoul, H., Caro, V., Cadar, D., Gabriel, M., Pahlmann, M., Tappe, D., Schmidt-Chanasit, J., Impouma, B., Diallo, A., Formenty, P., Van Herp, M., & Günther, S. (2014). Emergence of Zaire Ebola Virus Disease in Guinea New England Journal of Medicine, 371 (15), 1418-1425 DOI: 10.1056/NEJMoa1404505

Ice, Ice Baby: Bringing Frozen Viruses Back To “Life”

Back in 2003, a new class of giant, ancient viruses were found that preyed upon unsuspecting amoebas in the Paleolithic.  

Earlier this year, scientists published a study describing how they revived another one of these giant viruses, which has been frozen in Siberian permafrost for 30,000 years! We’ll discuss why they did this in a bit, but let’s first talk about how they did this.

Over the years, lots of cool stuff has been found well-preserved in ice. Otzi, a 5,000 year old “ice man” was a historic find in 1991. He went on to become a spokesperson for the GEICO auto insurance company.

Viruses are minute obligate intracellular parasites. In other words, they cannot replicate outside of a host cell, an attribute that gives them the unflattering distinction of being the worst houseguest ever. That’s right:  viruses storm into your home – unannounced – take off their coat and make themselves right at home. They ransack the place and raid your fridge without even asking. As if that wasn’t bad enough, you come home one day and catch the virus in the act of making babies – lots and lots of babies. Finally, this unruly family blows up your house as they leave, without so much as a “thank you”, and go on their merry way to invade other homes in your neighborhood.

While we can feel the pain that they cause, especially during cold and flu season, we can’t see the culprits. Viruses are really, really tiny - most are smaller than the molecular complex cells use to make proteins.

Many viruses are under 100 nM (0.1 micron), but some (like Ebola) are almost 1.0 micron. Compared to viruses, even a bacterium is enormous. 

So how does one find a virus in thousands of miles of ice? Virus hunters take an approach similar to finding a needle in a haystack. But in this case, instead of a magnet, the scientists use amoebas as “bait” to lure out viruses that might be chilling out in the permafrost.

Amoebas are single-celled organisms called protozoa that, like most cells, fall prey to viruses. By putting permafrost into amoeba cultures, scientists were able to screen samples for those that could kill the amoebas. And they found a “big” surprise.



Thick membrane or no, Pithovirus invades amoebas. Who knows…with this discovery, maybe scientists can devise a new treatment that targets the deadly brain-eating amoeba, Naegleria.

The virus spotted in these infected amoeba cultures resembled a so-called “pandoravirus” or “giant” virus. They are still microscopic of course, but considerably larger than the viruses we know of today (about 1.5 microns in length and 0.5 microns across). Not only are they larger in size, but they contain many more genes. By way of comparison, HIV contains less than 15 genes, but this giant virus has 500 genes. They christened this new giant virus “Pithovirus sibericum”, and it is the oldest virus ever to have been revived to date.

A “huge” find in the world of virology, Pithovirus is now growing in labs again after a 30,000 year slumber. Image taken from Legendre, et al.

Now why on earth would scientists bring a virus back from the dead? Are they mad? Are they trying to facilitate the apocalypse?

Of course not. As climate change continues to melt more and more ice, it is possible that these viruses are going to revive naturally. By resurrecting them in the lab in controlled conditions, researchers can get ahead of this curve by studying the virus. Study of the virus can help determine which one(s) pose a threat and, if so, vaccine and drug development efforts can get underway thanks to our knowledge of the virus. And don’t worry about Pithovirus – it was already found to be incapable of infecting animal cells.

Another reason these viruses are worthy of study is that they can reveal new insights into how cells evolved, since viruses can transfer their DNA to their hosts. They may even shed light on the greatest biological mystery:  the origin of DNA/RNA and how life came to be on Earth.

The same team of scientists isolated yet another ancient giant virus this year from the same permafrost and named it Mollivirus sibericum. You may also be wondering what Siberian virus hunters listen to while exploring those Hoth-like landscapes. I'll take a guess and hope that it is wrong...
 

Contributed by:  Bill Sullivan, Ph.D.
Follow Bill on Twitter.

