5 different types of human viruses

There are at least 25 viruses in the family Herpesviridae. Eight or more herpes virus types are known to infect man frequently.

Rotavirus is the most common cause of severe diarrhoea among infants and young children, and is one of several viruses that cause infections often called stomach flu, despite having no relation to influenza. It is a genus of double-stranded RNA virus in the family Reoviridae. By the age of five, nearly every child in the world has been infected with rotavirus at least once.

However, with each infection, immunity develops, and subsequent infections are less severe; adults are rarely affected. The virus is transmitted by the faecal-oral route. It infects and damages the cells that line the small intestine and causes gastroenteritis. In addition to its impact on human health, rotavirus also infects animals, and is a pathogen of livestock. Chickenpox is a highly contagious illness caused by primary infection with varicella zoster virus VZV.

It usually starts with vesicular skin rash mainly on the body and head rather than at the periphery and becomes itchy, raw pockmarks, which mostly heal without scarring. On examination, the observer typically finds lesions at various stages of healing.

Chickenpox is an airborne disease spread easily through coughing or sneezing of ill individuals or through direct contact with secretions from the rash. A person with chickenpox is infectious one to two days before the rash appears. They remain contagious until all lesions have crusted over. Immunocompromised patients are contagious during the entire period new lesions keep appearing. Crusted lesions are not contagious.

It takes from 10 to 21 days after initial infection for the disease to develop. Influenza is a viral infection that affects mainly the nose, throat, bronchi and, occasionally, lungs. Infection usually lasts for about a week, and is characterized by sudden onset of high fever, aching muscles, headache and severe malaise, non-productive cough, sore throat and rhinitis. The virus is transmitted easily from person to person via droplets and small particles produced when infected people cough or sneeze.

Influenza tends to spread rapidly in seasonal epidemics. Most infected people recover within one to two weeks without requiring medical treatment. However, in the very young, the elderly, and those with other serious medical conditions, infection can lead to severe complications of the underlying condition, pneumonia and death. The common cold also known as nasopharyngitis, acute viral rhinopharyngitis, acute coryza, or a cold Latin: rhinitis acuta catarrhalis is a viral infectious disease of the upper respiratory system, caused primarily by rhinoviruses and coronaviruses.

Common symptoms include a cough, sore throat, runny nose, and fever. There is no cure for the common cold, but symptoms usually resolve in 7 to 10 days, with some symptoms possibly lasting for up to three weeks. The common cold is the most frequent infectious disease in humans with the average adult contracting two to four infections a year and the average child contracting between 6 and Collectively, colds, influenza, and other upper respiratory tract infections URTI with similar symptoms are included in the diagnosis of influenza-like illness.

Sign in. 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.

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. Figure 1 — This is a picture of a phylogenetic tree.

Each sequence from a specific influenza virus has its own branch on the tree. The degree of genetic difference between viruses is represented by the length of the horizontal lines branches in the phylogenetic tree. The further apart viruses are on the horizontal axis of a phylogenetic tree, the more genetically different the viruses are to one another.

An influenza clade or group is a further subdivision of influenza viruses beyond subtypes or lineages based on the similarity of their HA gene sequences. See the Genome Sequencing and Genetic Characterization page for more information.

Clades and subclades are shown on phylogenetic trees as groups of viruses that usually have similar genetic changes i. Dividing viruses into clades and subclades allows flu experts to track the proportion of viruses from different clades in circulation. Note that clades and sub-clades that are genetically different from others are not necessarily antigenically different.

These proteins act as antigens. Antigens are molecular structures on the surface of viruses that are recognized by the immune system and can trigger an immune response such as antibody production. Therefore, for antigenically different viruses, immunity developed against one of the viruses will not necessarily protect against the other virus as well. Influenza A H3N2 viruses also change both genetically and antigenically.

Influenza A H3N2 viruses have formed many separate, genetically different clades in recent years that continue to co-circulate. Similar to influenza A viruses, influenza B viruses can then be further classified into specific clades and sub-clades. Influenza B viruses generally change more slowly in terms of their genetic and antigenic properties than influenza A viruses, especially influenza A H3N2 viruses. Influenza surveillance data from recent years shows co-circulation of influenza B viruses from both lineages in the United States and around the world.

However, the proportion of influenza B viruses from each lineage that circulate can vary by geographic location and by season.

Figure 2 — This image shows how influenza viruses are named. The name starts with the virus type, followed by the place the virus was isolated, followed by the virus strain number often a sample identifier , the year isolated, and finally, the virus subtype.