Holy influenza, batman!

Typically when we think of flying things and influenza viruses, the first images that come to mind are wild waterfowl. Waterbirds are reservoirs for an enormous diversity of influenza viruses, and are the ultimate origin of all known flu viruses. In birds, the virus replicates in the intestinal tract, and can be spread to other animals (including humans) via fecal material.

However, a new paper expands a chapter on another family of flying animals within the influenza story: bats.

I’ve written previously about the enormous diversity of microbes that bats possess. This shouldn’t be surprising–after all, bats are incredibly diverse themselves, encompassing about a fifth of all known mammalian species. Though rabies is probably the most famous bat-associated virus, other viruses that have been isolated from bats include Nipah and Hendra viruses, SARS coronavirus, Chikungunya virus, Japanese and St. Louis encephalitis viruses, Hantaan virus (a relative of the Sin Nombre hantavirus), and filoviruses, among many others. And of course, a bat->pig->human cross-species infection ended up being a plot line in the recent movie, Contagion (modeled after Nipah virus). However, bats still remain chronically under-studied, despite the fact that they can carry so many potential human pathogens.

This new research expands our knowledge of bat viruses a bit. The authors examined 316 bats from eight locations in Guatemala in 2009-10. Rectal swabs were obtained and screened for influenza virus using molecular methods (looking for influenza virus RNA). Three of the samples tested positive, and all were from little yellow-shouldered bats (Sturnira lilium). This could indicate some clustering and transmission of the virus within bat colonies–and indeed, two of the bats were from the same area in the same year (2009). However, the third bat was captured in 2010 at a location 50 km away from the other two, suggesting that the virus may be more widespread than in just one colony.

When we discuss the epidemiology of influenza viruses, we talk about two genes: the HA gene, which encodes the hemagglutinin protein and allows the virus to bind to host cells; and the NA gene, which encodes the neuraminidase protein and allows the virus to leave an infected cell and spread to others. This is where the “H1N1” or “H5N1” nomenclature come from. The novel bat virus was a completely new H type–type 17 (provisional, they note, pending further analyses). The NA gene was also highly divergent, but they are awaiting further analyses to more definitively classify this gene. (Currently there are 9 recognized types of NA genes).

Though they weren’t able to culture out the flu viruses, the authors did do some molecular work suggesting that these novel bat viruses could combine with human viruses and form a functional recombinant virus. What implications could this have for human health? Well, hard to say. We still know very little about all the implications of any distinct type of avian influenza virus, or swine influenza virus, much less something completely foreign like bat flu. It’s interesting that, like birds, influenza virus in bats was found in the intestine (though lung samples were also positive). Can it cause an intestinal infection as well as an upper respiratory infection (the latter being more common in other mammal species)? Does it cause any signs of disease in infected bats at all? If they can get this bat virus to grow, all sorts of interesting lines of research are just waiting.

The article also mentions that seroepidemiological studies are currently being carried out to better understand the epidemiology of bat flu. Looking at PubMed, there is one reference to some similar studies carried out in the early 1980s, but I can’t access anything beyond the title. There also is a report of H3N2 influenza in bats in Kazakhstan, but that article is in Russian and also not readily available. Either way, everything old is new again, and it looks like interest in bat influenza has resurfaced after a 30-year lull. Who knows what else we’ll find lurking out there as interest continues to increase in the wildlife microbiome.


Suxiang Tong, Yan Li, Pierre Rivailler, Christina Conrardy, Danilo A. Alvarez Castillo, Li-Mei Chen, Sergio Recuenco, James A. Ellison, Charles T. Davis, Ian A. York, Amy S. Turmelle, David Moran, Shannon Rogers, Mang Shi, Ying Tao, Michael R. Weil, Kevin Tang, Lori A. Rowe, Scott Sammons, Xiyan Xu, Michael Frace, Kim A. Lindblade, Nancy J. Cox, Larry J. Anderson, Charles E. Rupprecht, & Ruben O. Donis (2012). A distinct lineage of influenza A virus from bats PNAS Link.

Chickenpox parties–just a Facebook friend away

I’ve written a few times about chickenpox parties. The first link refers to a magazine article describing the practice; the second, a few years later, about a Craigslist ad looking to hold such a party “at McDonald [sic] or some place with toys to play on.”

