Scientists have long known that chimpanzees and other nonhuman primates can become infected with simian immunodeficiency virus, or SIV, a variant of HIV. It was thought, however, that only Asian macaque monkeys could die from the infection. But a new study published in Nature contradicts this assumption by finding that the virus can also be deadly to chimpanzees, humans’ closest relatives.
Some wild primates appear to have developed a way to keep SIV from becoming deadly, and scientists had hoped that studying chimpanzees could reveal how this mechanism works, possibly opening to the door to a human remedy. The new results suggest that it will not be possible to find the key to HIV immunity in the chimpanzee genome, as scientists had hoped. However, the study… sets the stage for researchers to gain insight into how HIV and SIV cause disease in their hosts by studying the responses of different primates to the viruses [Nature News].
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In September 2007, HIV research faced a serious setback: Scientists found that a promising HIV vaccine was actually increasing the rate of HIV infection, and the so-called STEP vaccine trial was immediately halted. The failure had a ripple effect, and caused researchers to call off another vaccine trial that operated on a similar principle. Since then, researchers have developed multiple explanations for why the vaccine upped the risk of infection. Now two new studies presented in Nature Medicine refutes the latest of these hypotheses, which gives researchers valuable information but ultimately leaves the mystery unsolved.
The recent theory held that some people responded more strongly than others to a component of the vaccine tested in the STEP trial, making them more vulnerable to HIV, which attacks immune cells that are actively responding to a pathogenic threat [Nature News]. Because the vaccine was constructed on the modified backbone of the virus that causes the common cold, the theory posited that white blood cells called helper T-cells jumped into action to combat this infectious particle. Unfortunately, HIV targets these T-cells, scientists reasoned, so vaccination actually gave HIV a larger target. This would explain why vaccination increased the risk of HIV infection.
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Circumcising men who are infected with HIV does not protect their female partners from the deadly virus, researchers have found. The Uganda-based study was stopped early due to “futility,” the researchers wrote in a study published in The Lancet, when it became clear that the women were not benefiting. The outcome was disappointing because circumcision has been shown to drastically reduce infection rates in men. But the researchers said that wide-scale circumcision is so effective in protecting men that [it] will still likely benefit women indirectly by reducing circulation of the virus in general [Reuters].
In 2007, the World Health Organization concluded that circumcising males reduced female-to-male transmission of the HIV virus by about 60 percent. The foreskin of the penis, which is removed during circumcision, is rich in cells that are particularly easy for the virus to infect. The theory is that removing this source of vulnerable cells makes infection more difficult [Reuters].
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Genetic “pieces” of the 1918 flu virus, which killed between 50 and 100 million people worldwide, were likely circulating between pigs and people two to 15 years before the pandemic struck, according to a new study published in Proceedings of the National Academy of Sciences.
Catch two different flu viruses at once and a new one can emerge, something scientists call reassortment. Birds are the ultimate origin of influenza viruses, but because pigs can catch both bird and human flu strains, they’ve long been recognized as a species mixing vessel [AP]. The research shows that lethal flu strains may be the result of such reassortment of pre-existing strains, not a sudden genetic “jump.” It’s a cautionary tale for those studying the current swine flu outbreak, say researchers, as the findings suggest that the swine flu virus could evolve slowly over many years into a more dangerous form.
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It’s unknown whether the swine flu virus will mutate to a more deadly strain in the coming year, but the federal government is preparing for the worst in case the pandemic continues to spread. At yesterday’s flu summit at the National Institutes of Health, Health and Human Services Secretary Kathleen Sebelius revealed the government’s provisions for a possible swine flu emergency.
The campaign to combat the swine flu is different from the strategy usually employed against the seasonal flu. One reason is that the swine flu appears to be most deadly to children and young adults, while the seasonal flu traditionally is most fatal to the elderly. Therefore, if mass vaccination becomes necessary, school-aged children will be among the first to be immunized; this likely will occur at school, in a manner reminiscent of the 1950s polio vaccination campaign. “We are likely to have a different target population,” Sebelius said. “We will be seeking partnerships with schools potentially and other vaccination sites.” Time will have to be spent writing consent forms so parents are not blindsided when schools ask to vaccinate their children, Sebelius said [Reuters]. States should also prepare a plan for closing schools if needed.
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Researchers have revealed that seasonal flu and swine flu cause different symptoms because they have different destinations in the body: the seasonal flu lodges itself mainly in the nasal passages, while the swine flu virus travels into the trachea and lung, and even makes its way to the intestines. It also replicates more quickly and causes more damage than the seasonal flu, according to a pair of studies published in Science.
Flu viruses wreak their havoc by binding to molecules on the surface of cells in mammals’ respiratory tracts, including humans. But the researchers found that the swine flu binds to surfaces that are unusually deep in the respiratory tract, such as the branches within the lungs known as bronchioles. The scientists used ferrets for the experiments because the animals respond to the flu much the way humans do. Research teams in the United States and the Netherlands found that the new H1N1 flu virus replicated more extensively in the respiratory tract, going to the lungs, whereas the seasonal flu virus stayed in the animals’ nasal cavity. The U.S. team also found that the new virus, unlike the seasonal one, went into the ferrets’ intestinal tract [Forbes], which explains the unusual symptoms of nausea and vomiting that some swine flu patients experienced.
