Smallpox: A New Kind of Computer Virus?

Source: Jan Bajtlik, New York Times

In 1975, smallpox was eradicated. Our war against one of humankind's greatest killers, with an estimated death toll of one billion people, was over. Humanity had won. There have been no cases of naturally occurring smallpox in almost four decades. 

And yet, as a New York Times op-ed argues, smallpox is just a mouse-click away. What could stop someone from searching up the genome and sending it out for synthesis? Scientists have it even easier; with the right machines, they could synthesize it from the comfort of their lab. Could inserting this synthetic genome into a human cell produce infectious virions?

Leonard Adleman, the op-ed author, says yes. He cites a 2002 study done by Cello, Paul and Wimmer at State University of New York at Stony Brook. In it, they succeeded in synthesizing a poliovirus genome from scratch and showing its moderate infectivity in mice. 

However, this is poor evidence that infectious smallpox could also be created in this way. First of all, poliovirus has a small RNA genome that is about 7,500 base pairs long. Smallpox has one of the largest DNA genomes, clocking in at around 200,000 base pairs. That alone is telling. Especially given the limitations of chemical DNA/RNA synthesis. Even for the small poliovirus genome, only small portions of it could be synthesized at a time. All of these short fragments would then have to be connected in the correct order. With a 200,000 bp long genome, that task would be herculean. 

Additionally, the smallpox DNA cannot infect cells all by its lonesome. It is a huge virus that carries with it many of the proteins it needs for replication and other functions. Without those, it cannot effectively propagate. Could the proteins be translated from the genome or also chemically synthesized? Perhaps. But that would be another major obstacle to overcome before creating a fully infectious smallpox virus. 

These two considerations alone severely undermine the validity of this op-ed's dire warning. Although there may be potential for bioterrorism from an adequately equipped lab and open-source infectious disease databases, especially with other viruses, the resurrection of smallpox is not on the horizon. 

References

1. http://www.nytimes.com/2014/10/16/opinion/resurrecting-smallpox-easier-than-you-think.html?_r=1
2. http://www.sciencemag.org/content/297/5583/1016.full
3. Knipe, D. M. & Howley, P. M. (Eds.). (2013). Fields Virology (6th ed.). Philadelphia, PA: Lipincott Williams & Wilkins. Accessed via OvidSP through Stanford.

Tina Ju

Densovirus as a Beneficial Virus

     So this isn't a human virus, but I think it's cool enough to be relevant. A new study released claims that Densovirus is a mutual symbiont of a moth (Helicoverpa armigera) and protects against baculovirus. This breaks a central dogma of viruses that states all viruses are detrimental to health. This study shows that Densovirus infection is beneficial to this moth. Helicoverpa armigera Densovirus-1 (HaDNV-1) is wide-spread in adult populations of these moths (>67%).  The study found a strong negative interaction between HaDNV-1 and nucleopolyhedrovirus. Bioassays also showed that moths infected with HaDNV-1 had increased resistance to nucleopolyhderovirus. The researchers found no negative effect on the moths from HaDNV-1 infection. Another interesting thing is the fact that the virus could be transferred horizontally and vertically.

    When I first read this, I thought it was pretty cool because it shows a virus being beneficial to their hosts. However, the moth is actually a global crop pest and nucleopolyhedrovirus is used in biopesticides against the moth. soo..... We need to make sure these moths don't get infected with densovirus.

Source: http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1004490

- Jimmy

Combatting Viruses with Bacteria

Dengue fever has rampantly spread throughout the glove, with now more than 2.5 billion people at risk and an estimated over 400 million infected. Dengue is spread by the A. Aegypti mosquito; due to climate change and an increase in urbanization, these mosquitos now have an increased range in infection and a greater density of possible hosts. With no known vaccine or cure for dengue virus, the most prudent form of disease control is to control vectors - the mosquitos. While insecticides are an attractive option, they can pose serious risk to via biomagnification and toxicity. Recently, Monash University in Australia has attempted to curb the growing Aegypti mosquito population by intentionally infecting these mosquitos with a bacteria known as Wolbachia. In lab, Wolbachia has been known to dramatically decrease the rate of viral replication of dengue; additionally, Wolbachia can be spread at the cellular level to young. Several populations of infected mosquitos have been released to yards and pools around Australia in an attempt to cause a bacterial epidemic in the Aegyptis population.