Clearly, as chickenpox cases have become more rare in recent decades due to the success of the chickenpox vaccine, moving toward social media to find infections is the way to go. It allows people to find such cases and expose their immunologically naive children to a serious virus, just as easily as googling Jenny McCarthy Body Count.” But now, it’s gone even farther, with parents on this Facebook page hooking up to not only find cases/parties, but also to ship contaminated samples through the mail:

Shipping any kind of microbial specimen is a huge pain in the rear, specifically because they have the potential to cause harm. Myself and any employees who do this shipping have to be specially trained, and we have to use a number of specialized shipping containers to mail samples, and take precautions to prevent any leakage etc. out of the packages. Yale has a nice overview of shipping specimens at the link–54 pages long. We also have to apply for permits to ship many of these organisms. Now, Varicella zoster (chickenpox) isn’t on their list as far as “select agents,” but secretions from a person thought to have or diagnosed with chickenpox would be considered a category B agent (moderate risk of harm):

Biological substances, such as diagnostic or clinical specimens from humans or animals that are known to harbor a pathogen or have a high probability of containing a pathogen.

How should you package these?

Triple packaging. Must pass a 1.8 meter or 4 foot drop test. Packages shipped by air must meet a 95 kPa or 14 psi pressure test of primary or secondary container.

You can see pages 10-11 of the pdf for more instructions. This isn’t as easy-peasy as “stick it in a Ziploc baggie.” These people are putting a dangerous substance in the mail with the possibility (remote, but there) of making people sick. What if your mail carrier had never had the chickenpox or the vaccine? What if s/he is immunocompromised in some way? These people are taking all the dangers of their “chickenpox parties” and putting them in the mail system. Thank you, Andrew Wakefield and Barbara Loe Fisher.

Now, to be generous, their information page has been changed since the story came out to note “ABSOLUTELY NO SENDING VIRUSES THROUGH THE MAIL. This will not be tolerated and will be deleted immediately. Local only.” However, c’mon–people still have messaging on Facebook and I doubt that’s really going to stop the determined ones. These people simply don’t care about anyone but themselves and are in denial about the fact that chickenpox can kill–the one woman who received samples didn’t even know the name of the person they were from. This is so many levels of irresponsible I don’t even know where to begin.

Finally, not surprisingly, they’re deleting any comments that run counter to their propaganda. I replied to a few comments noting that the link between chickenpox and subsequent Streptococcal infection, for example, and it was gone within 20 minutes. I also noted that both my grandmother (shingles which led to pneumonia) and an uncle I never knew (primary chickenpox followed by pneumonia when he was only a year old) died from Varicella infection. The virus isn’t a joke, and those of us who had it, like me, are at a much higher risk of developing complications via reactivation (such as shingles) than those who obtained immunity via the vaccine. I wish the vaccine had been available when I was a kid, and I am frustrated as hell that these types of “parties” still exist in the vaccine era.

[Update: at least in Tennessee, a US prosecutor is warning that these types of mailings are illegal].

Hemolytic uremic syndrome (HUS) in history–part 4: the bigger picture

As I’ve laid out this week (part 1, part 2, part 3), the realization that a fairly simple, toxin-carrying bacterium could cause a “complex” and mysterious disease like hemolytic uremic syndrome came only with 30 years’ of scientific investigation and many false starts and misleading results. Like many of these investigations, the true cause was found due to a combination of hard work, novel ways of thinking, and simple serendipity–being able to connect the dots in a framework where the dots didn’t necessarily line up as expected, and removing extraneous dots as necessary. It’s not an easy task, particularly when we’ve had mostly culture-based methods to rely on since the dawn of microbiology.

If you read start digging around in the evolutionary medicine literature, you’ll see that one oft-repeated tenet is that many more “chronic” and “lifestyle” diseases are actually caused by microbes than we currently realize. (I’ll note that there is active disagreement here in the field–one reason noted is that many of these diseases would decrease one’s fitness and thus they are unlikely to be genetic, but many of them also have onset later in life than the prime reproductive years, so–still controversial). But whether you agree on the evolutionary reasoning or not, I think it’s safe to say that those who make this claim (like the Neese & Williams book I linked) are probably right on the overall assertion that more and more of these “lifestyle/genetics” diseases are going to be actually microbial in cause than we currently realize.