Legendre, M., Lartigue, A., Bertaux, L., Jeudy, S., Bartoli, J., Lescot, M., Alempic, J., Ramus, C., Bruley, C., Labadie, K., Shmakova, L., Rivkina, E., Couté, Y., Abergel, C., & Claverie, J. (2015). In-depth study of , a new 30,000-y-old giant virus infecting Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.1510795112

 

Legendre, M., Bartoli, J., Shmakova, L., Jeudy, S., Labadie, K., Adrait, A., Lescot, M., Poirot, O., Bertaux, L., Bruley, C., Coute, Y., Rivkina, E., Abergel, C., & Claverie, J. (2014). Thirty-thousand-year-old distant relative of giant icosahedral DNA viruses with a pandoravirus morphology Proceedings of the National Academy of Sciences, 111 (11), 4274-4279 DOI: 10.1073/pnas.1320670111

Why Should You Care How Bacteria Fight Viruses?

Regular readers have been learning a great deal about the human immune system thanks to our ongoing series on allergies by Julia van Rensburg. But did you know that bacteria have an immune system of sorts, too? Yes, even germs get germs!* Bacteria are susceptible to a group of viruses called bacteriophages, or phages for short. Phages resemble early spacecraft and “land” on the surface of bacteria in order to inject their DNA/RNA, much like a syringe ejects its contents.

Houston, we have a problem! A phage has just injected its DNA into our cell!

Bacteria, which have been on Earth for some 3.5 billion years, have had plenty of time to evolve defense mechanisms against predatory phages. Just like human viruses, phages are a most unwelcomed guest. They barge into the cell unannounced, “borrow” cellular components without asking, and then use them to make baby viruses until the cell becomes so engorged with viral progeny that it explodes, releasing the huge viral family so that it can invade more bacteria and repeat the process all over again. Phages that burst the bacterium like this are called “lytic”, but there are other types that don’t blow the house up. These are referred to as “lysogenic” phages and can insert their genetic material into the bacterial genome, becoming a permanent resident of that bacterium. Even more sinister, the incorporated viral genome is copied like all the other bacterial genes when the bacterium divides, so it is inherited by the daughter cell!

Lytic phages will replicate until they blow the infected bacteria apart. In contrast, lysogenic phages can stick around forever, even getting passed on to future generations since the viral genome was inserted into the bacterial genome.

So that sucks – imagine if you had uninvited viral DNA shoved into your DNA – such viruses basically transform you into a GMO. Sorry to inform you, but up to 8% of your genome is already littered with lots of viral DNA. If you oppose GMOs, I hope you can still stand to be in your own skin!

Presently, we don’t know how to remove foreign DNA from our own. But bacteria have figured out a way to get rid of incoming phage DNA, which provides the basis for a type of bacterial immune system.

 

Some combinations work great together, like chocolate and peanut butter. But getting viral DNA stuck into your own DNA, a strategy used by many viruses including HIV, is not a welcome combination.

In 1987, scientists uncovered unusual repeat sequences in the genome of E. coli bacteria, which were later named “clustered regularly interspaced short palindromic repeats”, or CRISPR. In the early 2000s, scientists identified bacterial proteins interacting with CRISPR sequences (now called CRISPR-associated (Cas) proteins) and discovered that they provide resistance to phage infection. Through the efforts of many laboratories, it is now known that bacteria can use a phage invasion as a vaccination by incorporating some of the foreign DNA between CRISPR repeat sequences. This provides the bacteria with a “catalogue” – a memory system, if you will – of foreign DNA that it can pass along to future generations.

But CRISPR is not just a storage system. The bacteria can retrieve these sequences and hook them to Cas9, a nuclease enzyme that can cut DNA. When foreign DNA enters that bacteria, its CRISPR-Cas9 system can specifically target the invasive element and neutralize it.


Foreign DNA, such as that injected by a phage, can be neutralized by CRISPR/Cas9, which serves as a type of bacterial immune system. Bacteria can store foreign DNA sequences in its genome and express them as crRNAs that bind to Cas9. If the bacterium encounters foreign DNA that matches any of the sequences stored in its CRISPR array, the crRNA will deliver Cas9 to that invading sequence to chop it up.