http://www.abc.net.au/news/2014-10-30/bacteria-infected-mosquitoes-used-in-fight-against-dengue/5852846

http://www.plosntds.org/article/info%3Adoi%2F10.1371%2Fjournal.pntd.0002688

Alex Lindqwister

Stanford ER Surgeon being monitored for Ebola "out of an abundance of caution"

     A Stanford ER surgeon, Dr. Colin Bucks, is being monitored for Ebola "out of an abundance of caution." Dr. Colin Bucks is the medical director of disaster preparedness for Stanford Health Care and is a clinical assistant professor of surgery at Stanford medical school's department of emergency medicine. Dr. Bucks was volunteering in Liberia with International Medical Corps, a LA-based nonprofit that's not affiliated with Stanford in any way.
    Stanford Health Care announced last Thursday that Bucks would be isolated for 21 days "out of an abundance of caution" following his last known contact with an Ebola-infected patient. 21 days is the incubation period for Ebola. He has been healthy and asymptomatic since coming back. This response is interesting as we have learned that an Ebola-infected individual is only contagious when he/she is also symptomatic. It seems like an over-reaction and even Stanford Health Care admits that it's kind of a severe reaction. However, we do need to be careful just in case he's infected with a mutated strain that makes him contagious even when he's asymptomatic. This decision was made by Stanford Healthcare according to its emerging infectious disease response plan, which are based off CDC's guidelines.
   Dr. Bucks is on paid leave and is "very cooperative." County health officials take his temperature twice a day.
   I initially thought this was an overreaction, but it's actually a pretty chill quarantine. It sounds like a lot of resources are going into this. Speaking of lots of resources, all major hospitals are undergoing significant "Ebola training" for relevant employees. It's not the most cost effective approach and it'd be great if all that training money was put into Africa instead.

virologically yours
Jimmy

Source: http://www.bizjournals.com/sanfrancisco/blog/2014/10/ebola-stanford-surgeon-monitored-colin-bucks.html?page=all

The King of Terrors

        I am reading “The Mississippi Valley’s Great Yellow Fever Epidemic of 1878” by Khaled J. Bloom, and as you can imagine I have yellow fever on the brain.  The confusion that initially surrounded Yellow Jack—the name for yellow fever at the time—was deeply entrenched in the medical community.  Some health officials believed that filth and dirty water were the causes of yellow fever.  Others believed that there was something inherent in the atmosphere of cities that bred disease.  And others believed that it had something to do with moist, warm air.  All these theories were close to some type of truth, but they were muddled with panic and confusion.  It makes sense that the people of Southern United States couldn’t wrap their minds around this disease because the virus nearly decimated certain states.  In 1853 in New Orleans, Louisiana there were 40,000 cases with 11,000 deaths.  Memphis was hit so bad that when the disease returned in 1879, the federal government was considering destroying the entire city of Memphis.  The disease quickly became known as the King of Terrors.  Although the scientific community didn’t know much about yellow fever it did loosely understand that yellow fever was a disease intertwined not only with people but also with the environment.   

            Mosquito vector-borne diseases are tough for several reasons.  Firstly, the life cycles of mosquitos are complicated and include several stages with their own identities and properties.  Secondly, the ecology and preferred environment of mosquitos play a big part in mosquito-vector diseases.  Lastly, these guys can fly. Recently diseases such as yellow fever, dengue, and malaria have come up in the discussion of climate change (global warming!).  As temperatures increases and climates shift, the range of habitat for insect vectors also shifts.  Although there is merit to this idea, it seems to me like the histories of mosquito vector diseases have more to do with human activities and their effect on ecology than climate change do.  Several articles also suggest human factors as a major driving point for the spread of the mosquito.  Clearing forests, development into mosquito habitat, and everyday behavior play a large role in modifying the range of a mosquito. 

