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.
A fraction of these viruses both existing and newly evolved are capable of infecting humans. The distinction is potentially important as it implies different determinants of the rate of emergence of viruses with epidemic or pandemic potential: for off-the-shelf pathogens this rate is largely driven by the rate of human contact with a diversity of virus genotypes possibly rare genotypes within the non-human reservoir i.
Whichever of these two models is correct perhaps both , there is a clear implication that the emergence of new human viruses is a long-standing and ongoing biological process. Whether this process will eventually slow down or stop if the bulk of new virus species constitute extant diversity or whether it will continue indefinitely if a significant proportion of newly discovered virus species are newly evolved remains unclear, although this makes little difference to immediate expectations.
If anthropogenic drivers of this process are important then it is possible that we are in the midst of a period of particularly rapid virus emergence and, in any case, with the advent of new virus detection technologies, we are very likely to be entering a period of accelerated virus discovery. By no means all of these will pose a serious risk to public health but, if the recent past is a reliable guide to the immediate future, it is very likely that some will.
The first line of defence against emerging viruses is effective surveillance. This topic has been widely discussed in recent years [ 10 , 41 ], but we will re-iterate a few key points here. Firstly, emerging viruses are everyone's problem: the ease with which viruses can disperse, potentially worldwide within days, coupled with the very wide geographical distribution of emergence events [ 9 ], means that a coordinated, global surveillance network is essential if we are to ensure rapid detection of novel viruses.
This immediately highlights the enormous national and regional differences in detection capacity, with the vast majority of suitable facilities located in Europe or North America. Secondly, reporting of unusual disease events is patchy, even once detected, reflecting both governance issues and lack of incentives [ 10 ]. Thirdly, we need to consider extending the surveillance effort to other mammal populations as well as humans, because these are the most likely source of new human viruses.
Improving the situation will require both political will and considerable investment in infrastructure, human capacity and new tools [ 10 , 41 ]. However, the benefits are potentially enormous. It is possible to forestall an emerging disease event, as experience with SARS has shown. However, our ability to achieve this is closely linked to our ability to detect such an event, and deliver effective interventions, as rapidly as possible.
A better understanding of the emergence of new human viruses as a biological and ecological process will allow us to refine our currently very crude notions of the kinds of pathogens, or the kinds of circumstances, we should be most concerned about, and so direct our efforts at detection and prevention more efficiently. Viruses are also the most abundant biological form of life on the planet. The first thing a virion does is enter a cell and becomes a virus.
Next, it reproduces, creating viral protein and genetic material instead of the usual cellular products. A virus can then spread through a wide variety of means, such as touching, coughing and sneezing.
The body fights viruses by breaking down the viral genetic material via RNA interference. The immune system then produces antibodies that bind to viruses to make them noninfectious. Lastly, T cells are sent to destroy the virus.
Antiviral drugs can treat viruses by inhibiting viral development and slowing down disease progression. These drugs help fight the flue, chickenpox and forms of hepatitis. Vaccines create a herd immunity that helps prevent an outbreak. There are five different types of viruses: Conjugate vaccines, inactivated vaccines, live, attenuated vaccines, subunit vaccines and toxoid vaccines.
There are several ways people can slow the spread of a virus in lieu of drugs or vaccination. These include thorough and frequent hand washing, eating a fruit and vegetable-rich diet, using an alcohol-based sanitizer and getting enough sleep each night. Around the world, nurses contribute to the prevention, management and containment of viral outbreaks by caring for infected patients and educating the public on prevention strategies.
Advanced practice nurses also fill a leadership role that involves working with government leaders and advocating for health care equality. Across a variety of roles and specializations, nursing professionals fight viruses in numerous ways. Some of their methods are direct, such as preventing surgical infections. Others are legislative in nature, such as advocating for care equality by questioning imbalanced care delivery systems. Nurses also share their expertise with the public on a host of vital topics, such as care delivery models, infection prevention and the distribution of important resources.
Another type of subunit vaccine can be created via genetic engineering. A gene coding for a vaccine protein is inserted into another virus, or into producer cells in culture.
When the carrier virus reproduces, or when the producer cell metabolizes, the vaccine protein is also created. The end result of this approach is a recombinant vaccine: the immune system will recognize the expressed protein and provide future protection against the target virus.
The Hepatitis B vaccine currently used in the United States is a recombinant vaccine. Another vaccine made using genetic engineering is the human papillomavirus HPV vaccine. Two types of HPV vaccine are available—one provides protection against two strains of HPV, the other four—but both are made in the same way: for each strain, a single viral protein is isolated.
When these proteins are expressed, virus-like particles VLPs are created. Conjugate vaccines, however, are made using pieces from the coats of bacteria. These coats are chemically linked to a carrier protein, and the combination is used as a vaccine. The vaccines currently in use for children against pneumococcal bacterial infections are made using this technique. Researchers continue to develop new vaccine types and improve current approaches. For more information about experimental vaccines and delivery techniques, see our article The Future of Immunization.
Plotkin, S. Philadelphia: Elsevier; This hepatitis B vaccine was the first human vaccine produced by recombinant DNA methods.
Researchers inserted the code for the antigen into yeast cells, which produced more of the surface protein. The yeast-derived surface protein produced immunity to the hepatitis B virus. True or false? Killed or inactivated vaccines usually provide shorter length of protection than live vaccines. Article Menu [ ]. Vaccine Science [ ]. Biological Weapons, Bioterrorism, and Vaccines.
Cancer Vaccines and Immunotherapy. Careers in Vaccine Research. Ebola Virus Disease and Ebola Vaccines. Human Cell Strains in Vaccine Development. Identifying Pathogens and Transmission Vectors. Malaria and Malaria Vaccine Candidates. Passive Immunization. The Future of Immunization. Vaccines for Pandemic Threats. Viruses and Evolution. History and Society [ ]. Cultural Perspectives on Vaccination.
Disease Eradication. Ethical Issues and Vaccines. History of Anti-vaccination Movements. Influenza Pandemics. The Development of the Immunization Schedule. The History of the Lyme Disease Vaccine. The Scientific Method in Vaccine History.
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