Emergence Of New Viral Diseases In Humans Biology Essay

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Cross-species virus transmission had led to the emergence of new viral diseases in humans (Parrish et al., 2008). As discussed in the paper written by Parrish et al., these viral transmissions are creating epidemic diseases which result in new public health threats. Several recent examples include Ebola fever, severe acute respiratory syndrome (SARS), and influenza. Several of these diseases have been traced back to the original animal host. A table published by Parrish et al. (p. 458), suggests that SARS Corona Virus (SARS CoV), originated from bats. The table showing the origin of several viruses can be seen in Table 1 in the paper. From these animals, enzootic and epizootic viruses have been identified. These viruses have adapted to spread to humans, often via an intermediate host, and have caused severe illness in the human population.

TABLE 1.

Examples of viruses that transferred between hosts to gain new host ranges so that they cause outbreaks in those new hosts

Virus(es)

Original host

New host

Mechanism and/or time

Measles virus

Possibly cattle

Humans

Host switching and adaptation? Time not known; after the establishment of populations sufficient to allow transmission

Smallpox virus

Other primates or camels(?)

Humans

Host switching and adaptation? Time >10,000 yr ago?

Influenza virus

Water birds

Humans, pigs, horses

Host switching and adaptation, possible role of intermediate host; many examples. In humans viruses emerged in the period ~1910-1916 and in ~1957 and ~1968. Reassortment involved in 1957 and 1968 emergences. Earlier epidemic viruses not characterized. Changes in several genes required for success in new host

CPV

Cats or similar carnivores

Dogs

Host switching and adaptation; several mutations in the capsid control binding to the canine transferrin receptor. Arose in early 1970s, spread worldwide in 1978

HIV-1

Old World primates, chimpanzees

Humans

Host switching and adaptation; virus entered human population approximately in 1930s and spread widely in 1970s; multiple introductions likely to give the HIV-1 M, N, and O variants

SARS CoV

Bats

Himalayan palm civets or related carnivores; humans

Host switching, adaptation; some adaptation for binding to the ACE2 receptor in humans. 2003-2004

Dengue virus

Old World primates

Humans

<500 yr before present?

Nipah virus

Fruit bats

Humans (via pigs, or direct bat-to-human contact)

Host switching; adaptation may not be necessary: bat and human isolates identical in some outbreaks

Marburg virus and Ebola viruses

Reservoir host not proven (bats?)

Chimpanzees and humans

Host switching; adaptation not certain

Myxoma virus

Brush rabbits and Brazilian rabbits

European rabbits

Existing host range, required contact; spread widely in 1950s by human actions; high virulence, adaptation after host emergence

Hendra virus

Fruit bats

Horses and humans

Host switching; adaptation not reported

Canine influenza virus

Horses

Dogs

Host switching; adaptation to dog may be occurring

Microbiol Mol Biol Rev. 2008 September; 72(3): 457-470.

doi: 10.1128/MMBR.00004-08.

Copyright © 2008, American Society for Microbiology

Once the virus spreads to a new host, it can take one of three paths (p. 457). First, the virus can infect a single host and then be unsuccessful at spreading from there, essentially dying off. Second, the virus can infect a single host and spread from there to other people living in the same community or area. Eventually it will die-out of the population. This is referred to as an epidemic. Third, the virus can infect a host, spread into the surrounding environment, and adapt so that it can continue to infect the population (Parrish et al., 2008).

What determines which path a virus will take? Parrish et al., suggest several factors that must be examined when researching how or why a virus takes one path rather than another (p. 458). One variable to consider is the frequency and length of contact between the original host and the new host. This can be examined by looking at geographical and ecological separations of the two. Hundreds of years ago, the human population was much smaller. Humans lived in 'towns' (not in the jungle), and had limited interaction with animals. It wasn't until later, when humans began encroaching on animal habitats, be it for agricultural expansion or deforestation, or hunting for food that more frequent interaction became the norm. Along with more frequent exposure to animals came a change in human attitudes toward animals. People began domesticating animals and wildlife trade increased

(p. 459). Once contact became more common, more frequent, and longer lasting, the viruses were able to adapt successfully to switch from the original host to humans. After this, viral adaptation continued to make it possible to infect humans, and viruses continued to spread throughout the human population (p. 459-460). The more contact they had with humans, the more they could adapt to successfully infect more humans. An example is SIV in Old World primates. They were separated from humans, living in African jungles. When humans began to hunt them, the virus, which had adapted to infect humans, by way of the chimpanzee, became fully adapted and is know as HIV

(p. 460). Influenza A virus could travel long distances due to birds migrating and could reach animals like pigs and human populations on its own (p. 460). This still illustrates the need for a virus to come into contact with the new host in order for adaptation and infection to occur.

