Different human virus names




















Box Respiratory route i. Fecal-oral route: polioviruses, coxsackieviruses, hepatitis A virus, rotavirus, astrovirus, norovirus. Parenteral route i.

Vertical route e. Arthropod-borne route e. Rodent-associated transmission: Lassa fever virus, sin nombre, and other hanta viruses e. Understanding virus classification can lead to important generalizations regarding the prevention and treatment of viral infection and insights into the distribution and evolution of viruses.

In addition, insights from viral taxonomy play key roles in preventing and staunching the spread of viral disease at the population level. All references are available online at www.

National Center for Biotechnology Information , U. Principles and Practice of Pediatric Infectious Diseases. Published online Jul Robert David Siegel. Guest Editor s : Sarah S. Chief, Section of Infectious Diseases, St. Christopher's Hospital for Children, Philadelphia, Pennsylvania. Guest Editor s : Charles G.

Copyright and License information Disclaimer. All rights reserved. Elsevier hereby grants permission to make all its COVIDrelated research that is available on the COVID resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source.

TABLE Open in a separate window. Key References 5. Siegel R. Lipkin WI. The changing face of pathogen discovery and surveillance. Nat Rev Microbiol. Ho T, Tzanetakis IE. Development of a virus detection and discovery pipeline using next generation sequencing. References 1. Murphy FA.

Virus taxonomy. Fields Virology. Lippincott-Raven Publishers; Philadelphia: Condit R. Principles of virology. Fenner F. The classification and nomenclature of viruses: summary of results of meetings of the International Committee on Taxonomy of Viruses in Madrid, September J Gen Virol. Delwart EL. Viral metagenomics. Rev Med Virol. Microbe hunting in the 21st century. Transfusion transmission of highly prevalent commensal human viruses.

The 7th ICTV report. Arch Virol. A new family of vertebrate viruses: Toroviridae. 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.

We are grateful to colleagues in Edinburgh's Epidemiology Research Group and elsewhere for stimulating discussions and to two anonymous referees for thoughtful comments on the manuscript. National Center for Biotechnology Information , U. Author information Copyright and License information Disclaimer. This is an open-access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

This article has been cited by other articles in PMC. Abstract There are virus species that are known to be able to infect humans. Keywords: discovery curves, emerging infectious diseases, public health, risk factors, surveillance. Virus diversity and discovery a Survey of human viruses As a starting point for our survey, we used a previously published database see [ 5 ] obtained by systematically searching the primary scientific literature up to and including for reports of human infection with recognized virus species, using species as defined by the International Committee on Taxonomy of Viruses ICTV [ 6 ].

Open in a separate window. Figure 1. Table 1. Figure 2. Table 2. Emergence as a biological process a Non-human reservoirs More than two-thirds of human virus species are zoonotic, i. Figure 3. Figure 4. Conclusions The lines of evidence described earlier combine to suggest the following tentative model of the emergence process for novel human viruses. References 1. Levine A. History of virology. In Fields virology eds Fields B. Woolhouse M. Ecological origins of novel human pathogens.

Population biology of emerging and re-emerging pathogens: preface. B , — Parrish C. Molecular epidemiology of parvoviruses. Temporal trends in the discovery of human viruses. International Committee on Taxonomy of Viruses. Bebber D. Predicting unknown species numbers using discovery curves. Storch G. Diagnostic virology. The viruses within these categories share similar characteristics. 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.



0コメント

  • 1000 / 1000