MicrobiologyBytes

First it was foot and mouth virus.
Then it was bluetongue virus.
Now it is Schmallenberg virus.
So here’s 10 things you didn’t know about Schmallenberg virus:

1. Schmallenberg virus was first isolated in Schmallenberg, Germany, in November 2011.
2. Schmallenberg virus is a Bunyavirus, one of a large group of of negative-stranded RNA viruses.
3. Why should I care? In cows, Schmallenberg virus causes fever and a drastic reduction in milk production. In sheep it causes congenital malformations and stillborn lambs (also stillborn calves in cows).
4. Schmallenberg virus was first identifed in the UK on 23rd January 2012.
5. Like Bluetongue, Schmallenberg virus is transmitted by midges (Culicoides spp.), which means we will be unlikely to be able to eradicate it – vaccination of anaimals is the only likely effective response.
6. Where did Schmallenberg virus come from? The virus genome is most closely related to sequences of a different Orthobunyavirus called Shamonda virus which belongs to the so-called Simbu serogroup known to infect ruminants and be transmitted by midges. In other words, it has form. But whether it is newly evolved (unlikely) or just newly discovered we don’t yet know.
7. How did Schmallenberg virus reach the UK? We don’t know. It could have been due to animal movements, but since it was first identifed in eastern England, it’s possible that it arrived in midges travelling under their own steam.
8. Is Schmallenberg virus going to spread to other parts of the UK and other countries? Yes, you can bet on that (just like bluetongue did).
9. Can I catch Schmallenberg virus? Honest answer: We don’t know. Possibly, but there have been no reports of human illness from areas where the virus is known to exist, so I wouldn’t worry too much.
10. Where can I find the latest news about Schmallenberg virus? Right here.
11. OK, one last time, why should I care? Because Schmallenberg virus is going to cost European and probably worldwide ecomonies millions of pounds. And that will affect you.

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Among the negative RNA viruses, ambisense RNA viruses occupy a distinct niche. Ambisense viruses contain at least one ambisense RNA segment, i.e. an RNA that is in part of positive and in part of negative polarity. Because of this unique gene organization, one might expect ambisense RNA viruses to borrow expression strategies from both positive and negative RNA viruses. However, they have little in common with positive RNA viruses, but possess many features of negative RNA viruses. Transcription and/or replication of their RNAs appear generally to be coupled to translation. Such coupling might be important to ensure temporal control of gene expression, allowing the two genes of an ambisense RNA segment to be differently regulated. Ambisense viruses can infect one host asymptomatically and in certain cases, they can lethally infect two hosts of a different kingdom. A possible model to explain the differential behavior of a given virus in different hosts could be that perturbation of the translation machinery would lead to differences in the severity of symptoms.

The ambisense coding strategy is an unusual way of encoding genes that presumably allows the virus to temporally control expression of the viral proteins, in particular if coupling of translation to transcription enhances the level of vc-encoded versus v-encoded protein expression. In any event, translation itself and/or translational control appear to play an important role in regulation of gene expression of ambisense viruses. Ambisense viruses have two hosts in which they can replicate. In their vector or reservoir host, infection is usually asymptomatic. However, in another host, multiplication of the virus can be lethal. Replication/transcription experiments in different host cell types would be helpful to shed further light on the differences observed in different hosts. At present, there are many complementary ways to study ambisense virus replication/ transcription such as cell culture, in vitro assays and reverse genetics systems. Since ambisense viruses are the meeting point of different viral families and are able to replicate in different hosts whether plants or animals and have different behaviors depending on the host, it would be particularly important to better understand the complex replicative cycle of ambisense viruses, in order to find the means to alleviate the lethal aspects of these pathogens.

Expression strategies of ambisense viruses. Virus Research 93: 141-150, 2003. doi: 10.1016/S0168-1702(03)00094-7

Related:

• Negative sense RNA viruses
• MicrobiologyBytes: Arenaviruses
• MicrobiologyBytes: Bunyaviruses

The family Bunyaviridae contains more than 350 viruses that are distributed throughout the world. Most members of the family are transmitted by arthopods, and several cause disease in man, domesticated animals and crop plants. Despite being recognized as an emerging threat, details of the virulence mechanisms employed by bunyaviruses are scant. This article summarises the information currently available on how these viruses are able to establish infections when confronted with a powerful antiviral interferon system.

Viruses 2009, 1(3), 1003-102; doi: 10.3390/v1031003

Related:

• Bunyaviruses
• The Interferon Antiviral Response
• Interferon – 50 years on