Why do I agree with this claim? History is a great indicator. Many infectious diseases were thought to be due to complex interactions of genetics (or “breeding,” “lineage,” etc.) with “lifestyle.” Think of syphilis and tuberculosis in the Victorian era. Syphilis (and many other diseases which we know now to be sexually-transmitted infections) was considered a disease which affected mainly the lower social classes (“bad breeding”), and was thought to be rooted in both family history as well as an over-indulgence in sex or masturbation. Tuberculosis, because it affected those throughout the income spectrum, was still blamed on “poor constitution” in the lower classes, but was a disease of the “sensitive” and “artistic” in the upper classes. It was also thought to be due to influences of climate in combination with genetics. Or, look to more recent examples of Helicobacter pylori and gastric ulcers, which were also ascribed to dietary habits and stress for a good 30 years before their infectious nature was eventually proven. And from that same era, HIV/AIDS–which even today, some are still all too ready to write off as merely a behavioral disease, rather than an infectious one.

So, we still view many of these diseases of unknown etiology as multi-factorial, “complex” diseases. And undoubtedly, genetic predisposition does play a role in almost every infectious disease, so I’m not writing off any kind of host/pathogen interplay in the development of some of these more rare sequelae, such as HUS as a consequence of a STEC infection. But looking back over history, it’s amazing how many diseases which we view now as having a documented infectious cause were studied for years by researchers thinking that the disease was the result of exposure to a toxin, or diet, or behavior, or a combination of all three.

I’ve mentioned the example of multiple sclerosis in previous posts. Multiple sclerosis is an autoimmune disease; the body produces antibodies that attack and eventually destroy parts of the myelin sheath covering our nerves. The cause of MS, like HUS 40 years ago, is unknown, though it’s thought to be a combination of genetics and environmental influences. Going through the literature, it seems like almost everything has been implicated as playing a causal role at one point or another: pesticides, environmental mercury, hormones, various other “toxins,” and a whole host of microbes, including Chlamydia pneumoniae, measles, mumps, Epstein-Barr virus, varicella zoster (chickenpox), herpes simplex viruses, other herpes families viruses (HHV-6 and HHV-8), even canine distemper virus. They’ve done this looking at both microbe culture (from blood, brain tissue, CNS, etc.) as well as using serology and DNA/RNA amplification in various body sites. None have shown any strong, repeatable links to the development of MS–much like the spurious associations that were seen with adenovirus and HUS.

Although no microbial agent has been convincingly implicated to date, there are tantalizing hints that MS is caused by an infectious agent. There have been “outbreaks” of MS; the most famous occurred in the Faroe Islands in the 1940s. Studies of migrants show that the risks of developing MS seem to be tied to exposures in childhood, suggesting a possible exposure to an infectious agent as a kid. And one of the most common mouse models used to study MS has the disease induced by infection with a virus called Theiler’s murine encephalitis virus (TMEV). If it can happen in mice, why not humans?

It might seem implausible that infection with some microbe could lead to the eventual neurological outcomes of MS, but again, examples abound of weird connections between microbes and health outcomes. For STEC, it might not be intuitively obvious at first glance how a fecal organism could be a cause of kidney failure. The respiratory bacterium Streptococcus pyogenes usually causes throat infections (“strep throat”), but if left untreated, it can also cause kidney damage (glomerulonephritis) or even heart failure due to rheumatic heart disease. A microbial cause of MS could lie in a virus, bacterium, parasite, or fungus–maybe one that we haven’t even discovered yet, but that perhaps will pop up as we learn more and more about our metagenome. Perhaps 30 years down the road, the way we view many of these “complex” diseases will look as short-sighted as it does looking back at old HUS papers from today’s vantage point.

Measles in Iowa

We’ve had pertussis and mumps, so it was only a matter of time.

State health officials declared a “public health emergency” Tuesday after a test confirmed a case of measles in an unvaccinated Dallas County baby who apparently picked up the disease in India.

They said people who might have been exposed included passengers on an Americans Airline flight from Chicago to Des Moines May 11 and people who were at Mercy Medical Center or a Mercy pediatric clinic in downtown Des Moines May 14.

Dr. Patricia Quinlisk, medical director for the Iowa Department of Public Health, said many Americans falsely recall measles as a benign childhood illness. “I get asked by medical students, ‘Which disease are you most afraid of?’ And they expect me to say Ebola or SARS or something like that – but, it’s measles,” she said. “I don’t think people understand how bad it can be, how many people can get seriously ill and, unfortunately, how many people can die from this disease. It’s bad and it’s probably the most spreadable disease we have in our society.”


