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Richmond, VA - Nearly 4 million people in the U.S. are living with a potentially fatal virus in their bodies, but only a fraction know it. Hepatitis C, the Hidden Killer, can lie dormant in your liver, causing slow and silent destruction for decades.

Now, a new round of drugs is bringing new hope to doctors and their patients. Until recently, treatments for Hepatitis C have been almost as painful as the virus itself. Doctors have been working furiously over the past several years to develop a new generation of drugs to cure patients in less time, with less effort, and with less pain.

"The new drugs that we're using, almost everybody is cured. In fact, now it's rare for somebody in these clinical trials not to be cured," said Dr. Mitchell Shiffman, Medical Director of the Bon Secours Liver Institute in Richmond.

The new treatments are a far cry from ones dating back just three years ago. Before 2011, the year-long process of treating Hepatitis C produced limited results and extensive side effects.

"Because of these low cure rates and the high side effect rates, this is why the vast majority of patients with Hepatitis C in the country, who know they have the virus, have not been treated," said Shiffman.

Only 25% of Americans with Hepatitis C know they have it. Less than half of those people are seeking treatment. The risks and benefits of older treatments just don't weigh out for most patients.

"It's depressing to take those medications and get side effects and not be cured," said Shiffman.

The main culprit of these side effects is interferon, an injection that's been known to cause depression, flu-like symptoms and fatigue. Bryan McKernon is all too familiar with the side effects interferon causes. The 57-year-old learned he had Hepatitis when he was 30. Back then, Hep C wasn't even on the radar for most doctors.

So, McKernon went to the Bon Secours Liver Institute in Richmond, to meet with Dr. Shiffman.

"When we first met Bryan he looked very healthy, but his liver was already very diseased," said Shiffman.

Continue reading here:
Hidden Killer Part 2: The Promise of New Hepatitis C Treatments

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The mystery of colony collapse disorder in honeybees has a remarkable new suspect a plant virus that has made a spectacular jump across 1.6 billion years of evolution to infect insects.

The potential hive killer is tobacco ringspot virus, named for the discoloured circles it forms on infected leaves. It has at least 90 different plant hosts and is so difficult to get rid of that some farmers have stopped raising susceptible crops.

It often travels on pollen from one host to another by thumbing a ride in insects, including varroa mites, aphids and bees. But such viral hitchhikers usually stay in the gut or salivary glands, ready to make a quick jump to the next plant host.

So when a team of scientists from the US Department of Agriculture and Chinas Academy of Agricultural Science spotted it in honey bees they were not expecting to find that it had spread throughout the animals bodies, and was doing particularly well in wings, antennae, trachea, hemolymph (insect blood) and nerves.

Such jumps are not unheard of. Rhabodoviridae, the family of viruses that includes rabies, has members that have both plant and animal hosts. Shorter hops are routinely made between species by influenza and HIV famously transferred to humans from apes.

Common to all these viruses is the use of RNA rather than DNA to encode their genetic templates. RNA is the messenger molecule that tells cells how to build proteins. It is not as rigorously policed as DNA, and so is far more likely to have copying errors. As a result, viruses that rely on RNA mutate more often.

Tobacco ringworm virus was also found in varroa mites, which parasitize honeybees, and may play a role in spreading the disease.

The prime suspect in colony collapse disorder remains neonicotinoid pesticides, which were banned in the European Union in November 2013.

However, the case against them is far from proven, and researchers continue to hunt for other candidates, including viruses.

The US-China team screened six strong and four weak colonies over a year for tobacco ringspot and other viruses, deformed wing bee virus, black queen cell virus and Israel acute paralysis virus and found that higher concentrations presaged colony collapse, although no apparent disease symptoms were spotted in individual bees. The four weak colonies studied had collapsed by February.

More:
Plant Virus Jumps 1.6-Billion-Year Species Barrier Killing Honeybees

Threatwatch is your early warning system for global dangers, from nuclear peril to deadly viral outbreaks. Debora MacKenzie highlights the threats to civilisation and suggests solutions

Exactly 10 years after H5N1 bird flu exploded across south-east Asia, the virus is still widespread, and has been joined by new killer types of bird flu. Human cases of H7N9 flu are surging in south-east China, and a new type of bird flu, H10N8, has claimed its second human victim, in the same region.

