Monthly Archives: October 2011

Molecular Virology

Discovery of an Ebola-like virus in Spain

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Fans of Richard Preston’s The Hot Zone will know Ebola virus and Marburg virus as ones that causes their victims to die a horrific death, bleeding from every opening and turning organs into a bloody pulpy mess. Ebola outbreaks occur sporadically in central and west Africa, and despite extensive efforts, its still not known where the virus comes from. The best evidence is that bats carry the virus, and contact with bats or bat excrement in caves sparks the outbreaks. Ebola RNA has been detected in bats, but no one has been able to find live virus in bats.

But now a close relative of Ebola and Marburg viruses has been discovered in bats in Spain. And unlike Ebola and Marburg, which don’t cause disease in bats, it is possible that this newly identified virus is killing the bats. A recent bat die off in Spain killed several bat colonies in a little more than a week. So researchers searched for viral sequences in the bats and identified an new filovirus, and called it Lloviu virus, after the cave in which it was found. They found the same viral sequence in other caves that experienced die offs, and could not find evidence of the virus in healthy bats.

This finding is significant for several reasons. It is the first detection of a naturally occurring filovirus outside of Africa and The Philippines. The bats in Spain do not overlap with the known geographic range of Ebola and Marburg viruses so its unlikely that it would have been picked up there. There have been bat die offs across parts of western Europe, and it will be interesting to see if Lloviu virus is found at all these locations.

Also, it might be making the bats sick. The key word being might. In my class called “Microbial Wars” we have discussed Koch’s postulates and hopefully my students will recognize that these are far from fulfilled. Live virus has not yet been isolated from diseased animals, only detection of the viral genetic material. Researchers will need to demonstrate that experimental inoculation of bats with live Lloviu virus will cause the expected disease.

Cueva de Lloviu is frequented by tourists, so its possible that many people have been exposed to the virus without ever developing disease. So this is not a human health concern but it is an important discovery that may help us understand filoviruses better, especially with respect to their ecology.

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Evolution, Molecular Virology

Taking control of the host to spread virus laden goo

Viruses are experts at hijacking cells to replicate, manipulating the conditions in the cell to optimize viral processes. But they manipulate their hosts on a higher level too, sometimes manipulating host behaviour to increase the chances of transmission. Take rabies virus for example: the virus induces aggression, then replicates abundantly in the salivary glands and stimulates salivation. The aggressive host is driven to bite, spreading the virus to its next host.

The basis for these bahavioural changes is poorly understood, on both the viral and host ends. However an experiment published in Science recently identifies the genetic basis for host behaviour manipulation by a baculovirus that infects the gypsy moth. When a baculovirus infects its host, the host eventually dies in a gruesome death appropriately called “virus melt.” The insect is liquefied, and the gooey, virus laden liquid drips down from the remains of the host on to the leaves below. Unsuspecting insects will then eat the contaminated leaves, becoming infected themselves.

So how could a virus maximize the dissemination of said liquid? How about having the host climb to the top of the plant and stay there to die, dripping all the liquid on the leaves below? The normal behaviour of the gypsy moth is to climb up a tree and munch on leaves during the night, and hide in crevices or climb down to the soil during the day, thus avoiding predation by birds. This behaviour is regulated by a hormone, 20-hydroxyecdysone, which tells the gypsy moth when to stop feeding and move down the tree (it also regulates molting and pupation). Baculovirus infected gypsy moths, however, climb up but don’t climb back down, staying up in the tree to die.

Baculoviruses expresses a gene that deactivates 20-hydroxyecdysone and prevents the infected host from leaving its “feeding state” and descending the tree. When researchers deleted the gene from the virus, the infected gypsy moths displayed normal behaviour.

I’d love to see a transmission experiment to see if the presence of this gene really helps with transmission to the next host.

(Also discussed on TWiV)

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Epidemics, Guest Blogger, Uncategorized

I Don’t Want Dengue Fever

When a student is absent from class, they usually send me an email to explain why. Occasionally I get emails from students in my microbiology or virology classes explaining their absence from class as a result of some infectious disease and they actually seem excited about the fact that they are hosting a virus. Perhaps they feel that they are participating in the class on a whole new level or are appreciating and understanding what is going on in their body, despite feeling awful. However, I was surprised recently when I mentioned Dengue Fever and a student piped up and said “I’ve had that!” I asked Caitlyn to write about her experience, and she kindly agreed. While she is interested in learning more about the virus, I suspect she would have preferred to learn about it without first hand experience. Here is her story.

Contributed by Caitlyn Anderson ’13

Photos of Angkor Wat in Siem Reap, Cambodia. Taken by Caitlyn Anderson.

“I was infected with Dengue virus in Cambodia during the summer of 2007 while working as an intern for the Clinton Foundation. I knew before going that there was a Dengue epidemic across the country but was unwilling to give up the opportunity. It is likely that I was bitten by a mosquito carrying the virus while I was sight seeing in Siem Reap towards the end of my stay. The virus incubated within my body for a period of approximately 5 days. Thankfully, I was back on U.S. soil when the virus began to present itself. I remember feeling slightly odd as I worked the night shift at Starbucks. After I returned home I immediately went to bed. In the morning I had developed flu like symptoms with a fever of 100 degrees. My body began to feel achy and I remained in bed throughout the afternoon. By 3:00 pm my temperature had reached 103 degrees and by 5:00 pm, my temperature was up to 104 degrees and I could barely move. My mother immediately called my pediatrician who then instructed us to go to the Emergency Room. I had immense difficulties walking from my bed on the second floor to the car. When we got to Norwalk Hospital in Connecticut, I was unable to walk and required the assistance of a wheel chair. The initial reaction of the emergency room doctor who saw to me first was that I was presenting with Lyme like symptoms. However, the unbearable pain caused by the insertion of the IV into my arm was not indicative of Lyme disease so I was immediately admitted to the hospital for further tests and supportive care. A few hours later my fever had reached 105 degrees and was coupled with the sudden onset of rash covering my entire body. The virus began to affect my nervous system causing extreme skin tenderness. Infectious disease specialists were brought in to evaluate my case. A Haitian doctor was immediately convinced I had Dengue Fever because she had witnessed the disease many times. Unsure of which of the four strains I had been infected with, the doctors could not predict the clinical evolution of the disease.
My fever remained between 103 and 105 degrees for 3 days. I was treated with fluid intravenously and pain medication for my body aches and severe skin sensitivity. My body was packed with ice in an effort to lower my body temperature. While Dengue Fever is commonly referred to as “breakbone fever” because people often feel as if there bones are being crushed, I did not experience this sensation. My skin, rather than my bones and joints, was the greatest cause of my discomfort. On day 4 of my hospital stay, my fever began to go down to 100 degrees but I was transitioned to the telemetry unit so that my heart could be monitored more closely. I continued to receive IV fluids and pain medication. I remained in the telemetry unit until day 6 when I was moved to a general ward where I remained until my release from the hospital on day 8. My fever had completely dissipated but I was very weak and had trouble walking. When I returned home I slept for 16 hours a day for about a week and was able to return to school a few days later with a reduced academic schedule. About a month later I regained my strength was symptom-free.”

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