Tag Archives: Herpes

Hosts on a viral planet: When Herpes infects the eye

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In the summer of 1985, I was working in a cool lab, and about to enter the final year of my undergraduate degree in molecular biology and genetics.

And I was living with a girl.

In Aug. 1985, we got tickets to go see Neil Young and the International Harvesters at the CNE (the Canadian National Exhibition, or the Ex) and I fell ridiculously ill.

I was in bed for two weeks, barfing, and in agony – a great way to start a new relationship that would bear four beautiful daughters.

I made it out of bed to see Neil and the Harvesters.

The next day I went home to Brantford, Ontario, Canada.

I was really, really sick, my eye really, really hurt, and my parents suggested I go see the eye doctor.

Within 5 minutes, he diagnosed eye Herpes, prescribed a retroviral cream, and I was quickly cured.

Yeah, science.

I have been exceedingly public about this story in the fantastical hope that others may be spared some of the pain, or at least have it contained.

Sarah Zhang of The Atlantic writes – 33 years later – that Herpes simplex virus type 1 is best known as the culprit behind cold sores. When it’s not causing itchy, crusty sores on the mouth, it hides in the bundle of nerves that run through the face. And it’s super common. An estimated 50 to 90 percent of people harbor lifelong infections of HSV-1—largely without incident.

But in some cases, HSV-1 can run through that bundles of nerves in the face and erupt in the eye. Or maybe it gets into the eye from the outside. No one is really sure. In any case, HSV-1 can definitely infect the eye. (In case you’re wondering: HSV-1 can also cause genital infections, though it’s herpes simplex virus type 2 that is more commonly associated with genital herpes.)

Herpes in the eye is as bad as it sounds. The virus infects the cornea, forming tree-like branching ulcers across the eye. It can cause irritation, pain, sensitivity to light, and ultimately blindness if untreated. Herpes in the eye is a leading cause of blindness in the world. The cornea, after all, is a transparent layer of tissue at the front of the eye, whose job is essentially to let in as much light as possible. Infection can turn the cornea cloudy—permanently.

In most cases, herpes infections in the eye can be treated with antiviral drugs like Zovirax, but the herpes viruses are becoming increasingly resistant to these drugs. Scarred corneas can also be replaced with a transplant, but past infection makes the eye more likely to reject the new tissue. Plus, once you get herpes in the eye, it can keep coming back—just like cold sores. “For some patients that experience this, there’s absolutely nothing we do,” says Dan Carr, an HSV-1 researcher at the University of Oklahoma. “Essentially they’re going to go blind if something else doesn’t happen”—if new treatments don’t become available.

Enter now a surprising new study about herpes. Deepak Shukla, a virologist at the University of Illinois at Chicago, and colleagues have identified a molecule called BX795 that clears HSV-1 infections in human cells and in mice—with few side effects, it seems.

It’s a surprise because Shukla’s team originally threw BX795 onto HSV-1-infected cells thinking it would make the viruses grow better in the lab. (They were trying to study the virus’s basic functions.) That’s because BX795 is known to inhibit a enzyme called TBK1 that turns on the human immune response. Dampen the immune response, and you should get more viruses, right?

“We saw the opposite,” says Shukla. BX795 appears to play another role in yet another human enzyme that viruses hijack to synthesize their own viral proteins. Shukla’s team tested BX795 in cultured human cells, human corneas, and mice with herpes eye infections. It worked to suppress the herpes virus in all those cases—and often at lower concentrations than existing antiviral drugs.

Most exciting of all, BX795 could represent an entirely new class of drugs for herpes. Existing drugs generally work by inhibiting the virus’s DNA (or RNA) replication, blocking it from making more copies of itself. Since the drugs work in such similar ways, it’s easy for the virus to evolve resistance to all of them. “A second class is almost nonexistent. That’s where I think our discovery is really important,” says Shukla. BX795, remember, prevents protein synthesis instead. Shukla is now testing it to see if BX795 offers broad protection against other related viruses like those causing chicken pox and mono.

I spent the weekends of 1979 bagging rock, and while I thought I was just really bored, I had mono.

 

‘It’s a super-cool study’ Salmonella took down the Aztecs

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Eye herpes is a real thing.

I got it in 1984.

Probably from my ex roomate’s towel.

I was so sick for two weeks, although I did manage to crawl out of bed for a Neil Young show in Toronto (part of the International Harvesters tour) but then felt so sick afterwards I went home to Brantford.

One of my parent’s neighbours was my evy doctor, so I was in for a regular check-up and he detected it immediately.

Put me on some Acyclovir, which had just come out, and I was cured in no time.

Or temporarily. Viruses don’t go away.

We’re all hosts on a viral planet.

Mine has come back, in the form of a cold sore, probably because of the stress of buying a new house in an over-heated real-estate market and not selling ours.
I went to the chemist, got some drugs that aren’t really working, but at least I had that option.

Imagine 600 years ago, when Cortez from Spain dances across the water to what is now Mexico and there’s no chemist down the road.

Ewen Callaway of Nature writes one of the worst epidemics in human history, a sixteenth-century pestilence that devastated Mexico’s native population, may have been caused by a deadly form of salmonella from Europe, a pair of studies suggest.

In one study, researchers say they have recovered DNA of the stomach bacterium from burials in Mexico linked to a 1540s epidemic that killed up to 80% of the country’s native inhabitants. The team reports its findings in a preprint posted on the bioRxiv server on 8 February.

