Although Ebola viruses can cause fatal disease in humans and other primates, pigs can carry the infections with few ill effects. Now, Canadian scientists have shown that apparently healthy pigs can pass the deadliest species of Ebola to monkeys, even without ever coming into contact with them.
The study, published today (November 15) in Scientific Reports, marks the first time that the virus has spread between different species in a lab experiment, and suggests that pig farms could be facilitate such species-hopping in more natural conditions.
However, Gary Kobinger from the University of Manitoba, who led the study, cautioned that “we still don’t know if pigs are playing any role in the natural transmission or ecology of Ebola virus in Africa.”
“An epidemiological survey of wild and domestic pigs in sub-Saharan Africa is now necessary,” agreed Shigeru Morikawa from the National Institute of Infectious Diseases, Japan, who was not involved in the research.
Canadian scientists have shown that the deadliest form of the ebola virus could be transmitted by air between species.
In experiments, they demonstrated that the virus was transmitted from pigs to monkeys without any direct contact between them.
The researchers say they believe that limited airborne transmission might be contributing to the spread of the disease in some parts of Africa.
They are concerned that pigs might be a natural host for the lethal infection.
God help us all if this deadly virus spreads worldwide.
Terrified patients fled from a hospital in western Uganda as soon as news broke that a mysterious illness that killed at least 14 people in the region was Ebola, one of the world’s most virulent diseases.
Ignatius Besisira, an MP for Buyaga East County in the Kibaale district, said people had at first believed the unexplained deaths were related to witchcraft. “Immediately, when there was confirmation that it was Ebola … patients ran out of Kagadi hospital (where some of the victims had died),” he told the Guardian. “Even the medical officers are very, very frightened,” he said.
Government officials and a World Health Organisation representative confirmed the Ebola outbreak at a news conference in Kampala on Saturday. “Laboratory investigations done at the Uganda Virus Research Institute … have confirmed that the strange disease reported in Kibaale is indeed Ebola haemorrhagic fever,” they said in a joint statement.
Health officials said at least 20 people had been infected and of those 14 had died.
There is no treatment or vaccine against Ebola, which is transmitted by close personal contact and, depending on the strain, can kill up to 90% of those who contract the virus.
It has a devastating history in Uganda, where in 2000, at least 425 people were infected, of whom more than half died. Ebola was previously reported in the country in May last year, when it killed a 12-year-old girl.
The deadly Ebola virus has killed 14 people in western Uganda this month, Ugandan health officials said on Saturday, ending weeks of speculation about the cause of a strange disease that had many people fleeing their homes.
The officials and a World Health Organization representative told a news conference in Kampala Saturday that there is “an outbreak of Ebola” in Uganda.
“Laboratory investigations done at the Uganda Virus Research Institute…have confirmed that the strange disease reported in Kibaale is indeed Ebola hemorrhagic fever,” the Ugandan government and WHO said in joint statement.
Kibaale is a district in midwestern Uganda, where people in recent weeks have been troubled by a mysterious illness that seemed to have come from nowhere. Ugandan health officials had been stumped as well, and spent weeks conducting laboratory tests that were at first inconclusive.
Now, in a development that could transform how viral infections are treated, a team of researchers at MIT’s Lincoln Laboratory has designed a drug that can identify cells that have been infected by any type of virus, then kill those cells to terminate the infection.
In a paper published July 27 in the journal PLoS One, the researchers tested their drug against 15 viruses, and found it was effective against all of them — including rhinoviruses that cause the common cold, H1N1 influenza, a stomach virus, a polio virus, dengue fever and several other types of hemorrhagic fever.
The drug works by targeting a type of RNA produced only in cells that have been infected by viruses. “In theory, it should work against all viruses,” says Todd Rider, a senior staff scientist in Lincoln Laboratory’s Chemical, Biological, and Nanoscale Technologies Group who invented the new technology.
Because the technology is so broad-spectrum, it could potentially also be used to combat outbreaks of new viruses, such as the 2003 SARS (severe acute respiratory syndrome) outbreak, Rider says.
Other members of the research team are Lincoln Lab staff members Scott Wick, Christina Zook, Tara Boettcher, Jennifer Pancoast and Benjamin Zusman.
Few antivirals available
Rider had the idea to try developing a broad-spectrum antiviral therapy about 11 years ago, after inventing CANARY (Cellular Analysis and Notification of Antigen Risks and Yields), a biosensor that can rapidly identify pathogens. “If you detect a pathogenic bacterium in the environment, there is probably an antibiotic that could be used to treat someone exposed to that, but I realized there are very few treatments out there for viruses,” he says.
There are a handful of drugs that combat specific viruses, such as the protease inhibitors used to control HIV infection, but these are relatively few in number and susceptible to viral resistance.
Rider drew inspiration for his therapeutic agents, dubbed DRACOs (Double-stranded RNA Activated Caspase Oligomerizers), from living cells’ own defense systems.
When viruses infect a cell, they take over its cellular machinery for their own purpose — that is, creating more copies of the virus. During this process, the viruses create long strings of double-stranded RNA (dsRNA), which is not found in human or other animal cells.
As part of their natural defenses against viral infection, human cells have proteins that latch onto dsRNA, setting off a cascade of reactions that prevents the virus from replicating itself. However, many viruses can outsmart that system by blocking one of the steps further down the cascade.
Rider had the idea to combine a dsRNA-binding protein with another protein that induces cells to undergo apoptosis (programmed cell suicide) — launched, for example, when a cell determines it is en route to becoming cancerous. Therefore, when one end of the DRACO binds to dsRNA, it signals the other end of the DRACO to initiate cell suicide.
Combining those two elements is a “great idea” and a very novel approach, says Karla Kirkegaard, professor of microbiology and immunology at Stanford University. “Viruses are pretty good at developing resistance to things we try against them, but in this case, it’s hard to think of a simple pathway to drug resistance,” she says.