Dr. Asha Madia, a Mercy pediatrician, said the patient is an 8-month-old boy who had a fever, a rash and a mild eye infection. He has recovered. She said the boy was not vaccinated because such vaccinations generally are not given before age 1. But she said his family believes in vaccinations and had immunized the boy’s older sibling.

So this is unique in that the index case isn’t from a family who has eschewed vaccination (unlike this case in 2004), but in a child who was unvaccinated nevertheless due to his age. This is one reason the CDC just last month recommended the MMR vaccine in infants who would be traveling abroad, even if they are below the traditionally recommended age.

Story still developing, but for now it appears that this is the only case recognized. However, as Maryn recently pointed out, *any* measles outbreak isn’t cheap, due to the diligent surveillance that must be undertaken to make sure no one else comes down with the infection. Full information available here from the Iowa Department of Public Health.

Pigs with Ebola Zaire: a whole new can o’ worms

Ebola has long been associated with wildlife. From the early days, bats were viewed as a potential reservoir (though it wasn’t confirmed that they actually harbored the virus until 2005). Contact with wild animals–particularly primates which were butchered for food–was also long thought to be a risk factor, and now we know that primates can become ill with Ebola and pass the virus to humans.

What hadn’t been examined until 2008 were pigs. I mean, it’s not exactly the animal you associate with central Africa, where many of the Ebola cases have been concentrated. However, pigs are much more plentiful in the Philippines, where another Ebola subtype–Ebola Reston–is thought to lurk. The Reston strain actually was first documented in the United States, where twice it was associated with outbreaks in primates originating from the Philippines. When the facility in the Philippines was closed down in 1997, Reston disappeared for 11 years–until it surfaced in pigs in 2008.

The ecology of Ebola Reston in the Philippines isn’t known–unlike African Ebola strains (and their cousin, Marburg), no bats have been caught in that country and tested positive for the virus, though they probably serve as a reservoir of the virus in the Philippines just as they do in Africa. So it was a huge surprise when pigs from that country tested positive for Ebola Reston–and so did 6 of their human caretakers, suggesting cross-species transmission. (I should note here that the Reston strain has yet to be linked to any symptomatic infections in humans–the pig farmers who tested positive probably had no idea they’d been infected and did not show any clinical signs of illness). Pigs hadn’t previously been linked to any Ebola infection, so this brought in a whole other wrinkle when it came to Ebola transmission–the possibility of being exposed to Ebola via contaminated food, and the potential for pig populations to harbor the filovirus (and transmit it to their caretakers, as we have seen with outbreaks of Nipah and Hendra viruses).

A new study delves further into Ebola in pigs. Instead of using the Reston strain, they use the much-more-deadly Zaire strain. This is the one that movies are made about; the one which can cause outbreaks so nasty that they kill up to 90% of those who are infected. Why use Zaire instead of the Reston strain–the one which has actually infected pigs in nature? Well, the researchers wanted to find an animal that’s easier to work with than primates (there are all kinds of very strict regulations when it comes to working with non-human primates), so if pigs could work as a good model for human Ebola disease, that would make studying the virus just a bit easier. (In any case, for any live Ebola work, it still needs to be done in a biosafety level 4 environment, meaning complete spacesuits and the whole works).

The authors did 2 studies. In the first, they inoculated 6 pigs with Ebola Zaire, via a combination of intranasal, intraocular, and oral routes of infection. (Interestingly, no injection, which can be a key way Ebola is spread). They had an additional 2 pigs that they inoculated the same way with a saline solution, and housed them separately from the Ebola-inoculated animals. The goal of this experiment was to look at the pathogenesis of a virulent Ebola strains in the pig model. The infected animals all developed fevers and respiratory disease, with some internal hemorrhaging and evidence of airway replication by Ebola. Infectious virus was found at low levels in nasal washes and oral and rectal swabs; one animal also had a low level of virus in the blood. Higher levels of virus were found in various organs, including the heart and bladder, while the highest levels were found in lung tissue.