       When I mention the developed world, the specific area that I envision is Palo Alto, California.  And surprise surprise the yellow fever mosquito has almost made its way here to Palo Alto, the land of bike lanes and bistros.  In 2014 the San Mateo County Mosquito and Vector Control District found Aedes aegypti mosquitos at thirteen locations.  The first location was in Menlo Park at the Holy Cross Cemetery.  Furthermore this was the third mosquito in the Aedes genus that was found in Los Angeles, which isn’t too far away from Palo Alto.  Although there was no disease associated with these mosquitos, I think the Ebola epidemic suggests how easy viruses can move in this day and age. Unlike Ebola where an infected individual would have to cross an ocean to reach the US, an individual infected with yellow fever would have to travel up from any country in Southern America to reach the US.  No matter how improbable it seems like this would happen, it is possible, and that is what matters.

-Nalani Wakinekona

References

1. http://www.latimes.com/local/lanow/la-me-ln-yelllow-fever-mosquito-los-angeles-20141015-story.html
2. http://smcmad.org/data/aedes_aegypti/Press_Release_1_Yellow_Fever_Mosquito_Found_in_San_Mateo_County_Apr-2014.pdf
3. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240549/pdf/ehp109s-000141.pdf

No More Funding for Mutant Virus Development

The Obama administration recently announced that it will no longer fund research that focuses on creating "super-viruses," viruses that are evolved to be more deadly and more dangerous than the natural ones. This has significant implications for researchers in this field because the government is one of the main providers of funding for biomedical research. The government is justifying its action by claiming that developing and researching super viruses poses a threat to society. Opponents of the government's decision claim that researching the ways in which viruses can evolve is crucial in understanding them. Furthermore, inducing the mutations in certain virus before they occur in nature will be important in developing treatments. The government has stopped funding research and has recommended that sponsors, who provide the other sources of research, stop funding as well. It's waiting on the National Science Advisory Board for Biosecurity and the National Research Council to review the risks and benefits of this type of research to solidify a policy.

~Mariam


Sources
http://www.ajc.com/feed/technology/the-us-will-stop-funding-research-into-making/fnzkN/
http://gizmodo.com/the-u-s-will-stop-funding-research-into-making-mutant-1647865903

Viroids: a look at the smallest of the small and the origins of life

(shamefully stolen, but can’t find the original source.)

Last week in class we discussed 4 possible sources for viruses:

     1.  Viruses were present in primordial soup

           2. Viruses emanate from space (Fred Hoyle)

       3. Viruses assimilated from parts of other cells

       4.     Viruses are degenerate cells

The review“Viroids: Survivors from the RNA world?” from Annual Review of Microbiology, elaborates on the first possibility of sources for (plant) viruses and the rest of life. The article looks at the evidence from viroids and their close relatives to better understand their origins and the origins of life.  In addition to viroids, the review also discusses plant viroid-like satellite RNAs, retroviroids, and hepatitis delta virus (HDV), which have the smallest genome of animal viruses.

 According to this article, the consensus is that RNA emerged before DNA and proteins. DNA and proteins eventually took over life on earth, and relegated RNA to intermediate functions.  But are there survivors from this first RNA world?  

(more shameful stealing, http://pandasthumb.org/)

Primordial Soup – better known as the RNA World? 

Theories and thoughts on origins of viroids: 

       1.     Viroids are escaped introns. However, viroids do not seem to be simplified version of viruses or transposons because of their distinct reaction mechanisms. Additionally, viroids, such as PSTVd, weren’t found in the cellular DNA of normal plants.

       2.     Viroids are surviving relics of a precelllar evolution in an RNA World.

Most of the article’s evidence affirming viroids as the survivors of precellular ancestors relies on demonstrating that they could fit in an RNA world. 

Evidence for viroids as relics of an RNA World:

·        Viroids have small genomes and are nonprotein-coding RNAs.

  The underlying idea is the simplest is the oldest.

·        High G+C content and circularity

  The underlying idea is that this increases replication fidelity helps the genome replicate   completely, meaning greater stability.  The RNA world is possible!

·          A number of viroids have structural periodicity.

   The underlying idea is that in addition to being associated with protein binding, structural      periodicity may have allowed larger genomes to evolve. Modular evolution would have allowed for    high mutation rates, which would have shortened the evolutionary time required to make a complex    structure, and possibly allow for complex structures that may have not been directly selected.    Complex life could have come from an RNA world!

