Next the researchers adapted a statistical technique from the field of ecology to estimate that there were another three rare viruses unaccounted for in the samples, upping the estimate of viruses in the flying fox to Finally, this number was extrapolated to all 5, known mammals, yielding a total of at least , viruses.
Nonetheless, what we learn from exploring global viral diversity could mitigate outbreaks by facilitating better surveillance and rapid diagnostic testing. Anthony continues, adding that prevention is crucial when it comes to viral infections since antivirals are notoriously difficult to develop. The researchers say the initial estimate of , is just a starting point and will likely be considerably higher after accounting for additional viral families and employing high throughput sequencing methods developed at CII.
They also point to several unknowns, including whether or not the samples from flying foxes in Bangladesh are representative of all flying foxes, which range across Southern Asia; whether or not all mammal species harbor a similar number of viruses; and the extent to which viruses are shared from species to species as seen with the human, bovine, and avian viruses in the flying fox.
Furthermore, the cost of collecting samples could vary depending on habitat the flying fox expedition in Bangladesh was relatively low compared with similar undertaking for an animal living in more remote areas. With additional resources, they hope to expand the investigation to other species and viral families. Based on the cost to study viruses in P. I believe this would be money well spent, as the information would allow unprecedented study on the diversity and origins of viruses and their evolution.
However it is not at all clear that knowing all the viruses that could potentially infect humans would have an impact on our ability to prevent disease. We have known for some time that P. While it is not inconceivable that such information could be useful in responding to zoonotic outbreaks, the knowledge of all the viruses on Earth would likely impact human health in ways that cannot be currently imagined. Update 1: I neglected to point out an assumption made in this study, that detection of a PCR product in a bat indicates that the virus is replicating in that animal.
As discussed for MERS-CoV , conclusive evidence that a virus is present in a given host requires isolation of infectious virus, or if that is not possible, isolation of full length viral genomes from multiple hosts, together with detection of anti-viral antibodies. Obviously these measures cannot be taken for a study such as the one described above whose aim is to estimate the number of unknown viruses. Update 2: We discussed this estimate of mammalian viruses on TWiV The model was fitted to the data and evaluated using Markov chain Monte Carlo MCMC methods with flat prior information to calculate profile likelihood confidence intervals and the best fit parameters.
However, the binomial distribution B N , p can be accurately approximated by a Poisson distribution with parameter Np for the range of values of N and p of interest. We compared the model with the observed data by calculating the mean, trend in the mean and variance for the number of virus species discovered per year based on 5 million simulations using best fit parameter values.
The model reproduces the observed data well: observed mean and variance 3. Parameter estimates, however, are very uncertain owing to an unavoidable strong correlation between N and p [ 5 ]. The estimate of N is of particular interest: this has a central value of i. Thus, although there is considerable uncertainty as to the size of the human virus species pool, this analysis suggests that there are at least dozens of new species to be discovered, and possibly a very much larger number.
This projection, of course, makes no allowance for any improvements in virus detection technology nor changes in discovery effort. From our systematic literature review, we identified at least 14 putative new species of human virus first reported during the 5 years to inclusive table 2 , though this list is almost certainly incomplete.
Indeed, it would be unsurprising if it were exceeded, given the considerable recent interest in virus discovery and the advent of high throughput sequencing as a detection tool. Examples of putative new human virus species reported from to [ 11 — 24 ]. The discovery curve for virus families is shown in figure 1 b. Here, a family is included on the date of the first published report of human infection by a virus species from that family. Strikingly, no new families have been added to the list since , the longest such interval on record.
It should also be noted that there are three virus families that, although they do not contain any known human virus species, do contain species that infect other mammals: Arteriviridae several species including simian haemorrhagic fever virus ; Asfarviridae African swine fever virus ; Circoviridae including mammal infecting circoviruses as well as gyrovirus which infects chickens.
This suggests that the list of families containing human viruses may not yet be complete. More than two-thirds of human virus species are zoonotic, i. By far the most important non-human host taxa are other mammals, with rodents and ungulates most commonly identified as alternative hosts, followed by primates, carnivores and bats.
Some of these e. HIV-1 have much more recent origins [ 29 ]. Some of both kinds are believed to have originated in other mammal or bird species [ 30 ], including: HIV-1 derived from a simian immunodeficiency virus found in chimpanzees ; HIV-2 sooty mangabeys ; severe acute respiratory syndrome virus SARS; horseshoe bats ; hepatitis B, human T-lymphotropic virus HTLV -1 and -2, dengue and yellow fever all primates ; human coronavirus OC43, measles, mumps and smallpox all livestock ; and influenza A wildfowl.
A useful conceptual framework for thinking about the emergence of novel viruses is the pathogen pyramid [ 30 , 31 ] figure 3. The pyramid has four levels. The pathogen pyramid adapted from [ 30 ].
Each level represents a different degree of interaction between pathogens and humans, ranging from exposure through to epidemic spread. Some pathogens are able to progress from one level to the next arrows ; others are prevented from doing so by biological or ecological barriers bars —see main text.
Level 1 represents the exposure of humans to a novel pathogen; here, a virus. The rate of such exposure is determined by a combination of the distribution and ecology of the non-human host and human activities. This is likely to reflect both the molecular biology of the virus e.
Level 3 represents the subset of viruses that can not only infect humans but can also be transmitted from one human to another by whatever route, including via arthropod vectors. Again, this will mainly reflect the host—pathogen interaction, especially whether it is possible for the virus to access tissues from which it can exit the host, such as the upper respiratory tract, lower gut, urogenital tract, skin or for some transmission routes blood.