Now it seems that all of these viruses stem from a single, mother virus. Targeting it might stop it from spawning new, deadly viruses in the future.

Few people have heard of H9N2, but this virus was crucial in giving rise to the three dangerous bird flu viruses that have emerged so far in China H5N1, H7N9 and H10N8.

None of these viruses has yet evolved the ability to spread readily in people and potentially trigger a pandemic although we know H5N1 can, and H7N9 and H10N8 seem similar. But even if those viruses never go rogue, their cousins might, because the real problem is their common ancestor, which endowed them with the genes that make them dangerous.

"H9N2 is the enabler, the one to worry about," Robert Webster of St. Jude Children's Research Hospital in Memphis, Tennessee, told New Scientist. Bird flu is usually a gut infection in ducks, but H9N2 has evolved into a benign respiratory virus in chickens that has spread across Eurasia. When multiple flu viruses infect the same host, they can swap genes. They may be named for their various H and N surface proteins, but H5N1, H7N9 and H10N8 all got some or all of their "internal" genes from H9N2.

Those genes for the enzymes that replicate the viral genome, for example, or a protein that confuses a host's immune system can make these viruses dangerous, says Webster. Any of them might become pandemic if they acquire the right mutations to spread in people or hybridise with a normal human flu.

Closing Asia's ubiquitous live poultry markets would be the key to controlling N9N2, says Webster, as this is where H9N2 and its spin-off viruses spread, mingle and evolve and where humans catch them.

That is just what China is trying to do. As millions celebrate Lunar New Year this week with home-slaughtered poultry, Shanghai and three other cities have shut their live markets and officials are urging people to eat pre-slaughtered, frozen birds. The continued threat from China's bird flu may depend on whether that catches on. "It's the Year of the Horse in China," says Webster. "I hope they can get the stable door closed before the horse has bolted."

H7N9 emerged in south-east China last spring, infecting 136 people, a third of whom died. In response, Chinese flu scientists called for live poultry markets to be shut last April. Some were but they were re-opened when flu cases dropped in the following months.

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Threatwatch: Mother virus of China's deadly bird flu

The ailment that swept through the U.S. driving up pork, ham and bacon prices is gaining a foothold here. Farmers are fearful, and with good reason. Here is all you need to know about the killer virus:

What is PED?

Porcine epidemic diarrhea is a virus that kills suckling piglets, usually within five days. Older hogs are weakened and lose weight, but do not die in large numbers. It does not affect humans nor does it affect food safety. Considering that pigs produce just two litters a year, a PED attack can be devastating.

Will this affect my grocery bill?

Consumers in the United States are paying more for pork as a result of PED, and it is expected Canadian consumers will, too. Since its discovery, the virus has helped drive up bacon prices in the United States by about 15 per cent as it reduced the number of animals going to slaughter by about 1 per cent. There are predictions the 2014 U.S. herd could be cut by 3 per cent, and prices will rise more as people fire up their barbecues when the weather gets warmer. The virus hit when supply was already low; hog producers had culled their herds during 2011-2012 after a major drought drove up the cost of animal feed. (Consumers looking to beef for better prices might be disappointed. Cattle ranchers are also rebuilding post-drought. Wholesale beef prices in the United States have risen by 15 per cent in January.)

How widespread is PED?

Since being discovered in the United States last spring, the fast-spreading virus has been found in about 23 states and has killed between one million and four million pigs. In Canada, PED has been confirmed in a slaughterhouse in Quebec, and in Ontario at farms, one processing plant, a trucking facility and a yard where hogs are gathered for transport. Officials expect it to spread to other hog operations. (PED has been present in Asia and Europe for decades, and the strain in North America is believed to have come from China.)

How does it spread?

PED is passed through manure-to-mouth contact. The virus thrives in the cold and is easily carried on dirty boots, in hog transport trailers or manure pumping equipment. It can be spread by birds and other livestock that come in contact with manure-spread fields. Canada exports pigs to the United States and imports very few, so it is believed the virus came to Canada on an empty truck that had not been thoroughly cleaned.

What is being done to prevent its spread?

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What’s at stake for Canada as pig virus spreads