Archive for June, 2012

Seasonal Trivalent Inactivated Influenza Vaccine Protects against 1918 Spanish Influenza Virus Infection in Ferrets

8 June, 2012

See on Scoop.itVirology News

“The influenza virus H1N1 pandemic of 1918 was one of the worst medical catastrophes in human history. Recent studies have demonstrated that the hemagglutinin (HA) protein of the 1918 virus and 2009 H1N1 pandemic virus [A(H1N1)pdm09], the latter now a component of the seasonal trivalent inactivated influenza vaccine (TIV), share cross-reactive antigenic determinants. In this study, we demonstrate that immunization with the 2010-2011 seasonal TIV induces neutralizing antibodies that cross-react with the reconstructed 1918 pandemic virus in ferrets. TIV-immunized ferrets subsequently challenged with the 1918 virus displayed significant reductions in fever, weight loss, and virus shedding compared to these parameters in nonimmune control ferrets. Seasonal TIV was also effective in protecting against the lung infection and severe lung pathology associated with 1918 virus infection. Our data demonstrate that prior immunization with contemporary TIV provides cross-protection against the 1918 virus in ferrets. These findings suggest that exposure to A(H1N1)pdm09 through immunization may provide protection against the reconstructed 1918 virus which, as a select agent, is considered to pose both biosafety and biosecurity threats.”

 

So, all you doomsayers – and yes, NSABB, I’m talkin’ to YOU – as expected by some, the resurrected Spanish Flu virus is NOT going to be an all-conquering scourge that depopulates the planet if it gets out.  Basically, anyone who has either had the H1N12009pdm or the modern vaccine, is almost certainly protected against the old virus.

 

Graphic courtesy of Russell Kightley Media

See on jvi.asm.org

Adam Baker – Zombie Apocalypse Survival.

6 June, 2012

See on Scoop.itVirology News

Adam Baker, author of Outpost and Juggernaut, shares a few survival tips for surviving the zombie apocalypse.

 

I thought I’d include this useful little “how to survive” video, seeing as engineered rabies viruses and whatnot will shortly precipitate the Viral Zombie Apocalypse…B-)

See on www.youtube.com

Differential assembly of Hepatitis B Virus core protein on single- and double-stranded nucleic acid suggest the dsDNA-filled core is spring-loaded

5 June, 2012

See on Scoop.itVirology and Bioinformatics from Virology.ca

“Hepatitis B Virus (HBV) cores assemble on viral RNA, which is reverse transcribed within the core to the partially dsDNA genome of mature HBV. However, constraining dsDNA, a stiff polymer, within a core necessarily requires far greater capsid stability than constraining ssRNA. We hypothesized that, unlike ssRNA, dsDNA would be a poor substrate for assembly. We examined titrations of ssDNA and dsDNA with purified HBV core protein, Cp183, by EMSA, EM, DLS, and etheno-DNA fluorescence. Cp183 bound ssDNA with high affinity to form virus-like capsids. However, Cp183 bound dsDNA poorly, forming a mixture of irregular complexes. Nonetheless, we observed some normal cores in dsDNA assembly reactions, indicating that the energy required to bend DNA could be similar to the protein–protein association energy. This similarity of energies suggests that dsDNA stresses mature HBV cores, in agreement with calculation, which may be the basis for the virus maturation signal and DNA release.”

 

A great paper – and one which harks back to an age where many studies on viruses were biophysical, because the molecular biological techniques we use now had simply not been invented.  I note frequent reference to Bancroft, 1970 – to a paper on self-assembly of plant viruses.  I also like the concept of HBV cores as a Jack-in-a-box: ready to pop open to deliver the goodies.

See on www.sciencedirect.com

Endogenous RNA viruses of plants in insect genomes

5 June, 2012

See on Scoop.itVirology News

“Endogenous viral elements (EVEs) derived from RNA viruses with no DNA stage are rare, especially those where the parental viruses possess single-strand positive-sense (ssRNA +) genomes. Here we provide evidence that EVEs that share a sequence similarity to ssRNA + viruses of plants are integrated into the genomes of a number of insects, including mosquito, fruit flies, bees, ant, silkworm, pea aphid, Monarch butterfly, and wasps. A preliminary phylogenetic analysis places these EVEs as divergent relatives of the Virgaviridae and three currently unclassified plant viral species.”

I have covered this before, in ViroBlogy, (and here, in 2007)as an interesting and probably under-appreciated phenomenon.  I note Eddie Holmes and colleagues have now taken it much, much further – which incidentally lends significant credence to my supposition that virus/vector/plant coevolution was probably a fair bit more intimate than has been supposed, with the newly-emerged (in evolutionary terms) insects and their viruses meeting terrestrial plants and THEIR viruses.  And mixing everything up, as I have speculated elsewhere (Origins of Viruses).

I thank Jean-Marie Verchot for drawing my attention to this!

