Field of Science

A bat virus that can't fight your immune system

I have been too busy to go into this in much detail but I'm wondering whether anyone had any ideas as to why this virus (cedar virus - a newly discovered bat RNA virus) appears not to be able to combat the human innate immune system, specifically: HeLa cell secretion of beta interferon in cell culture.

 1) is this real?

2) does a virus have to be able to combat this part of the immune system?

3) why use a human  cell culture to study a bat virus? and finally,

 4) what does this mean for the virus in a bat?

Cedar Virus: A Novel Henipavirus Isolated from Australian Bats


The genus Henipavirus in the family Paramyxoviridae contains two viruses, Hendra virus (HeV) and Nipah virus (NiV) for which pteropid bats act as the main natural reservoir. Each virus also causes serious and commonly lethal infection of people as well as various species of domestic animals, however little is known about the associated mechanisms of pathogenesis. Here, we report the isolation and characterization of a new paramyxovirus from pteropid bats, Cedar virus (CedPV), which shares significant features with the known henipaviruses. The genome size (18,162 nt) and organization of CedPV is very similar to that of HeV and NiV; its nucleocapsid protein displays antigenic cross-reactivity with henipaviruses; and it uses the same receptor molecule (ephrin- B2) for entry during infection. Preliminary challenge studies with CedPV in ferrets and guinea pigs, both susceptible to infection and disease with known henipaviruses, confirmed virus replication and production of neutralizing antibodies although clinical disease was not observed. In this context, it is interesting to note that the major genetic difference between CedPV and HeV or NiV lies within the coding strategy of the P gene, which is known to play an important role in evading the host innate immune system. Unlike HeV, NiV, and almost all known paramyxoviruses, the CedPV P gene lacks both RNA editing and also the coding capacity for the highly conserved V protein. Preliminary study indicated that CedPV infection of human cells induces a more robust IFN-β response than HeV.

Schmallenberg virus hits Europe again but should we be worried?

Lambs, don't worry. I's not all that bad.

I wrote back in February this year (2012) of a worrying outbreak of disease spreading across North-Western Europe, starting in Germany and ending up in the UK and even Spain and Italy.

The disease, manifesting itself in the Spring lambing/calving season, as fetal deformaties in these ruminants (also now alpacas). Many of which lead to the death of the newborn animal. It was quickly uncovered that this illness was caused by a previously unheard-of virus (an orthobunyavirus if you wanna know) now named after the town it was sampled from: Schmallenberg.

To date, no cases of human infection have been reported. And currently, cases have severely decreased as we leaving lambing/calving season.

Back seven months ago we really didn't know an awful lot about this emerging virus apart from that it looked not much like anything we had seen before. We didn't know how it got to Europe, we didn't know if it was going to stay here and we didn't know what to do about it. It was predicted that the virus was spread by midge flies living across Europe during the summer of 2011, the animals exhibiting a flu-like illness that barely registered with farmers. But when it came to the spring and the then newly pregnant sheep or cows gave birth, it soon became evident what damage the virus had done in this group of individuals.

What has happened since the Spring?

The months following this initial characterisation was a worrying one but scientifically really interesting:

I wrote in May that we had discovered where the virus had come from. A Japanese group had sequenced a load of new viruses that were cousins on Schmallenberg. One of the reasons we didn't know where the virus originated was due to really not knowing much about the genetic diversity of the orthobunyaviruses.

Bunyavirus - segmented genome. Is Schmallenberg composed of  segments from different viruses?

They then compared their sequences with the German isolate from back in early 2010. It became quickly obvious that parts of the viruses segmented genome came from different viruses and was hence a 'recombinant'. Recombining - or joining - together 3 fragments from two different kinds of viruses. But now with further increased sampling of orthobunyavirus genomes, Schmallenberg appears to be firmly rooted in one particular viral group while another virus cousin seems to be a recombinant.

A couple of months later, a Danish group showed that they could detect Schmallenberg virus RNA in one particular group of midges: Cullicoides obsoletos in Autumn 2011, when the virus was spreading across Europe, including Denmark.  

Culicoides sp. Reported vector for Schmallenberg virus.

Europe's stance downgraded but is it still here?

But Defra reported in June that the lack of seriousness of Schmallenberg virus had caused them to downgrade their view on the disease after only 0.002% of the susceptible ruminant population was affected. And those that were infected caused little negative impact to the farming.
SBV is no longer considered an emerging disease and therefore affected Member
States will no longer be reporting to the OIE on a regular basis. It was agreed at the
OIE 80th General Session that the disease is low impact with no public health risk
and negligible risk posed by commodities such as meat, milk, semen and embryos.
Thankfully European Food Safety Authority (EFSA) earmarked a 3 millions Euros for researchers to look into the biology of how Schmallenberg virus infects and causes disease in animals. Although nothing ear-marked for vaccine research. But despite this downgrading, the virus is in the news again when scientists at the UK Institute for Animal Health report (although there's no paper available) that they are still seeing new evidence of infection in cows in one of their farms when they look for antibodies.  The evidence has not been repeated in mainland Europe.

The UK guys take this as evidence that the virus survived the winter in the UK midges and is beginning to spread across the country. Although I'm not sure how much this could be explained by some animals mounting a slower response to the virus from the season before that. But maybe a year is too long for this.

Depending on midge dynamics across the country, which is itself dependent on weather and temperature etc (midges don't like the cold and the rain). The extent of the virus spreading and infecting new animals may be blocked by some animals having already mounted an immune response against it from last year and could be protected. You could  predict that this could drive the virus into areas that were not affected a year ago.

OK - it might be here, but calm down.

But as Defra and the EFSA stress, this virus poses no risk to humans and has only - to date - had a small  effect on European farming industry. It is no bluetongue disease however, I'm sure it's distressing for the individual farmers and it could have a relatively large effect on single farms that have been heavily affected. But in general,  even if this virus does return this summer (and we see its effects next Spring) hindsight has shown us that we shouldn't be as worried as we were 6 month ago.

Who cares about ebola?

Allow me to play the Devil's advocate:

Ebola has struck again in Uganda, and to date, at least 15 people have died from it and a further 32 are in isolation in the country. This is the most recent outbreak in what appears to be an annual occurrence in Central Africa. What I'd like to know is: why do we care?

Numbers of African outbreaks since 1976 to 2012, based on CDC records. 

The African strains at least, of Ebola are probably not as fatal in humans as reported (see Vincent Racaniellos take here), as a disease it doesn't really effect all that many people and I think Africa has a lot more pressing public health issues than really worrying about a virus like this one - malaria, vaccination campaigns and malnutrition.

The ebola belt traces the area of rain/deciduous forest covering Central Africa from the Cote d'Ivore in the West to Uganda and South Sudan in the East. Somewhere inside that forest lies in wait, Ebola. 

Currently a lot of research is being carried out on Ebola and related viruses and we are making excellent progress in understanding how the virus infects and replicates in our cells but also how our body responds to it and how this leads to the fatal, often haemorrhagic, fever that is ebola.We are even beginning to understand how this virus, a virus of fruit bats, can spill over into other animal populations nearby, like primates and us. 

All this information could help lead to the development of antiviral molecules or even an ebola vaccine or even a potential preventative measure based on some sort of control of host species.

But are there more useful things for us to spend our money on? Which of the above areas of research would be the most cost effective and successful? Is research on ebola pursued on the back of a potential bioterrorism concern rather than on public health thinking?

Why should we care about ebola? Answers on a postcare below.