Effects of viruses on the human body

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. Your immune system may be able to fight it off. For most viral infections, treatments can only help with symptoms while you wait for your immune system to fight off the virus. Antibiotics do not work for viral infections. There are antiviral medicines to treat some viral infections. Vaccines can help prevent you from getting many viral diseases.

The information on this site should not be used as a substitute for professional medical care or advice. Contact a health care provider if you have questions about your health. Everywhere researchers have looked in the human body, viruses have been found. Viruses in the blood?

Viruses on the skin? Viruses in the lungs? Viruses in the urine? And so on. Viruses are contagious. Researchers have shown that just living with someone will lead to rapid sharing of the viruses in your body. Ultimately, we need to know what all these viruses in the human body are doing, and figure out whether we can take advantage of our virome to promote our health. It may seem counterintuitive, but harming our bacteria can be harmful to our health.

Just as an invasive wild animal species can breed out of control when it enters a new area without predators or pathogens think cane toads in Australia, or rats on tropical islands , so too would bacteria override our bodies without these regulating mechanisms.

Viruses also seem to be important in the regulation of our immune system. In humans, the hepatitis G virus can protect against HIV, while in mice herpesvirus is known to reduce autoimmune diseases.

These are diseases that are a major factor in many modern illnesses in humans, from asthma to irritable bowel syndrome. Many viruses are clearly very harmful to us and humans have evolved mechanisms to counter their attacks. Viruses share a deep evolutionary relationship with animals and plants. Every cell in your body is part of an unbroken chain of life that has extended over 3. Viruses have been an important part of that evolutionary waltz from the very start.

The more we learn about the virome, the more we come to see how some aspects are essential for a healthy life.