Pretty clever for tiny bacteria, huh? But here is where things get really interesting, or worrisome, depending on your appetite for paranoia. Scientists have adapted CRISPR/Cas9 to work in all sorts of cell types, including human. Cas9 acts as DNA shears that can cut wherever we tell it to by directing it with a “guide RNA” (analogous to how a crRNA operates in bacteria). This provides us with an unprecedented means to easily “edit” the genome of virtually any living thing, including stem cells and embryos. Furthermore, Cas9 has been modified to do more than just cut DNA; versions exist now that can insert new DNA sequences or switch out bad (mutated) DNA with good DNA.

In the hit TV show, Orphan Black, a group of clones discover that their DNA has been “barcoded” to designate them as intellectual property by their maker. Theoretically, CRISPR technology could have been used to tag DNA in this fashion.

The power of genome editing can be used for good. Several diseases, such as cystic fibrosis and sickle-cell anemia, are caused by a single mutation in one gene. CRISPR/Cas9 is a plausible tool that may be able to repair this defect. However, tinkering with one gene can have unforeseen repercussions on other genes, so this exciting technology could have adverse effects. In March, 2015, a group of scientists proposed a ban on editing the human genome, arguing that a greater understanding of how CRISPR/Cas9 works is required before we even consider applying it clinically.

Gene editing using CRISPR/Cas9 can be used to modify the genome of virtually any creature. One recent application is the creation of wheat that is resistant to a fungus that causes mildew.

Here is a video that shows how CRISPR/Cas9 works and some of the applications it may have down the road:

 

 

Contributed by:  Bill Sullivan

Follow Bill on Twitter.

*It should be noted that not all bacteria are “germs”; in fact, many species of bacteria inhabit our bodies to constitute our “microbiome” and provide important services to us. Learn more about your microbiome here.
 

Sander JD, & Joung JK (2014). CRISPR-Cas systems for editing, regulating and targeting genomes. Nature biotechnology, 32 (4), 347-55 PMID: 24584096

Garneau, J., Dupuis, M., Villion, M., Romero, D., Barrangou, R., Boyaval, P., Fremaux, C., Horvath, P., Magadán, A., & Moineau, S. (2010). The CRISPR/Cas bacterial immune system cleaves bacteriophage and plasmid DNA Nature, 468 (7320), 67-71 DOI: 10.1038/nature09523

Horie, M., Honda, T., Suzuki, Y., Kobayashi, Y., Daito, T., Oshida, T., Ikuta, K., Jern, P., Gojobori, T., Coffin, J., & Tomonaga, K. (2010). Endogenous non-retroviral RNA virus elements in mammalian genomes Nature, 463 (7277), 84-87 DOI: 10.1038/nature08695

Horvath, P., & Barrangou, R. (2010). CRISPR/Cas, the Immune System of Bacteria and Archaea Science, 327 (5962), 167-170 DOI: 10.1126/science.1179555

Baltimore, D., Berg, P., Botchan, M., Carroll, D., Charo, R., Church, G., Corn, J., Daley, G., Doudna, J., Fenner, M., Greely, H., Jinek, M., Martin, G., Penhoet, E., Puck, J., Sternberg, S., Weissman, J., & Yamamoto, K. (2015). A prudent path forward for genomic engineering and germline gene modification Science, 348 (6230), 36-38 DOI: 10.1126/science.aab1028

Outbreak! Time To Review The Origins Of Vaccination

The US is currently experiencing an alarming spike in the number of measles cases. Yes, measles! Don’t we have a vaccine for that virus? Yes, we do. It first became available in 1963 and was so effective that by 2000 the US declared it had eliminated measles. But in 2014, a record 644 cases suddenly appeared in 23 distinct outbreaks.

Measles is caused by a very contagious virus that infects the respiratory system, causing high fevers, coughing, and a nasty rash. Complications are common and can lead to life-threatening situations, especially in undeveloped nations. Measles has rarely been seen in the US in recent decades, but has made an alarming resurgence in 2014-15.

