A report published in JAMA Internal Medicine suggests that 20% of the American public believe that doctors and the government know that vaccines cause harm, and yet they continue to inoculate children. The survey found that, of the 1351 participants, 69% had heard of this conspiracy theory, making it the most widely known medical conspiracy theory mentioned in the survey. Of the 1351 participants 20% agreed with the conspiracy, and 44% disagreed. Whilst it is of course good news that twice the number of participants rejected rather than endorsed the conspiracy, what is troubling is the 36% of the public that are sitting on the fence.
Ed Rybicki's insight:
Well, I'd say that this would be a self-limiting phenomenon, except that it'd take too long. Maybe it's better to just educate them?
Pollination is an essential step in the reproduction of flowering plants and is also crucial in agriculture in regard to fruit development, seed output, and the creation of new varieties of plants. However, at least 18 viruses can infect the mother plant through the fertilized flower (horizontal transmission by pollen). Horizontal transmission by pollen is epidemiologically important for viruses infecting perennial crops, since pollen grains from infected trees continue to be scattered every year. The mechanism how pollination with virus-infected pollen grains causes systemic viral infection to healthy plants has been unknown since the first report of horizontal transmission by pollen in 1918.
Historically, this blog has focused on “news you can use,” but in the spirit of two-way communication, for this post I thought I would try something that might generate more discussion. I’m sharing my thoughts on an issue I’ve been contemplating a lot: the hazards of overly hypothesis-driven science.
When I was a member of one study section, I often saw grant applications that began, “The overarching hypothesis of this application is….” Frequently, these applications were from junior investigators who, I suspect, had been counseled that what study sections want is hypothesis-driven science. In fact, one can even find this advice in articles about grantsmanship .
Despite these beliefs about “what study sections want,” such applications often received unfavorable reviews because the panel felt that if the “overarching hypothesis” turned out to be wrong, the only thing that would be learned is that the hypothesis was wrong. Knowing how a biological system doesn’t work is certainly useful, but most basic research study sections expect that a grant will tell us more about how biological systems do work, regardless of the outcomes of the proposed experiments. Rather than praising these applications for being hypothesis-driven, the study section often criticized them for being overly hypothesis-driven.
Ed Rybicki's insight:
I love it: "the hazards of overly hypothesis-driven science"! Viva, that man, viva!
I am not a fan of “Science By Hype”, which I think I have made abundantly clear via Virology News and elsewhere. Thus, I pour scorn on the “We found a structure which will lead to an AIDS vaccine”, and “We found an antibody that will cure AIDS” type of articles, WHILE at the same time, appreciating the ACTUAL science behind the hype. If there is any, of course. Which is why I am torn, on the subject of a giant DNA virus purportedly found in 30 000 year-old Siberian permafrost. I am also a fan of zombies, hence the title. But seriously, now: here we are, with news media and semi- and fully-serious science mags all hailing the description in PNAS, no less, of “Pithovirus sibericum“. A giant virus, wakened from a 30 000 year sleep in Siberian permafrost, by the kiss of an amoeba. OK, by infecting an amoeba, but you see where I’m going here.
n June 2012, three men removing slag from a derelict copper mine in southwestern China fell ill with severe pneumonia and died. Six months later, researchers went spelunking in the mine—an artificial cave hewn from a hillside—in search of pathogens. After taking anal swabs from bats, rats, and musk shrews living in the cave, the team has discovered what it says is a new virus that may have felled the workers.
The presumed pathogen resembles a genus of viruses known as henipaviruses, two of which are deadly: Hendra virus, discovered 20 years ago in Australia when it started killing horses—since then, four people who came in contact with infected horses have died—and Nipah virus, the cause of periodic outbreaks in people in Southeast Asia since 1998. The third confirmed henipavirus, Cedar virus, was first reported in Australia in 2012; it does not appear to infect humans. For all three species, the animals that harbor the virus in the wild—the natural reservoir—appear to be fruit-eating bats called flying foxes.
The new virus, named Mojiang paramyxovirus (MojV) after the county in Yunnan province where it was found, joins a growing list of species that share genetic similarities with henipaviruses and members of the Paramyxoviridae family that includes henipaviruses. The bats and shrews in the Yunnan cave tested negative for the new henipa-like virus; three of nine rats were infected. “It is not totally surprising to find henipa-like sequences in rodents,” as rats are the natural reservoir for some paramyxoviruses, says Lin-Fa Wang of the Australian Animal Health Laboratory in Geelong, who was not involved in the Mojiang study. MojV “could be a ‘bridging’ virus between those in bats and rodents,” says Wang, one of the leaders of the team that discovered Cedar virus.