In the second experiment, they inoculated 3 new pigs in the same fashion, but then added in 4 additional (uninoculated) animals to stay with them, and kept 2 additional control animals in a separate area so that they could investigate pig-to-pig transmission of the virus. They did find viral RNA from the mucosa of all contact animals, and infectious virus was detected from 2 of 4, demonstrating that the virus can be passed among pigs. Not stated in the article was if the authors thought this was due to direct contact with respiratory secretions among the pigs, or via airborne transmission (a much more concerning route of transmission, as in humans, Ebola Zaire doesn’t seem to transmit well via air–typically it’s spread via close direct contact and bodily fluids).

Notably, pigs didn’t seem to develop severe systemic disease from Ebola, as primates do–the main symptoms exhibited were respiratory, which the pathology supports (finding little virus in the blood, but a lot in the lungs). This suggests that even for Ebola Zaire, infection in a pig could be mistaken for other respiratory diseases, such as influenza or PRRS virus (porcine respiratory and reproductive syndrome virus, which the initial pigs in the Phillipenes were co-infected with). So, Ebola may be circulating even more than we realize in the pig population, disguised by its commonplace symptoms.

A commentary published in tandem with the research article ponders the issue of foodborne Ebola, suggesting that this is a remote possibility and noting that butchering infected animals in the wild in Africa has certainly spread the virus. However, solely eating meat as a means of infection hasn’t been reported, and cooking likely destroys any risk (similar to influenza viruses). Like influenza virus, Ebola doesn’t seem to survive long in most environments, but it’s also noted that differences in African food storage (with little refrigeration) versus more typical cold storage may affect that as a risk factor, possibly prolonging the life of the virus when held in the cold. I think foodborne transmission is unlikely, but it can’t be completely ruled out right now.

Because of the respiratory symptoms, does this mean Ebola could enter the population via meat from animals that farmers don’t consider very ill, or put butchers at a heightened risk of infection during slaughter? This to me is more concerning than simple foodborne transmission. With Reston, at least no human symptoms have been observed, but if pigs (and potentially other animals?) can present with Ebola Zaire as a rather generic respiratory infection…well, that could spell trouble in a lot of different ways. It means that telling individuals to simply avoid sick-looking primates (and bats) is going to be even more woefully inadequate than it already is. Plus, it raises the remote-but-not-completely-outside-the-realm-of-possibility of someone intentionally spreading the virus via animals that are infected in this manner.

Science fiction? Maybe. Probably. Hopefully. But this research opens the door on many new lines of investigation and once again, raises even more questions.

Kobinger GP, Leung A, Neufeld J, Richardson JS, Falzarano D, Smith G, Tierney K, Patel A, & Weingartl HM (2011). Replication, Pathogenicity, Shedding, and Transmission of Zaire ebolavirus in Pigs. The Journal of infectious diseases PMID: 21571728

Ebola in Uganda: current and past outbreaks

Via H5N1 and other sources, there’s at least one new Ebola case in Uganda:

The rare and deadly Ebola virus has killed a 12-year-old Ugandan girl and health officials said on Saturday they expected more cases.

The girl from Luwero district, 75 km (45 miles) north of the capital Kampala, died on May 6, said Anthony Mbonye, the government’s commissioner for community health, in the first outbreak of the virus in Uganda in four years.

“Laboratory investigations have confirmed Ebola to be the primary cause of the illness and death. So there is one case reported but we expect other cases,” he said.

Though we’ve known about Ebola in Africa since 1976, Ebola wasn’t recognized in Uganda until a bit over 10 years ago. Now, this is the third outbreak in this amount of time. The first occurred in August of 2000; the first case died in Gulu on the 17th of September. Despite an investigation, doctors were unable to determine where or how she had contracted the disease. Her death was followed by the deaths of her husband, two children, and several other family members. This was reported to the Ministry of Health in October of that year, near the peak of the epidemic. An investigation and intervention to control the disease followed, and the epidemic was declared to be over in January of 2001. A total of 425 patients from 3 villages (Gulu, Masindi, and Mbarara) across Uganda were identified based on symptoms and/or laboratory data. 224 of them died, with a resulting mortality rate of 53%; an eerie echo of the 1976 Ebola outbreak in Sudan. Indeed, sequence analysis showed the infecting strain to be the Sudan subtype of Ebola; the first time this type had surfaced since the 1979 outbreak in Sudan. It is hypothesized that Sudanese rebels, who carried out regular attacks around Gulu, may have accidentally introduced the virus in some manner, though this has not been confirmed.