·         Some viroids have hammerhead ribozymes, the “finger print of the RNA world.”

   The underlying idea is that the small size and relatively low complexity of hammerhead ribozymes    make viroid replication in a pre-protein world possible.

YES IT IS

Is such a thing what actually happened? The jury is still out.

Pithy quotes from the review:

“Thus viroids are essentially transcriptional parasites, whereas viruses are essentially translational parasites. “

By Olivia

Can A Virus Make You Dumber?

That might be a possible indication of a recent study of the virus ATCV-1 done by pediatric infectious disease expert Robert Yolken and his team at Johns Hopkins University School of Medicine in Baltimore, Maryland. Chlorovirus ATCV-1 is a virus that typically infects a species of green algae found in lakes and rivers. However, it has recently been found in the brain tissue of human corpses and in the throats of people with psychiatric disease. And ATCV-1 doesn't just appear in humans who are ill or dead. The Johns Hopkins study found that in a sample of 92 healthy study participants, 43% of them had the virus. The participants who had the virus did significantly worse on tasks measuring cognitive functioning, including visual processing and attention span.

While Yolken and his colleagues controlled for factors such as age, sex, race, and education level in their study, the initial association they had found did not necessarily prove that the virus is the direct cause of the cognitive impairment. The presence of the virus might instead be an indicator of the presence of some third variable which is actually causing the cognitive decline. The researchers point out that it might mean the virus might just be taking advantage of the presence of some other factor that impairs the brain in some people, such as other infectious agents, heavy metals, or pollutants, the researchers say.

To determine causality, the team injected uninfected and infected green algae into the mouths of mice, knowing that infected mice would produce detectable antibodies. Both sets of mice were then put trough a series of cognitive tasks. Infected animals had poorer attention spans and they weren't as good as uninfected mice at remembering their surroundings. Though the virus has not yet been found in the brain itself, Yolken and the other researchers also looked at the hippocampi of both groups of mice and found that in the infected mice there had been changes in the activity of almost 1300 genes in the hippocampus, which is involved in memory.

How does the virus come to be present in the human body in the first place? Yolken and his team have not fully determined exactly how the virus infects people, but it turns out that ATCV-1 is just one of many microorganisms that inhabit human mucosal tissue, and it is found in algae in inland waters worldwide. As the researchers remark in their paper, the study indicates that "viruses in the environment not thought to infect humans can have biological effects".

By Kasiemobi Udo-okoye

Reference: http://www.pnas.org/content/early/2014/10/23/1418895111.full.pdf+html

Rat Race: Analysis of the hidden NYC Vectors

Rats are everywhere. Especially in cities. Disease is everywhere. Especially in cities. 

It seems then somewhat surprising that no study has yet surveyed local rat populations—until now.  C. Firth and PI Ian Lipkin recently published an in depth analysis of the lovely pathogens harbored by, arguably, our most ubiquitous furry friends in new york city.  And their results show that, not only do rats shelter a large variety of dangerous viruses, but that this study probably should have been conducted earlier.

Some of the most deadly human viral infections are zoonosis—meaning viruses that infect animals and enter human populations via close contact. Thus, this survey of 133 rats presents a nice sample (but probably incomplete) of what we might expect to find on these other city dwellers.  One of the main findings was the percent of Seoul virus (SEOV) a hantavirus. Other notable viruses detected included anellovirus, parvovirus, circovirus, picornavirus, flavivirus and rotavirus.  Nearly all of these viruses could be a public health concern. The rats all had high viral loads with the leading represented families being picornaviruses (1.8 picornaviruses per rat) and flaviviruses (.48 flaviviruses per rat)

On a more positive note, the research also found Hepatitis C like virus in the livers of many of the rats, providing a possible future model of Hep C in humans.

