A possible new herpes danger 
When thinking of infectious disease, it’s usually the simpler things we need to be vigilante of such as Influenza virus, Streptococcus (i.e.; respiratory disease), Giardia and E. coli (i.e.; intestinal disease) to Staphylococcus (i.e.; “flesh” diseases) to name a few. The advent of national health campaigns, hygiene and prevention practices, food supply monitoring, vaccines, and antibiotics have all to one degree or another made huge impacts towards ensuring improved human and animal health in this respect. In fact, the rapidly changing global environment makes all these tools ever more critical and important. Among the more relevant up and coming global issues in disease vigilance is the increasingly more urgent need to monitor for the risk of zoonotic disease (those diseases that can potentially jump from one species to another).
With the advent in the human and animal medical world of the concept of ONE medicine, this particular branch of infectious disease- this crossover through species barriers- can be more effectively brought front and center. It is becoming increasingly apparent that the dangers are real.
As our knowledge continues to expand into the genomic, biochemical, and evolutionary aspects of infectious elements from prions to parasites researchers, medical doctors, and veterinarians are beginning to realize the extent to which things might go bad.
The geographic porosity of an increasingly smaller world is opening up niches for these organisms giving them an opportunity to adapt and capitalize on new horizons. The plasticity and ability for organisms such as bacteria and viruses to adapt to new situations is simply astounding. The risk for a more dangerous zoonotic event to occur can- in spite of the better known cross over media favorites like bird influenza H1N5- also involve those infectious diseases that work under the rubric of similar species. For example, virus’s acting within the umbrella of the primate genera. This particular case report entails just such a condition that unfortunately, in this case has potentially deadly consequences for its non-host primates- including humans.
Titled “Naturally transmitted herpesvirus papio-2 infection in a black and white colobus monkey”, this case involves the transmission of herpesvirus papio-2 virus to a colobus monkey that originated from a nearby baboon zoo colony. Though, this study may be somewhat tangential to any immediate risk to the general public, it illustrates how factors can serve as either facilitators or key prerequisites for how animal to human infections of potentially deadly diseases could occur.
The authors describe the death of a colobus monkey at the
The herpesvirus papio-2 (HVP-2) is a simian virus that is endemic in wild and captive baboons. This virus affects over 90 percent of wild –caught baboons and over 80 percent of captive baboons are seropositive for this virus. The HVP-2 shares genome composition, organization, and has a close sequence homology to other primate simplexviruses. (i.e.; SA8, Bvirus, HSV 1 and 2). These viruses are so similar serologic anti-body testing can not offer a positive identification between them.
When simplexviruses infect their normal primate hosts the resulting disease is usually mild or even absent. For example, HSV infection in humans are mild primarily affecting the oral or genital mucosa forming vesicles and papules that eventually form ulcerative lesions – similar pathophysiology occurs in other primates affected by their particular “brand” of simplexvirus.
However the story changes if a primate alphaherpsvirus infects a non-host animal where the virulence of the virus can vary dramatically. For example HVP-2 thought only to infect baboons and African green monkeys has been isolated as causing fatal encephalomyelitis in humans and other primates. The commonly benign human HSV-1 has caused fatal disease in several monkey species, shrews, lemurs, and rabbits.
The capacity for these viruses to cause such severe neuro virulence seems related to their capacity to replicate in there hosts- facilitated replication equated to higher virulence. Scientists have been able to phylogenically separate the HVP-2 virus into two distinct clades related to this neuropathic or non- neuropathic quality. That is their ability- or not- to cause severe central nervous system signs in non-host animals. Interestingly, this virulent HVP-2 caused similar signs to their non-hosts as another virus; the previously mentioned and related B virus effected on humans- a very crucial detail.
The authors in this study were able to isolate this particular virus that killed the colobus monkey to the neuropathic phylogenic strains calling it HVP-2 C1490. Most importantly, they found that this particular strain causes very similar clinical signs and histological lesions that another HVP-2 – the HVP-2nv- as those created in mice.
They were able to deduce that the most likely source of the HVP-2 C1490 infect ion came from a large baboon colony located in the zoological park, possibly through fomite contamination. That is, certain toys- even though they were disinfected- were shared by the colobus and baboon groups and it is possible some virus survived the decontamination process.
The authors note “As highlighted by the infection of the colobus monkey of this report, HVP-2nv can be transmitted naturally from baboons to a non-host species and result in development of fatal encephalitis. Given the extreme neurovirulence of HVP-2nv in non-host species, HVP-2 should be considered a potential zoonotic risk”.
In addition to the more obvious considerations of modifying zoo animal practices these findings suggest larger, more ominous possibilities. Because of the similarities between the virulent HVP-2nv, HVP-2, and the B virus that kills humans, the authors have discovered a new potential zoonotic link that needs to be added to the data base of human virulent viruses- originating from the common mostly benign herpes simplexvirus genus no less.
This small case study illustrates the need for constant vigilance in the search for emerging disease, especially in an increasingly complex global community. Very interesting news indeed.
NOTE:
Aetiology has an excellent zoonosis series that starts in 2006. For some reason the link does not go through right now- but search 2006 emerging disease and zoonosis at the sight-should get you to the series page.
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