See on www.sciencedirect.com

Narcolepsy traced to specific [flu] vaccine batches

4 June, 2012

See on Scoop.itVirology News

“A new Swedish study shows that all Swedes who developed narcolepsy from the swine flu vaccine Pandemrix received the vaccine from 12 of the 35 batches, despite the claim by the responsible agency that no such connection exists.”

There are some slightly disturbing connections between the H1N1 2009 pdm virus and narcolepsy: the virus itself seems to have caused narcolepsy in some of those infected; now a vaccine is implicated – is this an innate property of certain of the virus proteins, possibly?

See on www.thelocal.se

PLoS Pathogens: Evolutionary Reconstructions of the Transferrin Receptor of Caniforms Supports Canine Parvovirus Being a Re-emerged and Not a Novel Pathogen in Dogs

3 June, 2012

See on Scoop.itVirology News

“Parvoviruses exploit transferrin receptor type-1 (TfR) for cellular entry in carnivores, and specific interactions are key to control of host range. We show that several key mutations acquired by TfR during the evolution of Caniforms (dogs and related species) modified the interactions with parvovirus capsids by reducing the level of binding. These data, along with signatures of positive selection in the TFRC gene, are consistent with an evolutionary arms race between the TfR of the Caniform clade and parvoviruses. As well as the modifications of amino acid sequence which modify binding, we found that a glycosylation site mutation in the TfR of dogs which provided resistance to the carnivore parvoviruses which were in circulation prior to about 1975 predates the speciation of coyotes and dogs. Because the closely-related black-backed jackal has a TfR similar to their common ancestor and lacks the glycosylation site, reconstructing this mutation into the jackal TfR shows the potency of that site in blocking binding and infection and explains the resistance of dogs until recent times. This alters our understanding of this well-known example of viral emergence by indicating that canine parvovirus emergence likely resulted from the re-adaptation of a parvovirus to the resistant receptor of a former host.”

 

Nice to see Colin Parrish is still working on canine parvoviruses: I remember playing a Nintendo game with him in Ithaca, NY in 1991, and talking about viruses….

It is interesting that the arms race between virus and host can revive, as it has in this case: for the canine lineage to have lost susceptibility to parvovirus, and then have the virus regain the ability to infect is an excellent example of how host-pathogen interactions can change.

See on www.plospathogens.org

Genome and proteome analysis of 7-7-1, a flagellotropic phage infecting Agrobacterium sp H13-3

1 June, 2012

See on Scoop.itVirology and Bioinformatics from Virology.ca

“The flagellotropic phage 7-7-1 infects motile cells of Agrobacterium sp H13-3 by attaching to and traveling along the rotating flagellar filament to the secondary receptor at the base, where it injects its DNA into the host cell.”

 

This is an interesting paper, because it describes a phage infecting Agrobacterium – and touches on a subject that has intrigued me for years, which is: How does a phage which attaches to a flagellum, get its genome inside the cell?  This throws some mud onto a previous model, which suggested a passive mode of transport like a well-oiled nut moving towards the head of a bolt, as in this case that would result in transport the other way.  Expectr more on this topic!

 

Image sourced from the paper

See on www.virologyj.com

What Do Human Parasites Do with a Chloroplast Anyway?

1 June, 2012

See on Scoop.itVirology News

“Apicomplexans are an important group of pathogens that include the causative agents of malaria, toxoplasmosis, and cryptosporidiosis. These single-celled eukaryotic parasites evolved from photosynthetic algae. A remnant chloroplast, called the apicoplast, is a telltale hold-over from this more benign past in the ocean. 1The apicoplast is essential for parasite growth and development and therefore a potential target for drug therapy. The fact that humans and animals lack chloroplasts suggests that using approaches to target the apicoplast may provide parasite specificity. What are the critical functions of the apicoplast that should be targeted? In addition to the obvious medical relevance this question has broader biological implications. Why do organisms maintain an ancient symbiotic relationship when the initial rationale for this relationship has fallen by the evolutionary wayside? A new study by Yeh and DeRisi provides important clues. Their work demonstrates that antibiotic-induced loss of the apicoplast in cultured malaria parasites can be chemically rescued by providing isopentenyl-pyrophosphate (IPP) in the medium. IPP is generated by the apicoplast resident isoprenoid biosynthesis pathway and is apparently the one apicoplast metabolite that the parasite cannot live without in the red blood cell. This finding could be of great importance for the development of drugs and vaccines. The ability to produce and maintain parasite lines that lack the apicoplast also offers exciting experimental possibilities for the future.”

 

Great review – and malaria is important enough to be considered an honorary virus (B-), so it is appropriate to cover it here.  The review also illustrates yet another aspect of the fascinating evolutionary propensity for eukaryotic algae, themsleves the result of endosymbiosis between a photosynthetic prokaryote and a eukaryote, for themselves becoming endosymbionts.

See on www.plosbiology.org