Full article can be found here: http://mbio.asm.org/content/5/5/e01933-14

---Lauren Sweet

700 year old virus isolated from the ice

Scientists have discovered a new virus. The DNA and RNA was isolated from 700-year-old Caribou feces, found in a drilled ice core. Two distinct viral genomes were isolated—one with a small circular DNA viral genome (ancient caribou feces associated virus, or aCFV) and one with a partial RNA viral genome (Ancient Northwest Territories cripavirus, or aNCV). The viral capsids were protected for 700 years by the extreme cold. These viruses are related to the geminivirus family (which infects plants). The viruses were no longer alive, but researchers were able to use a modern geminivirus multimeric clone to induce the DNA virus to infect Nicotiana Benthamiana in the lab. The researchers think that the virus came from foliage eaten by the caribou or from flying insects ingested at the same time as foliage.

It is very likely that as global temperature increase and more permafrost melts, many more ancient viruses, not unlike these will be exposed. Any number of viruses may be exposed and some of them may still be infectious. When considered with the giant virus uncovered in Siberia a few weeks ago, it may be wise to develop a stratagey to deal with these potentially dangerous ancient pathogens.

Madeleine Bousquet

References:

http://www.pnas.org/content/early/2014/10/23/1410429111

Dengue Vaccine Completes Phase III (and All Four Serotypes Are Terrified)

Sanofi Pasteur has developed a dengue vaccine candidate that successfully completed phase three clinical efficiency studies. The vaccine efficiency study was done throughout Latin America, and was shown to have an efficacy of 60.8%, protecting against all four of the dengue serotypes! This reduction in dengue disease cases was observed in children/ adolescents from the ages of 9-16, and who were on a 3 dose vaccination schedule. The vaccine candidate has also been shown to have a good safety profile, not only in this phase but in all previous ones as well.

It was reported by Sanofi that the vaccine resulted in a reduction of the risk of hospitalization by over 80%. The study shows that the vaccine was efficacious against dengue hemorrhagic fever (results that were also observed in a Sanofi study of the same vaccine in Asia). The vaccine will be presented in early November in Louisina. If the vaccine proves to be very efficacious, it would be a very important tool to be able to reach the goal of reducing mortality by dengue by 50% by 2020 as set by the World Health Organization.

As aforementioned, this was the second of two large-scale randomized, placebo controlled (and observed blind) trials. Total amount of children immunized in Latin America was 20, 875 (places in which they participated included Mexico, Brazil, Honduras, Colombia, and Puerto Rico), and the schedule was comprised of the vaccine at zero, six and twelve months.

To read more, see the full article at http://www.sanofipasteur.com/en/articles/sanofi-pasteur-s-dengue-vaccine-candidate-successfully-completes-final-landmark-phase-3-clinical-efficacy-study-in-latin-america.aspx

Dengue-astically yours,

Meche Peterson

Ebola Just Went Digital

Ebola Virus fears are now being used to bait unsuspecting emailers into infecting themselves with a virus of another kind – the digital kind. Emails with titles like "Ebola Outbreak Now WORSE Than We’re Being Told" and "EBOLA Outbreak — FEMA Storing 250,000 Plastic Coffins" have been popping up in inboxes worldwide, and when clicked on, infect the computer in question with trojan viruses allowing hackers to remotely operate the computer's webcam, keyboard, take screenshots, access data, and so forth.

My moral obligation to condemn this aside, I would first like to note: this is a fantastic extension of the "virus as obligate parasite" paradigm, and the philosophical implications of a digital virus using a psychological abstraction of a real-world virus to spread itself merit an entire blog post by themselves. The digibiology of memes and chain-letters is truly fascinating.

But in reality, this does bring up a troubling notion: that the impact of a virus, or really any other form of pandemic, can extend beyond the epidemiology of the pathogen itself. And the act of doing so is really not all that different from a virus going airborne, or entering any other route of transmission. First, the concept of the virus first infects the minds of a population in the form of fear, then in some minds that concept mutates into fear plus the possibility of exploitation. Then the exploitation potential is isolated by a subset of this population and distilled into some other, more transmissible form (most likely a meme or chain-letter). In most cases this manifests itself in a harmless manner (bit.ly/ZQ3kSc), but in some cases, a meme-progenitor has been "infected" by the knowledge of digital virus design – they see the logical exploitative value of combining the two, and the ebola digivirus is born.