This is a function of both the transmissibility of the virus how infectious an infected host is, and for how long and properties of the human population how human demography and behaviour affect opportunities for transmission. From previous reviews of the literature [ 25 , 26 , 34 ], it is possible to put approximate numbers of virus species at each level of the pyramid. We do not have a good estimate of the total species diversity of mammalian and avian viruses; however, we can get an indirect indication of the magnitude of the barrier between level 1 and level 2.
It has been reported elsewhere R. Critchlow , personal communication that of the virus species known to infect domestic animals livestock and companion animals —to which humans are presumably routinely exposed—roughly one-third are also capable of infecting humans. The species barrier exists: but it is clearly very leaky. Based on data from [ 25 ], roughly 50 per cent of the viruses that can infect humans can also be transmitted by humans level 3 , and roughly 50 per cent of those are sufficiently transmissible that R 0 may exceed one level 4.
That a significant minority of mammalian or avian viruses should be capable of extensive spread within human populations or of rapidly becoming so [ 35 ] is consistent with experience: there are several examples within the past hundred years alone HIV-1, SARS, plus variants of influenza A and many more in the past few millennia e. The most straightforward explanation for this is the much more rapid evolution of viruses especially RNA viruses , allowing them to adapt to a new human host much more quickly than other kinds of pathogen.
Moreover, identification of drivers is usually a subjective exercise: there are very few formal tests of the idea that a specific driver is associated with the emergence of a specific pathogen or set of pathogens.
In many cases, this would be a challenging exercise: many drivers have only indirect effects on emergence e. Other ideas about drivers of emergence are even harder to test formally.
King , personal communication. A slightly different way of thinking about drivers of emergence is to draw an analogy between emerging pathogens and weeds A. Dobson , personal communication. The idea here is that there is a sufficient diversity of pathogens available—each with their own biology and epidemiology—that any change in the human environment but especially in the way that humans interact with other animals, domestic or wild is likely to favour one pathogen or another, which responds by invading the newly accessible habitat.
This idea would imply that emerging pathogens possess different life-history characteristics to established, long-term endemic pathogens. As noted earlier, the most striking difference identified so far is that the majority of recently emerging pathogens are viruses rather than bacteria, fungi, protozoa or helminths. For viruses, one of the key steps in the emergence process is the jump between one host species and humans [ 37 ].
For other kinds of pathogen, there may be other sources of human exposure, notably environmental sources or the normally commensal skin or gut flora. Various factors have been examined in terms of their relationship with a pathogen's ability to jump into a new host species; these include taxonomic relatedness of the hosts, geographical overlap and host range.
Two recent studies provide good illustrations of the roles of host relatedness and geographical proximity. Streicker et al.
A broad host range is also associated with the likelihood of a pathogen emerging or re-emerging in human populations [ 26 ]. An illustrative case study is bovine spongiform encephalopathy BSE. After BSE's emergence in the s, well before it was found to infect humans as vCJD , it rapidly became apparent that it could infect a wide range of hosts, including carnivores. This was in marked contrast to a much more familiar prion disease, scrapie, which was naturally restricted to sheep and goats.
With hindsight, this observation might have led to public health concerns about BSE being raised earlier than they were. Host range is a highly variable trait among viruses: some, such as rabies, can infect a very wide range of mammals; others, such as mumps, specialize on a single species humans. Moreover, for pathogens generally, host range seems to be phylogenetically labile, with even closely related species having very different host ranges [ 27 ].
Clearly, the biological basis of host range is relevant to understanding pathogen emergence. One likely biological determinant of the ability of a virus to jump between species is whether or not they use a cell receptor that is highly conserved across different mammalian hosts. We therefore predicted that viruses that use conserved receptors ought to be more likely to have a broad host range. To test this idea, we first carried out a comprehensive review of the peer reviewed literature and identified 88 human virus species for which at least one cell receptor has been identified.
Although this is only 40 per cent of the species of interest, 21 of 23 families were represented; so this set contains a good cross-section of relevant taxonomic diversity. Of these 88 species, 22 use non-protein receptors e. For the subset of proteins where amino acid sequences data were also available for cows, pigs or dogs, we found very similar patterns. The result is shown in figure 4. The most striking feature of the plot is that there are no examples of human viruses with broad host ranges that do not use highly conserved cell receptors i.
Statistical analyses requires correction for phylogenetic correlation: viruses in the same family are both more likely to use the same cell receptor and more likely to have a narrow or broad host range.
This can be crudely but conservatively allowed for by testing for an association between host range and receptor homology at the family, not species, level. Number of virus species with broad blue bars or narrow red bars host range as a function of the percent homology of the cell receptor used see main text.
We conclude that the use of a conserved receptor is a necessary but not sufficient condition for a virus to have a broad host range encompassing different mammalian orders. It follows that a useful piece of knowledge about a novel mammalian virus, helping to predict whether or not it poses a risk to humans, would be to identify the cell receptor it uses.
However, this may not always be practicable: at present, we do not know the cell receptor used by over half the viruses that infect humans, and this fraction is considerably smaller for those that infect other mammals. The lines of evidence described earlier combine to suggest the following tentative model of the emergence process for novel human viruses.
First, humans are constantly exposed to a huge diversity of viruses, though those of others mammals and perhaps birds are of greatest importance. Moreover, these viruses are very genetically diverse and new genotypes, strains and species evolve rapidly over periods of years or decades.
0コメント