Archive for April, 2016

Protection of Cattle against Rinderpest by Vaccination with Wild-Type Peste des Petits Ruminants Virus

30 April, 2016

Although rinderpest virus (RPV) has been eradicated in the wild, efforts are still continuing to restrict the extent to which live virus is distributed in facilities around the world and to prepare for any reappearance of the disease, whether through deliberate or accidental release. In an effort to find an alternative vaccine which could be used in place of the traditional live attenuated RPV strains, we have determined whether cattle can be protected from rinderpest by inoculation with vaccine strains of the related morbillivirus, peste des petits ruminants virus (PPRV). Cattle were vaccinated with wild-type PPRV or either of two established PPRV vaccine strains, Nigeria/75/1 or Sungri/96. All animals developed antibody and T cell immune responses to the inoculated PPRV. However, only the animals given wild-type PPRV were protected from RPV challenge. Animals given PPRV/Sungri/96 were only partially protected, and animals given PPRV/Nigeria/75/1 showed no protection against RPV challenge. While sera from animals vaccinated with the vaccine strain of RPV showed cross-neutralizing ability against PPRV, none of the sera from animals vaccinated with any strain of PPRV was able to neutralize RPV although sera from animals inoculated with wild-type PPRV were able to neutralize RPV-pseudotyped vesicular stomatitis virus.

Sourced through Scoop.it from: jvi.asm.org

I have written before in ViroBlogy about the eradication of rinderpest, and what a big deal that was – and here are people taking the gloomy view of wanting to have vaccines against it in case it gets used as a bioweapon, or escapes from fridges or freezers somewhere.

Not that these concerns aren’t valid – but surely it would be a better idea to use recombinant viruses expressing rinderpest envelope glycoproteins, rather than another live virus related to rinderpest which needs to be eradicated itself?
Just asking – but a recombinant poxvirus would seem to me to be a MUCH better option!

See on Scoop.it – Virology News

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Dengue Virus Antibodies Enhance Zika Virus Infection

26 April, 2016

We tested the neutralizing and enhancing potential of well-characterized broadly neutralizing human anti-DENV monoclonal antibodies (HMAbs) and human DENV immune sera against ZIKV using neutralization and ADE assays. We show that anti-DENV HMAbs, cross-react, do not neutralize, and greatly enhance ZIKV infection in vitro. DENV immune sera had varying degrees of neutralization against ZIKV and similarly enhanced ZIKV infection. 

Conclusions / Significance 

Our results suggest that pre-existing DENV immunity will enhance ZIKV infection in vivo and may increase disease severity. A clear understanding of the interplay between ZIKV and DENV will be critical in informing public health responses in regions where these viruses co-circulate and will be particularly valuable for ZIKV and DENV vaccine design and implementation strategies.

Zika virus graphic from Russell Kightley Media

Sourced through Scoop.it from: biorxiv.org

This is a big deal: a really big deal.  While people have been speculating around the issue for months now – yes, you, Neil Bodie! – this prepub appears to provide proof that prior immunity to the related dengue virus(es) may enhance Zika virus infection, without neutralising infectivity.  This is termed “antibody-dependent enhancement” (ADE), and is also a major factor in dengue haemorrhagic fever which results from ADE due to reinfection with a different dengue type.

It is also interesting because this is one of the first high-profile uses of the online preprint archive bioRxiv (STUPID name!) for a virology paper – which may open the floodgates, as people see what a good idea it potentially is.
The possibility that ADE exacerbates Zika infection means that the manifestations of Zika may be very different depending upon the seroprevalence of dengue and possibly yellow fever virus antibodies in the target population: where this is very low – as in the USA or Europe – there may be no real problem.  Where the seroprevalences are high – as is the case in Brazil and much of Central America – Zika infections may be much more severe.
We will wait and see.

See on Scoop.it – Virology News

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New Zika Mouse Model Mimics Human Disease

6 April, 2016

Researchers develop another mouse model of Zika virus infection that mimics the disease in humans.

Sourced through Scoop.it from: www.the-scientist.com

…and strains from Africa, Polynesia and Asia were used in it – and all did the same thing?  Interesting…meaning there is no clear differentiation between “original” (=older) African strains and more recent incarnations?  Meaning, obviously, that background immunity due to endemicity will probably prevent the nastiness seen in adult infections in S America?  Possibly…watch this space!

See on Scoop.it – IDM News

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