This would all be pointless abstract theory were it not for the fact that these viruses are causing tangible harm around the world. We have officially entered an age in which ideas and information can harm us, and while in the case of ebola the relative harm is small, it is easily foreseeable – say, with the advent of a flu-inspired chain virus – that digital harm could exceed physical.

WELCOME TO THE METAVIROCALYPSE! (® Billman Portmanteaus, Inc.)

By Matthew Billman

Sources:

http://www.sfgate.com/business/article/Computer-virus-exploits-Ebola-fears-5848299.php

http://blog.sfgate.com/techchron/2014/10/24/ebola-related-computer-viruses-disguised-as-public-health-tips/

http://tech.firstpost.com/news-analysis/ebola-virus-being-used-as-bait-to-spread-malware-symantec-229524.html

And colds too! Stay healthy this week 6 and beyond!

--Joe

Clash of infectious agents: bacteria helps prevent malaria and dengue infection

A team of scientists from Johns Hopkins University has uncovered a novel way to prevent malaria and dengue: by introducing microbial agents of the genus Chromobacterium (Csp_P) to the guts of mosquito vectors, scientists were able to induce immunity to both Plasmodium and dengue virus. Successful Csp_P colonization in Anopheles and Aedes (the vectors for malaria and dengue, respectively) activates a mosquito immune response that helps prevent the establishment of viral and parasitic infection. In vitro tests also suggest Csp_P may directly interact with invasive agents and produce anti-pathogenic molecules that inhibit pathogen survival in the mosquito's gut. This observation has a further implication: the toxins Csp_P uses to kill pathogens in mosquitoes can be studied to help produce drugs to treat malaria and dengue in humans.

Csp_P has also been shown to have entomopathogenic activity, as a significant portion of mosquitoes colonized by Chromobacterium during testing died shortly after initial Csp_P ingestion. All of this data suggest the possibility of using Csp_P as an efficacious malaria and dengue vector control measure: by lacing sugar-baited traps (currently used to spread insecticide) with Csp_P, public health officials can both kill most mosquitoes that feed from the traps and prevent any surviving mosquitoes from spreading malaria and dengue.

In is important to note, however, that since Csp_P appears to be such a toxic agent, it may exhibit damaging effects on human cells in addition to invasive organisms. The research on Csp_P remains in its infancy, so further testing will show whether or not it can be used to safely control disease.

http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1004398

-Nick Simon

Children's Human Rights Seminar on Ebola

Last Thursday, I attended the Children's Human Rights Seminar discussing emergency medical response in humanitarian crises. The seminar was broadcast as a panel on Ebola, but was much more broadly focused, as two of the panelists had no direct involvement in the outbreak whatsoever.

The Panel was composed of Erica Kochi, Eric Talbert, and Brad Adams, each of which had dealt extensively with children's human rights and humanitarian crisis response in their own regard. Erica Kochi sparked my interest, as she was the co-chief of UNICEF's innovation team. As the lead of innovation at UNICEF, she talked about her focus on development of communication, supply chain management, and education. Although she spoke little about her personal role in the Ebola outbreak, she did mention that UNICEF's innovation tech team has been working on improving mobile networks in Liberia in order to try and disseminate public health information to people in the region.

This immediately made me wonder how many people had access to cell phones in Liberia and West Africa overall. According to a national survey done in Liberia in 2013, mobile phone penetration stands at 42 percent, meaning that 42 percent of the 4.2 million Liberians have access to a phone. I was unable to find more information about UNICEF's involvement in distribution of Ebola outbreak information via SMS, but it seems that this is a viable avenue to educate citizens of Liberia about the disease with a relatively low cost.

Eric Talbert had much more of a direct role in the Ebola outbreak, as his non profit organization Emergency USA had already established one Ebola treatment center and is in the process of creating another. Professor Siegel quickly questioned Eric if these treatment centers would be utilized in the future, bringing up the issue of sustainability of foreign aid in the region. Eric's response was a little dismissive, however Bob's question is a very valid one. Ebola is not the only disease that Western African nations are battling against. As a company providing new Ebola treatment centers in West Africa, Emergency USA should seize the opportunity to create long lasting clinical facilities that will aid the population indefinitely. The failed health systems of many of these countries continue to propagate the growing number of deaths and incident cases in these countries. Therefore, Emergency USA has the ability to attack the root of the problem not only in the next few months, but for many years to come.