This is potentially the first genetic evidence of the pathogen that caused the massive decline in native populations after European colonization, says Hannes Schroeder, an ancient-DNA researcher at the Natural History Museum of Denmark in Copenhagen who was not involved in the work. “It’s a super-cool study.”

In 1519, when forces led by Spanish conquistador Hernando Cortés arrived in Mexico, the native population was estimated at about 25 million. A century later, after a Spanish victory and a series of epidemics, numbers had plunged to around 1 million.

The largest of these disease outbreaks were known as cocoliztli (from the word for ‘pestilence’ in Nahuatl, the Aztec language). Two major cocoliztli, beginning in 1545 and 1576, killed an estimated 7 million to 18 million people living in Mexico’s highland regions.

“In the cities and large towns, big ditches were dug, and from morning to sunset the priests did nothing else but carry the dead bodies and throw them into the ditches,” noted a Franciscan historian who witnessed the 1576 outbreak.

There has been little consensus on the cause of cocoliztli — although measles, smallpox and typhus have all been mooted. In 2002, researchers at the National Autonomous University of Mexico (UNAM) in Mexico City proposed that a viral haemorrhagic fever, exacerbated by a catastrophic drought, was behind the carnage2. They compared the magnitude of the 1545 outbreak to that of the Black Death in fourteenth-century Europe. 

In an attempt to settle the question, a team led by evolutionary geneticist Johannes Krause at the Max Planck Institute for the Science of Human History in Jena, Germany, extracted and sequenced DNA from the teeth of 29 people buried in the Oaxacan highlands of southern Mexico. All but five were linked to a cocoliztli that researchers think ran from 1545 to 1550.

Ancient bacterial DNA recovered from several of the people matched that of Salmonella, based on comparisons with a database of more than 2,700 modern bacterial genomes.

Further sequencing of short, damaged DNA fragments from the remains allowed the team to reconstruct two genomes of a Salmonella enterica strain known as Paratyphi C. Today, this bacterium causes enteric fever, a typhus-like illness, that occurs mostly in developing countries. If left untreated, it kills 10–15% of infected people.

It’s perfectly reasonable that the bacterium could have caused this epidemic, says Schroeder. “They make a really good case.” But María Ávila-Arcos, an evolutionary geneticist at UNAM, isn’t convinced. She notes that some people suggest that a virus caused the cocoliztli, and that wouldn’t have been picked up by the team’s method.

Krause and his colleagues’ proposal is helped by another study posted on bioRxiv last week, which raises the possibility that Salmonella Paratyphi C arrived in Mexico from Europe.

A team led by Mark Achtman, a microbiologist at the University of Warwick in Coventry, UK, collected and sequenced the genome of the bacterial strain from the remains of a young woman buried around 1200 in a cemetery in Trondheim, Norway. It is the earliest evidence for the now-rare Salmonella strain, and proof that it was circulating in Europe, according to the study. (Both teams declined to comment on their research because their papers have been submitted to a peer-reviewed journal – good for them, dp).

“Really, what we’d like to do is look at both strains together,” says Hendrik Poinar, an evolutionary biologist at McMaster University in Hamilton, Canada. And if more ancient genomes can be collected from Europe and the Americas, it should be possible to find out more conclusively whether deadly pathogens such as Salmonella arrived in the New World from Europe.

Herpes for all in Australia: First the carp — THE CARP – now turtles

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Following an impassioned speech by Australian deputy PM Barnaby Joyce (right, not exactly as shown) on government plans to deliberately infect invasive carp with herpes, an increasing number of green sea turtles on barnaby.jonesAustralia’s Great Barrier Reef, with pollution being investigated as the prime culprit.

The animals have a turtle-specific herpesvirus that causes fibropapillomatosis – a condition in which disfiguring tumours grow on the eyes, flippers, tail, shell or internal organs.

“The tumours are benign but can grow up to 30 centimetres in size and block the turtles’ vision, says Karina Jones of James Cook University in Townsville, Australia. “This means they can’t find food or see predators or boats.”

Turtles with tumours are also more vulnerable to other infections, she says. “Severely affected turtles are quite skinny and have other pathogens affecting them – that’s why they die.”

The unpublished results of surveys by Jones’s team this year show that herpesvirus is most prevalent within a narrow stretch of Cockle Bay at Magnetic Island, a popular tourist destination in the middle of the reef. Roughly half the turtles in this hotspot have fibropapillomatosis, compared with less than 10 per cent of turtles sampled across the rest of Cockle Bay.

The cause remains unclear, but environmental contaminants are at the top of the suspect list. “We see these tumours in turtles in very localised hotspots around the world where there is heavy human activity,” says Jones.

Herpes, hepatitis A, swine flu — beer pong transmits disease?

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No beer pong? What is college life without beer pong?

Last year, some publication at the University of California at Los Angeles – UCLA – warned students that beer pong, a communal drinking game, could be a source of infectious disease like herpes.

The N.Y Times reports tomorrow that students at Rensselaer Polytechnic Institute in Troy, N.Y., are being asked to refrain from playing beer pong after an outbreak of illness that officials feared might be swine flu.

The story notes that what used to be O.K. is not anymore, as the flu has ushered in new standards of etiquette that can be, in turns, mundane, absurd and heartbreaking.

Heartbreaking and beer pong. College life is tragic.