Such information could prove crucial to the public health response to the swine flu, which so far has sickened more than 77,000 people worldwide, killing at least 332, according to the World Health Organization.
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In the first confirmed case of drug-resistant swine flu worldwide, a Danish patient developed resistance to Tamiflu, the antiviral treatment used for flu prevention and treatment. The patient recovered and did not appear to have passed the resistant strain to others. While a drug-resistant virus could make it harder to treat and prevent the spread of the flu, experts maintain that the isolated case is not a cause for alarm, and say Tamiflu is still effective against the swine flu.
A spokesman for Tamiflu manufacturer Roche says the Danish patient developed drug-resistant swine flu while taking the drug as a preventative to avoid the contraction of swine flu…. He was probably already infected with the virus, and resistance to the drug emerged because he was given the lower preventative dose [The Wall Street Journal]. This type of resistance is known as drug-induced resistance, as opposed to naturally occurring resistance, in which a strain itself mutates to become unresponsive to a medication.
The U.S. Centers for Disease Control and Prevention continues to recommend Tamiflu to treat the flu, along with another flu drug, Relenza. The World Health Organization also is expected to keep supporting the use of Tamiflu. Tamiflu-resistant strains of the seasonal flu have been found in Japan, which has used more than half the world’s supply of the drug each year. But those strains were weak and did not spread. A Tamiflu-resistant strain of the H5N1 bird flu was also isolated from a Vietnamese patient being treated with low-dose Tamiflu in 2005, but it also died out [The New York Times].
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Seasonal flu outbreaks typically taper off in the warm and humid summer months, as the influenza virus can’t survive as long in those conditions as it does in the cold, dry air of winter. But the current outbreak of the H1N1 swine flu virus is quite different than a typical flu season, and may produce a very different pattern of infection: It may produce an extended year-round flu season that disproportionately hits young people, health officials said on Thursday…. “The fact that we are seeing ongoing transmission now indicates that we are seeing something different” [Reuters], said Daniel Jernigan of the Centers for Disease Control and Prevention.
The swine flu outbreak, which the World Health Organization officially declared a pandemic last week, has continued to spread around the world, although its fatality rate remains fairly low. Health officials estimate that at least 100,000 people in the United States have been infected, 1,600 people have been hospitalized, and 44 have died. In another difference from typical seasonal flu outbreaks, the swine flu has disproportionately infected young, healthy people. Jernigan says its likely that older people have been exposed to a similar virus to the H1N1 virus at some point, which gives them some immune response to the current virus, while children are believed to have a “complete lack of immunity to this particular virus” [Reuters], he said.
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The World Health Organization is expected to officially classify the ongoing H1N1 swine flu outbreak as a pandemic in the next couple of days, but health officials are taking pains to stress that the “pandemic” label only indicates that the virus is spreading through communities in more than one region of the globe–it does not mean that the virus is killing everyone in its path.
WHO official Keiji Fukuda explains: “It does not mean that the severity of the situation has increased or that people are getting seriously sick at higher numbers or higher rates than they are right now…. One of the critical issues is that we do not want people to ‘over-panic’ if they hear that we are in a pandemic situation” [Reuters].
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Hydrogen peroxide can kill viruses and bacteria, and it’s been used for generations to sterilize wounds and help them heal faster. But a new study published in the journal Nature shows that the substance may also serve as a Pied Piper for white blood cells, summoning them to the site of a wound to promote healing.
Damaged tissue hails a variety of cells to defend the body from infectious agents; one type is white blood cells, which kill by initiating a “respiratory burst,” which releases highly reactive antimicrobial molecules, including hydrogen peroxide produced by the body itself [ScienceNOW Daily News]. But it wasn’t until now that researchers noticed that hydrogen peroxide appeared at the injury site an average of 17 minutes before the immune cells arrived. Study coauthor Phillipp Niethammer explains that after nicking the tail of a zebrafish, “I saw something bursting at the wound,” he says, “but I didn’t see leukocytes there.” That bursting, experiments revealed, was hydrogen peroxide… [I]t appeared as if hydrogen peroxide was bringing leukocytes to the wound rather than the other way around [ScienceNOW Daily News]. Further investigations revealed more about the chain of post-injury events.
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While initial public panic about the swine flu outbreak has largely subsided, the virus continues to spread through our species: The World Health Organization has tallied more than 10,000 cases worldwide, with 80 deaths confirmed. As patterns begin to emerge regarding who gets infected with the H1N1 flu virus, health officials are beginning to map out strategies for a potential wide-spread vaccination campaign.