Unfortunately, 2015 is shaping up to be a bad year for measles, too, largely due to a multi-state outbreak propagated by so-called anti-vaxxers attending Disneyland in California. A study published last month showed that this single incident has spread measles to seven states and two additional countries and was due to parents who declined to vaccinate their children. Sadly, many of those who were infected were innocent bystanders of this misguided decision - they could not be vaccinated due to age or a legitimate medical condition.

We’ve recently discussed some of the fears the anti-vaccine movement cites to justify their opposition to vaccination, much of which stems from the completely fraudulent studies of the disgraced doctor, Andrew Wakefield. But perhaps it is worthwhile to take a trip back in time to review the origins of vaccination, which begin with the horrifying disease called smallpox.

Referred to as “the Speckled Monster”, smallpox is caused by an extremely contagious virus with a signature “dumb-bell” appearance.

Once infected with the smallpox virus, the victim becomes covered head to toe with burning pustules. The virus can also infect internal organs, which usually meant death in less than a month. Those lucky enough to survive the infection were left badly scarred and disfigured. Humanity has been struggling with this dreadful affliction since at least 1100 BC. We know this because the mummy of Egyptian pharaoh Ramses V contains the signature pockmarks caused by smallpox. Recent genetic studies suggest that the smallpox virus emerged 3000 to 4000 years ago in east Africa.

Smallpox is one of a number of infectious agents that has been a major factor in steering the course of history. Smallpox was instrumental in the conquering of the Aztecs in 1521 by Hernan Cortes and the Incas by Pizarro in 1533. Disturbingly, the early Puritan settlers in North America considered smallpox a “miracle” that purged their “New World” of the Native Americans.

The first advance in treating smallpox, which hinted at a new era of medicine, was made around 950 AD in China. Someone took note that smallpox survivors never got the disease twice and got the idea that maybe by giving someone a tiny bit of the disease on purpose would protect them from the real thing. To do this, they took the scabs from someone who looked like they were beating the infection, ground them into a powder, and blew them up the nose of someone who hadn’t caught smallpox yet. It sounds disgusting, but it worked! The scab-sniffers got very mild cases of smallpox but recovered.

By the late 1600s, the Chinese practice of delivering smallpox scabs into healthy people to prevent the disease had been refined and spread to the Turkish Empire. As shown above, a drop of pus from a person beating smallpox was scratched into the skin to “inoculate” another person and prevent him or her from getting the full-blown disease. The technique spread to England thanks to Lady Mary Wortley Montagu, wife of the ambassador to Turkey in the early 1700s.

These primitive vaccination efforts carried a great deal of risk compared to today’s methods. Since the individual was being inoculated with live smallpox virus, there was always a chance of developing full-blown smallpox and dying, along with the risk of transmitting smallpox to others. To offset the latter, England instituted “inoculation stables”, woeful low-cost sheds where peasant children were sent to stay until they either died or recovered from the smallpox inoculation.

Enter Dr. Edward Jenner. Born in 1749, he did time in an “inoculation stable” as a young lad. Smallpox may not have scarred his skin, but his experience in the stable scarred him psychologically. He decided to dedicate his life to finding a better way to beat the “Speckled Monster”. Just like the Chinese in 950 AD, keen observation is what led Jenner to an amazing breakthrough. But Jenner’s eureka moment didn’t occur in the lab or in the hospital. It came to him while observing…milkmaids.

Milkmaids had a reputation for always being pretty, with clear and smooth skin, largely because they never seemed to suffer smallpox and the extensive scarring it left in its wake. There was even a saying at the time, “If you want to marry a woman who will never be scarred by the pox, marry a milkmaid.”

In talking to milkmaids, Jenner learned that they frequently caught cowpox, a very mild disease carried by the cattle they handled every day. The milkmaids who caught cowpox would develop a few pustules on their hands that resolved on their own fairly quickly. But when Jenner proposed that cowpox was protecting the milkmaids from smallpox, most people wrote the idea off as superstitious nonsense.     

Jenner knew he had to conduct an experiment to prove the naysayers wrong. Jenner somehow convinced the parents of a young boy named James Phipps to be the guinea pig in his experiment. Jenner took cowpox pus from a milkmaid’s hand and scratched it into James’s arm. As expected, the boy developed a mild case of cowpox and recovered from it, unscathed. He called the process "vaccination" based on the Latin word for cow, "vacca". 