The strength of attraction between capsid proteins (CPs) of cowpea chlorotic mottle virus (CCMV) is controlled by the solution pH. Additionally, the strength of attraction between CP and the single-stranded RNA viral genome is controlled by ionic strength. By exploiting these properties, we are able to control and monitor the in vitro co-assembly of CCMV CP and single-stranded RNA as a function of the strength of CP–CP and CP–RNA attractions. Using the techniques of velocity sedimentation and electron microscopy, we find that the successful assembly of nuclease-resistant virus-like particles (VLPs) depends delicately on the strength of CP–CP attraction relative to CP–RNA attraction. If the attractions are too weak, the capsid cannot form; if they are too strong, the assembly suffers from kinetic traps. Separating the process into two steps—by first turning on CP–RNA attraction and then turning on CP–CP attraction—allows for the assembly of well-formed VLPs under a wide range of attraction strengths. These observations establish a protocol for the efficient in vitro assembly of CCMV VLPs and suggest potential strategies that the virus may employ in vivo.
Ed Rybicki's insight:
I do love it when a paper is published that could have been done pretty much any time in the last 40 years - and with one of my favourite viruses, that I played with a LOT back there before 1980.
Ultracentrifugation, pH meters, ionic strength determinations, EM...all tried and true, and used 40+ years ago. OK, they also used cloned BMV RNA 1 cDNA, and did 3-D image reconstruction from EMs, but hey, they needn't have done that! Nice, straightforward physicochemical studies, on a well-characterised virus, with good, simple conclusions.
Namely, that assembly of the virus is NOT just a simple mix-CP-and-RNA-and-it-will-happen, but that it depends upon both pH, for modulating ionic interactions,and ionic strength for modulating ionic interactions AND the "hydrophobic effect", as we used to know it.
While their conclusions are relevant for assembly of heat- and nuclease-resistant nano particles in vitro, I wonder if they are physiologically relevant: if "correct" assembly depends upon first, turning on CP-RNA attraction (ionic strength shift), and second, turning on CP-CP attraction (pH shift) - where in the cell does that happen?
In their own words, "It is generally accepted that the cytoplasm of plant cells is maintained near neutral pH with ionic strength of approximately 0.1 M. Our in vitro results show that these conditions are insufficient for nucleocapsid formation in the absence of cellular host factors."
Yeeee-ee-eesssss...precisely. What happens in the cell? The answer could lie in the one thing they don't report, but that some of the heroes of my distant youth - people like JB Bancroft and Thom Hohn, both quoted (from 1970 and 1969 respectively) in this paper, DID do. Namely, investigate what happens at different CP and RNA concentrations, at constant pH and ionic strength.
You see, it was shown 30+ years ago - and I have been lecturing on it since then - that CP and RNA for viruses like BMV / CCMV and MS2 form different complexes with their cognate partners at different molecular ratios. That is, at low CP:RNA ratios, a high-affinity complex is formed, which is basically a ribonucleoprotein complex without structure. Increasing the CP:RNA ratio for both MS2 and CCMV, as I recall (maybe Dick Verduin was involved with CCMV), results in further lower-affinity association of CP with both RNA and already-bound CP - which acts as a nucleation complex - to result in full capsid assembly.
I note that the process in both cases was shown to be specific, for low CP:RNA ratios: that is, it was cognate CP and RNA doing the high affinity nucleation complex formation.
And these guys deliberately used a heterologous RNA...albeit one from a related virus, but still: what would have happened if they'd used CCMV RNA?
Still - great paper, taking me back to when I wrote an essay on "Assembly of Spherical Plant Viruses" in my Honours year in 1977, quoting quite a few of the same references these folk did. Ah, simpler times...B-)
Highly contagious virus kills 59 people in Guinea, with fears the disease may have spread to neighbouring Sierra Leone.
Ebola has killed at least 59 people in Guinea and there are fears the virus may have spread to neighbouring Sierra Leone, world health officials have said.
Cases of the disease, which can kill 90 percent of those infected, have been registered in three southeastern towns and in the Guinean capital, Conakry, since Februrary 9. They are the first recorded cases in the country.
"It is indeed Ebola fever. A laboratory in Lyon, France, confirmed the information," Damantang Albert Camara, a government spokesman, told the Reuters news agency.
Ed Rybicki's insight:
38 years on, it continues to pop out of the bush - due almost certainly to the "bush meat" trade. So it goes when you mess with nature....
