TWiV 447: Un-impacting an elephant

The glorious TWiVerati un-impact their email backlog, anwering questions about viruses, viruses, viruses, viruses, viruses, and more. You should listen – our fans ask great questions!

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TWiV 446: Old sins die hard

The TWiV hosts review an analysis of gender parity trends at virology conferences, and the origin and unusual pathogenesis of the 1918 pandemic H1N1 influenza virus.

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The first human virus discovered

PlaqueOn the wall of a Columbia University Medical Center building just across the street from my laboratory is a plaque commemorating two participants in the discovery of a mosquito vector for yellow fever virus.

The plaque reads:

Aristides Agramonte, Jesse William Lazear, Graduates of the Columbia University College of Physicians and Surgeons, class of 1892. Acting Assistant Surgeons, U.S. Army. Members of the USA Yellow Fever Commission with Drs. Walter Reed and James Carroll. Through devotion and self-sacrifice they helped to eradicate a pestilence of man.

Yellow fever, known in tropical countries since the 15th century, was responsible for devastating epidemics associated with high rates of mortality. The disease can be mild, with symptoms that include fever and nausea, but more severe cases are accompanied by major organ failure. The name of the illness is derived from yellowing of the skin (jaundice) caused by destruction of the liver. For most of its history, little was known about how yellow fever was spread, although it was clear that the disease was not transferred directly from person to person.

Cuban physician Carlos Juan Finlay proposed in 1880 that a bloodsucking insect, probably a mosquito, was involved in yellow fever transmission. The United States Army Yellow Fever Commission was formed in 1899 to study the disease, in part because of its high incidence among soldiers occupying Cuba. Also known as the Reed Commission, it comprised four infectious disease specialists: U.S. Army Colonel Walter Reed (who was the chair); Columbia graduates Lazear and Agramonte, and James Carroll. Lazear confirmed Finlay’s hypothesis in 1900 when he acquired yellow fever after being experimentally  bitten by mosquitos who had fed on sick patients. Days later, he died of the disease.

The results of the Reed Commission’s study proved conclusively that mosquitoes are the vectors for this disease. Aggressive mosquito control in Cuba led to a drastic decline in cases by 1902.

The nature of the yellow fever agent was established in 1901, when Reed and Carroll injected filtered serum from the blood of a yellow fever patient into three healthy individuals. Two of the volunteers developed yellow fever, causing Reed and Carroll to conclude that a “filterable agent,” which we now know as yellow fever virus, was the cause of the disease.

Sometimes you don’t have to wander far to find some virology history.

Update 6/16/17: The statement on the plaque that Agramonte and Lazear “helped to eradicate a pestilence of man” is of course incorrect, as yellow fever has never been eradicated. Recent large outbreaks of yellow fever in Brazil and Angola are examples of the continuing threat the virus poses, despite the availability of a vaccine since 1938.

TWiV 445: A nido virology meeting

From Nido2017 in Kansas City, Vincent  meets up with three virologists to talk about their careers and their work on nidoviruses.

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TWiV 444: Astro Kate, The Right Stuff

From ASM Microbe 2017 at New Orleans, Vincent and Rich meet up with Kate Rubins to talk about becoming an astronaut, space travel, and doing science in space.

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A conversation with Islam Hussein of Virolvlog

From ASM Microbe 2017 in New Orleans, I speak with Islam Hussein about his science career, how he became interested in science communication, and his video blog in Arabic, Virolvlog.

Virolvlog meets TWiV

Islam Hussein of Virolvlog interviews me about my career in virology and my interests in communicating science, at ASM’s Microbe 2017 in New Orleans.

TWiV 443: On a leaf, no one can hear you scream

The TWiVsters reveal the puppet master: an RNA virus injected with wasp eggs that paralyzes the ladybug so that she protects the cocoon until the adult emerges.

You can find TWiV #443 at microbe.tv/twiv, or listen below.

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Bodyguard manipulation by a virus

Coccinella septempunctata with Dinocampus coccinellae cocoonHost behavior alteration by viruses is known to assist the development of another organism. An example is a parasitoid wasp that injects viruses along with eggs into a caterpillar. The viral genomes encode proteins that subvert the caterpillar immune response, allowing the wasp larva to develop. A similar strategy may enable safe development of a wasp by a ladybeetle.

The parasitoid wasp D. coccinellae lays its eggs inside a ladybeetle. After 20 days of larval development, a prepupa emerges from the ladybeetle and fabricates a cocoon between the beetle’s legs. At the same time, the ladybeetle becomes paralyzed. It remains on top of the cocoon (pictured; image credit), protecting it until an adult wasp emerges. Remarkably, some ladybeetles then resume their normal lives!

Given what we know about how parasitoid viruses can alter the manipulation of their hosts, it was only logical to search for a virus that paralyzes the ladybeetle. Sequencing of RNA from the heads of parasitized ladybeetles revealed the presence of an RNA virus which the authors call D. coccinellae paralysis virus, DcPV. The virus is a new member of a Iflaviruses, a family of picornavirus-like, (+) strand RNA viruses that infect insects. DcPV was found in wasps in Poland, Japan, and The Netherlands, confirming its cosmopolitain nature.

Viral particles were observed in cells lining the wasp oviducts, but not in the lumen. Viral genomes were undetectable in wasp eggs, became more abundant during hatching, and ceased to replicate in adult wasps. The levels of virus in the ladybeetle abdomen and head increase with time to egress, suggesting that it was transmitted from the wasp larvae to the host. In ladybeetles where the wasp egg did not develop, viral replication does not occur.

DcPV appears to be neurotropic. Before larval egression, no changes were observed in the nervous system of the ladybeetle, but glial cells were full of virus particles. After egression, vaculoles developed in glial cells and neurons degenerated. This damage was less severe in beetles that survived and recovered from paralysis. An expansion of glial cells in these hosts might explain how normal brain functions were restored.

Insects respond to infection with an RNA-based antiviral response. Components of the RNA based immune system were down-regulated during larval development, possibly by viral proteins, allowing virus to invade the nervous system. Resumption of the antiviral reponse might enable recovery of the ladybeetle after emergence of the wasp.

It appears that DcPV is a wasp symbiont that manipulates the behavior of the ladybeetle host to ensure development of wasp offspring. This hypothesis can be tested by removing DcPV from infected wasps, or by adding DCpV to uninfected hosts, and determining the effect on larval development.

We now realize that animals are actually holobionts: an aggregate of eukaryotes, bacteria, and viruses. Therefore host-parasite interactions are really holobiont-holobiont interactions.

TWiV 442: The New York Tim

Freelance science journalist Tim Requarth joins the TWiVers to explain why scientists should stop thinking that explaining science will fix  information illiteracy.

 

You can find TWiV #442 at microbe.tv/twiv, or listen below.

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