The next step was to see if the cowpox vaccination protected the boy from real live smallpox. So Jenner, probably with shaking hands, inoculated James with smallpox pus taken fresh from a victim at the height of the illness. Each day they waited for what must have seemed like an eternity, but James never came down with smallpox. Jenner was not only right, but his success also inspired others that we do not have to take infectious disease lying down. We can fight it.

Jenner tried 20 more times to inoculate James Phipps with smallpox, but the boy never showed a single pustule. What did James get for being used as a lab rat? Jenner built him a cottage, which is today the Jenner Museum.

So what is actually happening here? How does vaccination protect someone against an infectious disease? Unbeknownst to Jenner, we now know that microbes cause infectious disease – viruses, bacteria, fungi, and parasites. We also know that we are equipped with an immune system that battles these foreign invaders. A vaccine trains the immune system to recognize an invader before it conquers too much territory. Microbial invaders consist of foreign proteins (called antigens) that are recognized by immune cells as “non-self”. These immune cells take up to two weeks to fully kick into gear and destroy the invaders. In some cases, the invaders grow too fast or produce toxins and the immune system just can’t outpace the infection.

But when the immune system wins, it remembers the invader. If the pathogen dare challenge you again, your immune system reacts much more quickly, usually destroying the invader before you even experience symptoms. Vaccination allows your immune system to preview antigens from a weakened form of the virus (like smallpox from a pustule of a recovering patient) or a related virus that causes little or no disease (like cowpox), so it will be “primed and ready” for the real invader if it should come along.
 

With the first vaccination came the first anti-vaxxers. James Gillray, who drew this infamous cartoon in 1802, misled people into believing that Jenner’s cowpox inoculation would “bovinize” people, causing them to give birth to calves or have them spring out of the body. 

The word “virus” comes from a Latin word meaning “poisonous force”. Humanity has been battling these forces for thousands of years and through persistence and hard work, we finally hit upon a remarkably safe and effective antidote. To refuse the antidote may seem like a personal choice, but as evidenced by the recent measles outbreak, it puts all of us in danger.

Contributed by:  Bill Sullivan

Follow Bill on Twitter. Google+.

Majumder, M., Cohn, E., Mekaru, S., Huston, J., & Brownstein, J. (2015). Substandard Vaccination Compliance and the 2015 Measles Outbreak JAMA Pediatrics DOI: 10.1001/jamapediatrics.2015.0384

Babkin, I., & Babkina, I. (2015). The Origin of the Variola Virus Viruses, 7 (3), 1100-1112 DOI: 10.3390/v7031100

Marrin, Albert. “Dr. Jenner and the Speckled Monster”, Dutton Children’s Books, New York, 2002.

Attack Of The Germs!

No one likes being sick, especially with the flu. The body aches, the fevers, and the congestion all leave us desperate for ways to end the misery. Indeed, it’s growing increasingly hard to ignore the commercials telling us to stock up on flu-fighting products, like disinfectants and hand sanitizers. But how much do these items really help you avoid becoming the flu’s next victim, and do they have other consequences that we should be aware of?

Let’s first take a look at how many of the popular disinfectants work. Cleaners like Lysol have different types of salts in them that kill germs by disrupting important protein interactions, which causes the pathogen to stop functioning normally. These salts can also work by breaking up the membrane that surrounds bacteria and some viruses, essentially breaking open the pathogen and causing everything inside it to leak out. In both of these cases, the germs stop growing or are killed altogether.

Alcohol-based hand sanitizers work in a similar manner. At concentrations of at least 60%, ethyl alcohol (or ethanol) is effective at killing some viruses, including influenza viruses. Ethanol works by changing the shape of proteins, and therefore interferes with their ability to properly interact with other proteins. Ethanol can also disrupt membranes.

 

Image of Influenza virus from the CDC highlighting proteins on the outer surface that help the virus infect cells, and the viral genome located inside.

While killing off the germs that can make us sick sounds like a good way to stay healthy, the problem with using disinfectants and sanitizers to do this is that these products kill nearly all of the microbes in our environment. While there are many microbes that make us sick, there are also many that we need to help keep us healthy. If we kill those microbes off too, then we may put ourselves at risk for developing other health problems. 

