Reacción a "The first case of human infection with the Shamonda virus has been identified in a patient with pre-existing conditions who died in France"

This virus has been known in Nigeria since the 1960s and has been detected retrospectively in Japan and South Africa, but it had not been detected in Europe until this year (Germany, France and Switzerland) and a geographical spread such as the one it has now experienced had never been documented before.

It is an orthobunyavirus belonging to the Simbu serogroup, specifically to subclade B of this orthobunyavirus serogroup, in which, to my knowledge, no human infections have ever been detected before, although infections have been recorded in animals (the Akabane virus, for example). Expert virologists did not foresee any risk to humans from this virus, but within the Simbu serogroup there are several viruses—Oropuche and Madre de Dios, for example—which belong to subclade A of the Simbu serogroup and which are indeed infectious to humans and cause clinical problems. As far as we know, these orthobunyaviruses that are pathogenic to humans are largely confined to the Americas, and in Europe the only research being carried out is aimed at understanding the extent to which potential native vector species in Europe might act as significant vectors for these viruses. Risk assessments regarding the introduction of these viruses indicate a low risk; however, there may always be imported cases that could serve as significant routes of introduction if the virus finds competent vectors for its replication and transmission on our continent.

Bunyaviruses are viruses with very high mutagenic potential (they include, for example, the Crimean-Congo haemorrhagic fever virus in the genus Orthonairovirus), because, like the influenza virus, they are RNA viruses with a segmented genome. In this case, the genome of these viruses consists of three segments. Thus, apart from the usual mutations that typically occur over time due to errors in nucleotide assembly caused by malfunctioning viral polymerases, these viruses can exchange large fragments of RNA with one another (recombination) and even exchange entire segments of their genome when different variants replicate within the same cells of a vector or host (rearrangement).

I am unaware of any evidence to suggest that the Shamonda virus was the cause of the clinical case documented in France. It may be that the detection of the virus is not the cause of the patient’s illness and death (as the patient had other secondary clinical conditions that could have compromised their immune function), but rather that the presence of the viral genome was simply detected following exposure to bites from infected vectors. The ECDC is investigating the public health risks in order to provide a response.

It is important to bear in mind that there is already evidence of recombination between Shamonda viruses and other orthobunyaviruses, with serious clinical consequences for horses in some areas where these new viruses emerged; it is therefore not unreasonable to think that this new virus may have undergone changes that enable it to infect humans and cause them problems. We must wait for further updates to determine whether it may have any clinical impact – such as the identification of its complete genome and details of the human clinical case – but the virus itself is causing a multitude of clinical problems in livestock, which is why it is being treated as an emerging virus in Europe.

In Spain, this virus is already circulating in livestock, but we do not yet have clear evidence of its spread beyond occasional reports of problems or detection in animals. This indicates something important: that in Spain we have competent vectors for this virus. Experience with the Schmallenberg virus, which also belongs to subclade B of the Simbu serogroup, showed that its spread across Europe following its first detection in Germany was very rapid, taking place in less than a year. It is possible that the Shamonda virus – not necessarily the virus that may have caused clinical problems in people in France – is currently spreading across Spain because this is still the season when Culicoides are abundant; they do not disappear from most of the country until the end of the year. We will no doubt soon have information from surveillance studies indicating this spread, but it is to be expected that by 2027 the virus will have reached almost the whole of the country, at least mainland Spain.

If it were to be demonstrated that the Shamonda virus circulating in animals has the potential to cause disease in humans, this would have a major impact on public health policies. Should the impact be limited to only a sector of the population with immune system problems, the impact would be much less severe than if it were to affect perfectly healthy people. Controlling Culicoides is extremely complex, not only because of their diversity but also due to their wide distribution and their presence in natural, rural and urban environments. However, control measures for these insects do exist in environments where a risk can be inferred, and we have a great deal of information on the location of these vectors in Spain.