TWiV 372: Latent viral tendencies

TWiVOn episode #372 of the science show This Week in Virology, the TWiV-osphere introduces influenza D virus, virus-like particles encoded in the wasp genome which protect its eggs from caterpillar immunity, and a cytomegalovirus protein which counters a host restriction protein that prevents establishment of latency.

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TWiV 234: Live in Denver

Episode #234 of the science show This Week in Virology was recorded before an audience at the 2013 General Meeting of the American Society for Microbiology in Denver, Colorado. Vincent and Kathy spoke with Nels Elde and Tom Shenk about their work on the evolution of virus-host conflict and how viruses influence the cell metabolome.

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TWiV 189: Five postdocs in Glasgow

On episode #189 of the science show This Week in Virology, Vincent returns to the Centre for Virus Research at the University of Glasgow and meets with postdocs to discuss their science and their careers.

You can find TWiV #189 at

TWiV 165: The email zone

T4 tatooHosts: Vincent Racaniello, Dickson DespommierRich Condit, and Alan Dove

Vincent, Dickson, Rich, and Alan answer listener questions about XMRV, cytomegalovirus, latency, shingles vaccine, myxomavirus and rabbits, and more.

Please help us by taking our listener survey.

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Weekly Science Picks

Dickson – Creation
Rich –
America’s Science Decline
AlanOut of context science
Vincent – The Scientist Top 10 Innovations 2011

Listener Pick of the Week

Jim – Christoph Adami: Finding life we can’t imagine (TED)
TimPatient Zero (Radiolab)
Mary – Natural Obsessions by Natalie Angier
Jimmy –
Science Exchange

Send your virology questions and comments (email or mp3 file) to, or call them in to 908-312-0760. You can also post articles that you would like us to discuss at and tag them with twiv.

TWiV 47: Vertical vaccine farm

twiv-200Hosts: Vincent Racaniello and Dick Despommier

On episode #47 of the podcast “This Week in Virology”, Vincent and Dick discuss influenza virus-like particle vaccines produced in insect and plant cells, rapid sharing of influenza research, and answer listener questions about cytomegalovirus, viral evolution and symbiosis and much more.

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Links for this episode:
A Farm on Every Floor
Influenza virus-like particles in insect and plant cells
PLoS Currents: Influenza
Transmission of 2009 H1N1 influenza virus to turkeys [Thanks Debbie!]
Baxter produces Vero cell H1N1 vaccine [Thanks Peter!]
Boundaries of Darwinism podcast [Thanks David!]
Phages in human intestine: papers onetwothree [Thanks Terry!]
Post-exposure varicella vaccine [Thanks Patricia!]
Open science movement hereherehere, and here [Thanks Jim!]
Graduate programs in virology [Thanks Greggory and Blake!]
Post-exposure Marburg and Ebola vaccines [Thanks John!]
Vaccinia infection in the laboratory [Thanks Russ!]
Animations of bacteriophage T4 life cycle [Thanks Jim!]

Weekly Science Picks
Vincent Bionumbers
Dick Ocean: An Illustrated Atlas by Sylvia A. Earle, Linda K. Glover

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TWiV 33: Live in Philly

twiv-200Episode 33 of the podcast “This Week in Virology” was recorded before an audience at the ASM General Meeting in Philadelphia. Vincent, Alan, Dick, and Raul Andino discussed increased arterial blood pressure caused by cytomegalovirus infection, restriction of influenza replication at low temperature by the avian viral glycoproteins, first isolation of West Nile virus in Pennsylvania, and current status of influenza.

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Persistent viral infections

persistence-of-memoryIn contrast to acute viral infections, persistent infections last for long periods, and occur when the primary infection is not cleared by the adaptive immune response. Varicella-zoster virus, measles virus, HIV-1, and human cytomegalovirus are examples of viruses that cause typical persistent infections. A chronic infection is a type of persistent infection that is eventually cleared, while latent or slow infections last the life of the host.

There is no single mechanism responsible for establishing a persistent infection; a key feature is reduction in host defenses and the ability of the virus to kill cells. Many arenaviruses, such as lymphocytic choriomeningitis virus, do not kill cells and will cause a persistent infection if the host cannot clear the virus. In some persistent viral infections there are alternate cycles of virion production and quiescence. An example is Epstein-Barr virus, the agent of infectious mononucleosis. After the initial bout of fever, sore throat, and swollen lymph glands, the virus establishes a dormant infection in which the viral genome persists in cells of the immune system. Periodically the infection is reactivated and infectious virions are shed in the absence of clinical symptoms. These reactivations lead to transmission of the infection to new hosts.

Bovine viral diarrhea virus infection is another example of how persistence is regulated by the interplay of the host immune response and viral cell killing. This virus establishes a lifelong persistent infection in most of the world’s cattle. The infected animals produce no detectable anti-viral antibody or T-cells. The virus is passed from the mother to fetus early in gestation. Infection does not stimulate the production of interferon (IFN), and therefore the adaptive immune system is not activated. Because infection does not kill cells, a persistent infection ensues.

Many infections persist because viral replication interferes with the function of cytotoxic T-lymphocytes (CTLs), immune cells that are extremely important for clearing viral infections. Infected cells are recognized when CTLs detect viral antigens on the cell surface. This recognition process requires presentation of the viral peptides by major histocompatibilty complex (MHC) class I proteins. Many viral proteins interfere with different steps of the MHC class I pathway, including the synthesis, processing, and trafficking of the protein. Even transport to the cell surface of viral peptides – produced from viral proteins by the large protein complex known as the proteasome – may be blocked.

An amazing example of such immune modulation occurs in cells infected with cytomegalovirus (CMV). This betaherpesvirus causes a common childhood infection of little consequence in healthy individuals. The infection is never cleared, and the virus persistently infects salivary and mammary glands and the kidney. When latently infected individuals are immunosuppressed by drugs or HIV infection, viral replication ensues with life-threatening consequences. CMV persists in the host because the viral genome encodes multiple proteins that interfere with MHC class I presentation of viral antigens. One viral protein blocks translocation of peptides into the lumen of the endoplasmic reticulum, while two other viral proteins cause degradation of MHC class I proteins before they reach the cell surface.

There are many more examples of how virus infections modulate the immune response, leading to persistent infection. Not surprisingly, many of the processing or regulatory steps that are targets of viral modulation were not even known until it was discovered that they were blocked by virus infection.

Peterhans, E. (2003). BVDV and innate immunity Biologicals, 31 (2), 107-112 DOI: 10.1016/S1045-1056(03)00024-1

Bornkamm, G. (2006). The infectious kiss: Newly infected B cells deliver Epstein-Barr virus to epithelial cells Proceedings of the National Academy of Sciences, 103 (19), 7201-7202 DOI: 10.1073/pnas.0602077103

WIERTZ, E. (1996). The Human Cytomegalovirus US11 Gene Product Dislocates MHC Class I Heavy Chains from the Endoplasmic Reticulum to the Cytosol Cell, 84 (5), 769-779 DOI: 10.1016/S0092-8674(00)81054-5