Ebola returned to Uganda in August of 2007, causing 149 illnesses and 37 deaths until the outbreak was declared over in February of 2008. This mortality (36%) was significantly lower than most Ebola outbreaks. Interestingly, when scientists tested this virus, it also reacted strangely with their assays. Therefore, they determined the entire molecular sequence of the virus, and found that it was a whole new strain of Ebola, which they named Ebola Bundibugyo.

I couldn’t find any other details about the current outbreak–how she was infected, if she’s actually the index case or if there were previous deaths that have not yet been confirmed. (The girl died at the hospital–previous deaths may have gone unrecognized if they had died at home). I’m sure more details will be coming in the next days and weeks. What we’re left with now is the knowledge that in 11 years’ time, Uganda is now on its third Ebola outbreak. These have occurred in 3 different areas of the country (Gulu is toward the north, Kampala region in the south near Lake Victoria, and Bundibugyo in the southwest, almost due west of Kampala) and with 2 different strains (thus far). This again feeds my morbid fascination with the virus–what does this mean about Ebola reservoirs in Uganda? Are these cases bat-acquired? Other wildlife? Spillover from other countries, as suggested with the 2000-1 outbreak? As always, Ebola outbreaks tend to raise more questions than they answer.

[UPDATE: via Crawford Killian, CDC says current outbreak is due to Sudan strain.]

Margulis does it again

We all know of once-respected scientists who ended up going off the deep end, adhering to an unproven idea despite massive evidence to the contrary. Linus Pauling and his advocacy of megadoses of Vitamin C, or Peter Duesberg’s descent into HIV denial. It’s all the more disappointing when the one taking a dive is a woman, since there are, compared to men, relatively fewer female “big names” in the sciences. So when one goes from views that were, perhaps, outside of the mainstream (but later proven largely correct) to complete science denialism, it makes it all the more depressing. Even worse, mainstream popular science magazines like Scientific American (with this article by Peter Duesberg) and Discover (Duesberg again) give these ideas reputable press. And now Discover has done it again by giving “maverick” biologist Lynn Margulis a profile in their latest issue. More after the jump.
Continue reading “Margulis does it again”

“Pox” by Michael Willrich

Next to Ebola, my favorite virus would probably be smallpox (Variola virus). I mean, now that it’s eradicated in nature, what’s not to love about the mysteries it’s left us–where it came from, why it was so deadly (or, not so deadly, as in the emergence of the “mild” form, variola minor), and will a new poxvirus emerge to take its place? The topic is particularly germane since the debate still rages on about the fate of the world’s smallpox stocks. Smallpox has killed untold millions and influenced the destiny of societies; and as Michael Willrich details in his new book, Pox: An American History, the legacy smallpox has left us is still alive and well today.
Continue reading ““Pox” by Michael Willrich”

Twittering in the classroom

Readers may be interested in participating in this, from Dave Wessner at Davidson College:

Building on a project I piloted last fall, I will explore the potential role of Twitter more intentionally this fall in a course I teach on HIV/AIDS at Davidson College. I invite you to join me in this exploration.

Here are a few details:
Basically, I am interested in extending the class conversation outside the classroom walls and beyond the appointed class hours. I want the students to begin thinking on their own about what aspects of the subject (HIV/AIDS, in this case) truly interest them. I want to move away from the professor as purveyor of all information model. I want students to improve their ability to critically analyze information from disparate sources.

With Twitter, students can gather information from a wide variety of sources, some very reliable, some less reliable. They also can post information/questions/thoughts and get feedback from a wide variety of sources – again, some reliable and some not. Finally, Twitter provides a platform that they can easily access in their dorm room, the student union, or the local coffee shop (at any time of the day or night). And accessing Twitter, I hope, will not seem as overtly class-related to the students as accessing, for instance, course material via Blackboard.

This fall, I am requiring the students in my seminar to have a Twitter account. Students will post items on a regular basis, using the hashtag #BIO361. We also will devote some time on a regular basis to discussing items or responses from Twitter. Our first post probably will be on the first day of classes – Tuesday, August 24, 2010.

For this project to work most effectively, we need a critical mass of people outside of our class to participate. If you, your students, friends, or colleagues would like to join us, please do. We will appreciate any new comments, retweets, or responses. I’m looking forward to an engaging discussion throughout the semester.

This is up and running now, so keep an eye on #BIO361 and @dawessner.