The first cases went unrecognized. Ebola had never been seen in Guinea before, so when people became ill with fever, muscle pain, vomiting, and diarrhea, health workers initially assumed Lassa fever or yellow fever—both endemic in the region—were to blame. No one put the pieces together until late March. By then, the virus had been spreading for months. Now, health workers are struggling to contain the outbreak, which has already killed more than 100 and has affected at least two neighboring countries. At the same time, scientists are combing the forests, and the genome of the virus itself, looking for clues to how this strain—well known in Central Africa—ended up so far west, and whether its spread suggests people in forested areas all across sub-Saharan Africa are at risk.
Ebola is not a complete stranger to West Africa. In the mid-1990s, two outbreaks hit chimpanzees in Taï National Park in the Ivory Coast, and one researcher studying the animals was infected. (She survived.) "We expected to find the Taï strain," says Sylvain Baize, a virologist at the Institut Pasteur in Lyon, France, who with his colleagues sequenced some of the first samples of the virus from Guinea. To their surprise, it turned out to be Ebola Zaire, the deadliest of the five known Ebola species.
"We have no idea how it's moved from Central Africa to Guinea," says primatologist Christophe Boesch of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany. A leading suspect is fruit bats. In Central African rainforests, several species have shown evidence of infection with Ebola without getting sick. And at least one of the species, the little collared fruit bat, Myonycteris torquata, has a range that stretches as far west as Guinea. "We've always been very suspicious of bats," says William Karesh of EcoHealth Alliance in New York City, who studies the interactions among humans, animals, and infectious diseases.
Some people think of tobacco as a drug, whereas others think of it as a therapy — or both. But for the most part, it's hard to find people who think of the tobacco plant in terms of its medical applications. Qiang Chen, an infectious disease researcher at Arizona State University, is one such person. His team of scientists conducted an experiment,published today in PLOS ONE, that demonstrates how a drug produced in tobacco plants can be used to prevent death in mice infected with a lethal dose of West Nile virus. The study represents an important first step in the development of a treatment for the mosquito-borne disease that has killed 400 people in the US within the last two years.
Ed Rybicki's insight:
Thanks to @Ken Yaw Agyeman-Badu. Now I know Qiang "Shawn" Chen and the ASU crowd, and they're a smart bunch - and they're almost certainly using the same vector system we do.
Strange thing, that: using a plant virus-based vector system in tobacco to make monoclonal antibodies to combat an arbovirus. Full-on molecular zoo!
In recent years Nigeria has experienced sporadic incursions of highly pathogenic H5N1 avian influenza among poultry. In 2008, 316 poultry-exposed agricultural workers, and 54 age-group matched non-poultry exposed adults living in the Enugu or Ebonyi States of Nigeria were enrolled and then contacted monthly for 24 months to identify acute influenza-like-illnesses. Annual follow-up sera and questionnaire data were collected at 12 and 24 months. Participants reporting influenza-like illness completed additional questionnaires, and provided nasal and pharyngeal swabs and acute and convalescent sera. Swab and sera specimens were studied for evidence of influenza A virus infection. Sera were examined for elevated antibodies against 12 avian influenza viruses by microneutralization and 3 human viruses by hemagglutination inhibition.
Tomorrow, the World Health Organization (WHO) is expected to officially certify that south-east Asia, formerly one of the regions with the worst levels of polio, has eradicated the disease, after India found new no cases in the previous three years. (The WHO counts India as part of south-east Asia.) To understand why that matters, read this heart-breaking profile of Rukhsar Khatoon, the...
A possible case of Ebola has been detected in Canada after a passenger returned from Africa where dozens have died from the virus.
"All we know at this point is that we have a person who is critically ill who travelled from a country where these diseases occur," said Denise Werker, joint director of health in Saskatchewan province in western Canada.
She said the casualty had been in Liberia and had developed the symptoms after landing in Canada.
He or she would not have been contagious when travelling and was now in isolation pending test results.
Aid workers and health officials in Guinea are battling to contain western Africa's first outbreak of the deadly Ebola virus as neighbouring Liberia reported its first suspected victims.
At least one child has died since the outbreak began in November, with others vulnerable due to a lack of vaccinations.
An outbreak of measles is threatening the lives of children in Guinea, one of West Africa's poorest countries.
The UN children's agency UNICEF says one child has been confimed dead since the outbreak began in November, but the real number may be much higher.
A UN survey shows only 37 percent of children in Guinea get all the vaccines they need to stay healthy, making the majority vulnerable. Thirty-seven cases of measles have been confirmed in the capital Conakry.
Ed Rybicki's insight:
Makes one sad: kids in New York getting measles because their parents are too stupid to vaccinate them; kids in Guinea getting it because they're too poor.