Although we did not talk much about the children affected by the Ebola outbreak, overall,the panel spurred an interesting discussion about disease control and international aid. Hopefully UNICEF and Emergency USA will provide the region with meaningful infrastructural developments that will curb the epidemic and be of use to Western African nations in the future.

- Marcus Munoz

Using Antibodies to Fight Ebola

As we discussed in class, one of the ways that immunity can be passed onto another person is through passive immunoprophylaxis. This has been one treatment that has been used on multiple Ebola patients in the US. Patients who have had Ebola and have since recovered have antibodies in their blood that target the Ebola virus. These antibodies help the patients fight against the Ebola virus.

Plasma is the liquid portion of the blood where the antibodies can be found. One method to bolster the immunity of a person who is currently fighting the Ebola virus has been to transfuse blood plasma, which contains the anti-Ebola antibodies, into patients that are currently infected. This technique has been applied to the Dallas nurse who was infected, Dr. Kent Brantley and is now being used on the infected NYC doctor.

While it looks like this method of treatment for Ebola is effective, no scientific study has been done on it, and there are no statistics that can support that the transfusion of plasma is actually effective. In the African patients who had previously been treated with this method, and even the Americans who have had this passive immunoprophylaxis treatment, there are many variables that complicate the understanding of plasma transfusion effectiveness in the treatment of Ebola. In Africa, many of the patients received differing levels of care which could affect the supposed effectiveness of antibody transfusion. In the American patients, many of them were also receiving experimental drugs alongside any plasma transfusion treatments they may have been undergoing.

In order to better study the effectiveness of plasma transfusion in the treatment of Ebola, a $3.7 million dollar grant has been given to scientists to study the treatment in Guinea. Hopefully, this will give us some insight into how the antibodies work, and perhaps lead to further research that can help us manufacture Ebola antibodies in bulk for treatments!

http://www.thedailybeast.com/articles/2014/10/26/blood-is-ebola-s-weapon-and-weakness.html

-Anna Duan

Measles Outbreaks among Amish in Ohio

            The year of 2014 has seen a dramatic increase in measles outbreaks. Several Amish missionaries to the Philippines brought back the virus, which has spread throughout communities in Ohio. The virus halted wedding season and church in the spring to avoid further spreading. The Amish are not against vaccinations in principle, yet it is culturally uncommon. Furthermore, rumored health disadvantages of vaccinations over the past decade have decreased measles vaccinations among children countrywide, Amish or not, creating a serious health risk.

            Measles is caused by the Morbillivirus, an RNA virus in the paramyoxyviridae family. It is a respiratory disease that causes cough runny nose and a trademark rash. About 2 in 1,000 patients with measles pass away, usually from complications such as pneumonia. This disease is highly contagious and new outbreaks concern medical staff around the country.

            Dr. William Schaffner at Vanderbilt University describes the severity of the measles outbreak and suggests that everyone should be vaccination, especially when going abroad to other countries to avoid bring measles back to the United States.  Measles hospitalizes 15% of those infected and is a huge health risk among the young and old.  He says that bottom line there is no valid medical reason to avoid vaccination, only rewards for both the individual and society.

            An estimated 33,000 Amish live in Ohio yet only about a quarter have vaccinations. Because many Amish children have never had any shots, the vaccines are especially hard to give to scared children.  The 341 cases as of late June represent the largest measles outbreak in recent US history.  Interestingly in 2005, journalist, Dan Olmstead, produced an “Age of Autism” series noting that the Amish have very few children with autism and for the few cases, the children happened to have been vaccinated, contributing to the misguided debated about vaccinations causing autism and contributing to decreased vaccination rates in the US. Despite it being culturally uncommon, many Amish are seeking medical help and receiving the vaccine to slow the spread of the virus.

--Will St. Amant

Sources:

http://www.npr.org/blogs/health/2014/06/24/323702892/measles-outbreak-in-ohio-leads-amish-to-reconsider-vaccines

http://www.cnn.com/2014/05/23/health/ohio-measles/

http://viralzone.expasy.org/all_by_species/86.html

http://www.cdc.gov/measles/