Young people are particularly prone to infection, researchers say. Preliminary studies of family transmission showed that when one member gets infected, the most likely to follow are those under 18, not parents or grandparents [The New York Times]. The virus’s spread through the young has led to the closing of schools in infection hotspots–Japan is the most recent country to shut school doors–but most cases in young people have not been severe. The people who do get more serious cases that lead to hospitalization have tended to have underlying health conditions like heart problems, lung ailments, immune diseases, and diabetes. Surprisingly, obesity has also emerged as a risk factor.
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All’s fair in the fight against the AIDS virus–including medical sneak attacks. Researchers have devised a novel strategy to attack HIV by completely bypassing the immune system and instead tricking the muscles into producing virus-fighting proteins.
The quest for an HIV vaccine has been given a bad prognosis recently, due to increasing agreement that the human immune system isn’t clever enough to outsmart the ever-changing surface of the virus [Technology Review]. But using the new technique, researchers were able to protect monkeys from infection by the simian immunodeficiency virus (SIV), the animal virus most closely related to HIV. While lead researcher Philip Johnson cautions that there’s no guarantee that the vaccination process will work in humans, he’s eagerly looking forward to human trials in a few years.
Most efforts at blocking AIDS have sought to stimulate the body’s immune system to produce antibodies that fight the disease. This model has worked for diseases such as measles and smallpox. It hasn’t done as well with HIV/AIDS; test vaccines have failed to produce a protective reaction. So Johnson decided to try something different. “We used a leapfrog strategy, bypassing the natural immune system response that was the target of all previous HIV and SIV vaccine candidates,” Johnson said [AP].
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The swine flu virus that has infected almost 6,500 people in 33 countries is not the product of a lab accident, World Health Organization officials declared yesterday.
The health officials were arguing against a hypothesis that emerged earlier this week. An Australian researcher named Adrian Gibbs who was has been involved in the development of antiviral flu drugs issued a report suggesting the new strain may have accidentally evolved in eggs scientists use to grow viruses and drugmakers use to make vaccines. Gibbs said he came to his conclusion as part of an effort to trace the virus’s origins by analyzing its genetic blueprint. “One of the simplest explanations is that it’s a laboratory escape,” Gibbs said…. “But there are lots of others” [Bloomberg]. Gibbs said this new virus had evolved faster than other flu viruses found in pigs, which he said suggested that it combined with other viruses being used in a lab. He argued that the virus could have then escaped into the general population.
But at a press conference, WHO official Keiji Fukuda announced that the hypothesis had been investigated and rejected. “Based on that evaluation by all of the laboratories, the conclusion is that this group of scientists feels that the hypothesis does not really stand up to scrutiny,” Dr. Fukuda said. “The evidence suggests that this is a naturally occurring virus and not a laboratory-derived virus” [MedScape]. He did not go into specifics of the investigation, but did say that the virus’s mutation rate was typical.
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A “fast and dirty” analysis of the spread of swine flu thus far has led researchers to believe that the virus will eventually turn into a true pandemic infecting about a third of the world’s population–but they hasten to add that the analysis also suggests that the flu doesn’t have a devastating death rate.
Lead researcher Neil Ferguson, a member of the World Health Organization’s emergency committee for the outbreak, says: “This virus really does have full pandemic potential. It is likely to spread around the world in the next six to nine months and when it does so it will affect about one-third of the world’s population. To put that into context, normal seasonal flu every year probably affects around 10% of the world’s population every year, so we are heading for a flu season which is perhaps three times worse than usual” [BBC News].
The analysis, published in Science, also roughly estimates that the flu has a fatality rate of .4 percent, meaning that it kills 4 people out of every 1,000 infected. That makes the swine flu virus about as dangerous as the virus behind a 1957 pandemic that killed 2 million people worldwide. But it’s not nearly as lethal as the bug that caused the 1918 Spanish flu pandemic [ScienceNOW Daily News]. Seasonal flu has a fatality rate of less than .1 percent, and kills more than 250,000 people each year.
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In an ironic twist to the swine flu epidemic, an infected farm worker has infected a Canadian herd of pigs with the virus, and the development is a bad public relations blow for the pork industry. The outbreak came on an isolated Alberta farm after a farm worker returned from Mexico on April 12 and had contact with pigs on the farm two days later. On April 24, pigs began showing signs of influenza; about 220 of the 2,200 pigs on the farm were found to be infected with H1N1 [The Globe and Mail]. The farm remains quarantined although the human and all the pigs have recovered from the flu.
World Health Officials note that the virus hasn’t yet been found in other pigs, including any pigs in Mexico–although epidemiologists are testing pigs in the towns where the flu first emerged in humans. The WHO has also begun calling the virus by its scientific name, H1N1, to avoid confusing consumers (the virus is passing from human to human with sneezes and coughs, like a seasonal flu virus). There is no risk of contracting influenza from pork products. Flu viruses are fragile: They can survive only hours outside a live body – human or animal – and are easily destroyed in meat by cooking [The Globe and Mail].
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