On and within our bodies live millions and millions of good microbes that do things from helping us digest food, to helping keep bad microbes out of our bodies. These good microbes encompass the population known as the microbiome. The microbiome populations shift depending on the location of the body. For example, we have good bacteria that live on our skin, the population of which differs from the population of good bacteria that live in our digestive tracts. There is increasing interest in exploring the functions of the different microbiome populations, and many studies are showing that the microbiome has important roles in keeping us healthy. For example, it is thought that irregularities in the gut microbiome population may have a role in some inflammatory bowel diseases like Crohn’s disease and ulcerative colitis. It is possible that killing off the beneficial microbes in and on our bodies counteracts any good effect from killing off germs.

 

Keeping our good microbes around is only part of the story. According to the CDC, we are currently on the brink of a public health crisis due to the increasing numbers of microbes that are becoming resistant to common antibiotics. Due to our overuse and misuse of antibiotics, we have created strains of bacteria that are no longer susceptible, or able to be killed, by standard treatments. As bacteria populations are constantly exposed to antibiotics, many of those bacteria will be killed because they are sensitive to the antibiotic, but there will be some that are naturally able to withstand the actions of the antibiotic. Eventually, the population of bacteria that was initially a mix of sensitive and resistant will transition to a population of bacteria that is completely resistant, as all of the susceptible bacteria are killed off. What is the impact on us? In 2013, the CDC reported that at least 2 million people in the United States become infected with antibiotic-resistant bacteria, and that at least 23,000 of these people die from their infections.

Perhaps the most well-known case is MRSA, or methicillin-resistant Staphylococcus aureus. Staph bacteria are common and normally cause minor skin infections; however, MRSA has been highlighted in the media several times over recent years due to the outbreaks of invasive infections it has caused due to its resistance to standard antibiotics. MRSA is but one example of the bacterial strains that develop resistance to antibiotics due to constant exposure to them.

As we continue the cycle of overuse and misuse of antibiotics, we eventually will find ourselves at a point where no antibiotics will be effective against bacterial pathogens. Many public health experts suspect that point is near. There is reason to believe that constant use of disinfectants will eventually lead to the development of germs that are resistant to those disinfectants, just as we see happening with bacteria and antibiotics.

So how do we keep ourselves healthy without potentially setting ourselves up for other health problems later? We can start by limiting our use of disinfectants, and go back to simpler, tried-and-true methods of preventing the spread of communicable diseases. Despite the popularity of disinfectants and hand sanitizers, the CDC still maintains that hand-washing is one of the best ways to avoid spreading and catching viral and bacterial infections from others. Wash your hands before you eat, and avoid touching your hands to your eyes and nose.  If you are sick, do your best to sneeze or cough into the crook of your elbow (i.e., do the “Dracula sneeze”) rather than into your hands, and wash your hands frequently to avoid spreading your germs to others.

 

Of course, use soap that does not contain antimicrobial additives, like triclosan, to avoid encouraging the development of strains resistant to this compound. Soap is a potent killer of germs all by itself - it does not need supplemental antibiotics. While some companies are moving away from including triclosan, it is still present in many products, so be sure to check your labels.

Disinfectants have their place; they’re good for cleaning up food preparation areas that have come into contact with raw meat, for example. And, in times when you’re without clean water and soap, hand sanitizer can be a great tool for keeping your hands clean. But as with most things in life, these items should be used with care and arguably in balance with other washing methods in order to avoid creating greater problems down the line.

Contributed by:  Kelly Hallstrom
Visit Kelly’s blog, You Don’t Have To Be A Rocket Scientist
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CDC Threat Report on Drug-Resistant Bacteria:

http://www.cdc.gov/drugresistance/threat-report-2013/

CDC and hand washing:

http://www.cdc.gov/handwashing/

 

Greenblum, S., Turnbaugh, P., & Borenstein, E. (2011). Metagenomic systems biology of the human gut microbiome reveals topological shifts associated with obesity and inflammatory bowel disease Proceedings of the National Academy of Sciences, 109 (2), 594-599 DOI: 10.1073/pnas.1116053109