In addition to demographic barriers that viruses had to overcome to transmit, there are host barriers at the cellular level that must be overcome (p. 460). Viruses are selective in that they infect the same kind of tissue in a particular host. The process that viruses use to infect this tissue include receptor binding on/to the cells they plan to infect, entry into the cells, taking over the cell, and genetic replication and expression. Each of these steps requires the virus to adapt in order to overcome the barrier. In addition, viruses have to defend against the human innate antiviral response. This paper by Parrish et al., offers several points of discussion on these topics (p. 460-462).

First, before virus replication and innate response is even considered, genetic separation is examined. HIV has been repeatedly passed from chimpanzees to humans, both of whom are closely related (both are of the primate order). But viruses can also be passed from an original host to a new host even if they are from different orders. The SARS CoV was passed from bats (order Chiroptera), to civets (order Carnivora), and to humans (order Primates). Additionally, feline panleukopenia virus (FPV) was passed to dogs (same order, different families). Avian influenza can pass to humans and other mammals (same class). New studies have shown that equine influenza H3N8 can pass to dogs (different orders) and avian H5N1 can pass to cats (different classes). Parrish et al., suggest that these infections are more likely to occur due to increased contact and the ability of a virus to adapt than how closely related the animals are (p 460).

Receptor binding is a critical step in viral infections. This barrier must be overcome if a virus is to infect a new host cell. The receptors on the cells in the new host must recognize the virus in order for them to enter the cell. Changes in the virus must have occurred in order for the new host cells to have receptors that will recognize them. The virus must recognize something in the cell to target. For example, tissue that is infected by avian and mammalian viruses is different. Therefore, they both must target the same binding site such as a protein or, in this case, the same acid - sialic acid, in the cells. These cells are in different places in different animals (the intestinal tracts of waterfowl and in the respiratory tracts in humans). It is critical that the virus can find and recognize sialic acid, or any other receptor, in order to infect the host.

Another barrier for the virus, once inside the cell, is the mechanisms that the cells may use to restrict viral infection, for example, from retroviruses. An example is HIV-1 and SIV-1-like viruses. Certain cells have proteins that block infections when these viruses move on to the next cell. The human protein APOBEC-3G is an example of this. It gets packed into the cell when the virus replicates and gets passes on to the next cell, stopping the virus from infecting the cell by inactivating it. According to Parrish et al., the exact mechanism is not known, but these cell responses occur in several cells to protect against several viruses (p. 461). Other proteins affect binding sites in cells which also makes the virus inactive. A table from Parrish et al. shows some genes of poxviruses that can control viral host range in this way.

TABLE 3.

Genes of various poxviruses that have been found to be associated with the control of viral host rangea

Gene

Protein typeb

Cultured cells with defect in virus tropism

Myxoma virus genes

M-T5

Ankyrin repeats

Rabbit T cells; human tumor cells

M-T2

TNF receptor

Rabbit T cells

M-T4

ER localized

Rabbit T cells

M1 1L

Mitochondrial

Rabbit T cells

Vaccinia virus genes

E3L

PKR inhibitor

Human HeLa cells, chicken embryo fibroblasts

K3L

dsRNA-binding protein

Hamster (BHK) cells

B22R/SPl-1 genes

Serpin

Human AS49 keratinocytes

C7L

Cytoplasmic

Hamster Dede cells

K1L

Ankyrin-repeats

Pig kidney: PK13 cells

Rabbitpox virus gene

SPl-1

Serpin

Pig kidney: PK15 A594

Ectromelia virus gene

p28

E3-ubiquitin ligase

Mouse macrophages

Cowpox virus gene

C9L/CP77/CHOhr

Ankyrin repeats

Chinese hamster: W-CL9+grows in CHO cells, W-K1L/C9L+grows on PRK13 cells

aAs can be seen, there are many different genes that control infection of cells from different host species through a variety of mechanisms. (Adapted from reference 79 with permission from Macmillan Publishers Ltd.)

bTNF, tumor necrosis factor; ER, endoplasmic reticulum; PKR, protein kinase R; dsRNA, double-stranded RNA.

