TWiV 370: Ten out of 15

On episode #370 of the science show This Week in Virology, the TWiVomics review ten captivating virology stories from 2015.

You can find TWiV #370 at

TWiV 361: Zombie viruses on the loose

On episode #361 of the science show This Week in Virology, the TWiVsters discuss Frederick Novy’s return from retirement to recover a lost rat virus, and evidence for persistence of Ebolavirus in semen.

You can find TWiV #361 at

Sushi protects mosquitoes from lethal virus infections

mosquito brainAs far as I know, mosquitoes do not eat sushi. But mosquito cells have proteins with sushi repeat domains, and these proteins protect the brain from lethal virus infections.

Mosquitoes are vectors for the transmission of many human viral diseases, including yellow fever, West Nile disease, Japanese encephalitis, and dengue hemorrhagic fever. Many mosquito-borne viruses enter the human central nervous system and cause neurological disease. In contrast, these viruses replicate in many tissues of the mosquito, including the central nervous system, with little pathological effect and no alteration of behavior or lifespan. The defenses that allow such persistent infection of mosquitoes are slowly being unraveled.

A protein called Hikaru genki, or Hig, is crucial for controlling viral infections of the mosquito brain. Originally discovered in the fruit fly Drosophila, Hig is produced mainly in the brain of Aedes aegyptii, the natural vector for dengue and yellow fever viruses. Experimental reduction of Hig mRNA or protein in the mosquito leads to increased replication of dengue virus and Japanese encephalitis virus. This increase in viral replication is accompanied by more cell death in the mosquito brain, and decreased survival.

How does Hig protein impair virus replication? The Hig protein of A. aegyptii binds dengue virus particles via the E membrane glycoprotein. As Hig protein is located on the cell surface, binding to virus particles prevents virus entry into cells. Impairment of endocytosis is limited to insect cells – introduction of Hig into mammalian cells had no effect on virus replication. Clearly other components of insect cells must participate in the Hig-mediated antiviral mechanism.

The antiviral activity of Hig protein depends on the presence of sushi repeat domains, also known as complement control protein (CCP) domains. These consist of 60 amino acid repeats with four conserved cysteines and a tryptophan. The CCP domain is found in many proteins of the complement system, a collection of blood and cell surface proteins that is a major primary defense and a clearance component of innate and adaptive immune responses. The sushi domain mediates protein-protein interactions among complement components. Capturing the dengue and Japanese encephalitis viruses by the A. aegyptii Hig protein is just one example of the virus-binding ability of proteins with CCP domains. An insect scavenger receptor with two CCP domains is a pattern recognition receptor that recognizes dengue virus and recruits mosquito complement to limit viral replication. Some CCP containing proteins are virus receptors (complement receptor 2 binds Epstein-Barr virus, and membrane cofactor protein is a receptor tor measles virus).

Because the Hig antiviral machinery is largely limited to the mosquito brain, it is possible that it prolongs mosquito life to allow virus transmission to other hosts. Transmission of virus to other hosts requires replication in the salivary gland, which cannot take if the mosquito dies of neural infection. I wonder why humans do not have have similar mechanisms to protect their neural tissues from virus infections. Is neuroinvasion a less frequent event in humans, compared with mosquitoes, thereby providing less selective pressure for protective mechanisms to evolve?

TWiV 301: Marine viruses and insect defense

On episode #301 of the science show This Week in Virology, Vincent travels to the International Congress of Virology in Montreal and speaks with Carla Saleh and Curtis Suttle about their work on RNA interference and antiviral defense in fruit flies, and viruses in the sea, the greatest biodiversity on Earth.

You can find TWiV #301 at

Virology lecture #16: Persistent infections

Download: .wmv (331 MB) | .mp4 (68 MB)

Presented by guest lecturer Saul Silverstein, Ph.D.

Visit the virology W3310 home page for a complete list of course resources.

TWiV 62: Persistence of West Nile virus

The_Persistence_of_MemoryHosts: Vincent Racaniello, Dickson Despommier, and Alan Dove

On episode #62 of the podcast This Week in Virology, Vincent, Dickson, and Alan discuss STEP HIV-1 vaccine failure caused by the adenovirus vector, presence of West Nile virus in kidneys for years after initial infection, adaptation of the influenza viral RNA polymerase for replication in human cells, and the significance of the D225G change in the influenza HA protein.

Click the arrow above to play, or right-click to download TWiV #62 (47 MB .mp3, 66 minutes)

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Links for this episode:

Weekly Science Picks
Dick Smallpox – The Death of a Disease by DA Henderson
Alan Olympus Bioscapes Digital Imaging Competition
Vincent Microbe Magazine

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