The third idea is the determinants of efficient viral spread. These internal viral mechanisms allow the virus to adapt and spread. They include how fit the virus is at infecting the new host, the mode of transmission, and recombination or reassortment (p.462-465). If the virus is to adapt to become the right match to infect a new host (e.g. humans) it must change and recognize cells within the human body to attach to, as discussed above. During this process, however, Parrish et al. suggest that the virus changes enough so that the old host may not recognize it any more (p. 462). This is a trade-off that may or may not be advantageous for the virus. It may become successful at infecting the new host, but it may lose the ability to infect the old host. This can be seen in Figure 2 and 3 of the paper, reprinted below. More studies need to be done in this area.

FIG. 2.

Diagrammatic representation of the steps involved in the emergence of host-switching viruses, showing the transfer of viruses into the new host (e.g., human) population with little or no transmission. An occasional virus gains the ability to spread in the new host (R0 > 1), and under the right circumstances for transmission those viruses will emerge and create a new epidemic. (Adapted from reference 3 with permission from Macmillan Publishers Ltd.)

Microbiol Mol Biol Rev. 2008 September; 72(3): 457-470.

doi: 10.1128/MMBR.00004-08.

Copyright © 2008, American Society for Microbiology

FIG. 3.

The steps involved in the emergence of host-switching viruses, showing the host and viral processes that can be involved in the transfer and adaptation process (based on data from reference 149).

Microbiol Mol Biol Rev. 2008 September; 72(3): 457-470.

doi: 10.1128/MMBR.00004-08.

Copyright © 2008, American Society for Microbiology

A second determinant of viral spread is the mode of transmission. The discussion in Parrish et al. suggests that viruses that spread through a vector (from arthropods for example) may not spread as easily or successfully, due to the number of hosts that they have to infect, i.e. the original host, the vector, and the new host (p. 462). Viruses may be more successful at infecting a new host if they do not occupy a vector.

A third determinant of viral spread is the process of recombination, or reassortment for segmented genomes. This process can combine stronger, more advantageous genetic material that will allow a virus to survive longer (and not die out). This process can insert new genetic information quickly, and reduce errors or genetically 'bad' genes on a regular basis, allowing the virus to become more stable in its new environment (p. 463). Influenza is a great example of this; as a segmented virus, different segments can move from an old host to a new host quickly. It can also move to several different hosts (from pigs to birds to humans) making it a well adapted virus. Recombination of HIV can be seen in Figure 5 of the paper.

This paper was extremely interesting to me. The most interesting concepts to me are the role of host genetic separation and the viral fitness trade-offs. Parrish et al., suggest that contact between the old host and the new host is more important than host genetic separation when it comes to a virus adapting and infecting a new host. I completely understand that contact is necessary, but I would like to conduct research on viruses to find out if there are any that are more distantly related that have been able to adapt and infect humans. I would like to know what the biggest separation is and find out how it could have happened. Obviously, some of this research may already exist and I need to find it and read it.

The idea of viral fitness trade-offs is interesting as well. I think these two concepts are related. If a virus has changed so much that it is now 'fit' in a new host, and 'not fit' in an old host, can we still always find evidence about which old host it came from? How do we trace back to the old host? If it is not 'fit' for the old host anymore, is there evidence of it existing there? And, if there is not evidence, how do we know how much genetic separation truly exists? As a novice to the study of viruses, I may be asking questions that have already been answered. These studies may have already been completed. If so, I want to read them and continue with this kind of research. I am fascinated with viruses and there ability to adapt and survive for thousands, hundreds of thousands of years! In addition, I now know that viruses can be used to treat disease/illness. The more we learn about them collectively, the more we can use them to cure illness together.

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