Cross-Species Virus Transmission

Cross-Species Virus Transmission and the Emergence of New Epidemic Diseases Synopsis

Throughout history there has been a rapid increase in the amount of human viral diseases. According to the article Cross-Species Virus Transmission and the Emergence of New Epidemic Diseases by Parrish et al, the presence of these diseases is only new to us. Viruses have been evolving in such a way that diseases once thought to only affect certain animals have become human epidemics, such as HIV and various influenza viruses. Along with the viral evolution, human behavior has been changing in such a way to make us more available to these diseases. Before, we limited our contact with certain species. However, changes in travel, farming, population expansion, and even sexual practices that put use in closer proximity to new animals can also put us at risk for new diseases. Although the human body may have its own natural defenses, it is evident that viruses are evolving in ways to get around them.

In the beginning, the article highlights three main points that are necessary for a virus to cause an epidemic in a new host species. First, the virus must infect what is known as a “dead-end host” (Parrish, et al., 2008). A dead-end host is a host that does not infect others, either because of incapacitation or by isolation. Infecting a dead-end host firstly gives the virus a need to survive in order to induce evolution, but it also gives the virus time to evolve. Second, the virus must cause a series of outbreaks in the new host before it dies out. Last, the outbreaks must go on to infect others with in the population. This means that through evolution, the virus has to gain a way to be spread within the new population, not just from old species to new species. It also means that the carriers of this virus must be kept healthy for a while in order to transmit the virus to others. The article also makes a point to mention that before epidemic viruses such as influenza, smallpox, and HIV were seen in humans, they were unknown to us.

The article goes on to describe the difficult process of such a viral evolution. Firstly, the virus must some how overcome multiple barriers in order to infect the new host. Geographical barriers may be broken due to human behavior. HIV could not have become an epidemic with out an increase in “primate-to-human exposure” (Parrish, et al., 2008) and incidentally SIV (simian immunodeficiency virus). Traveling, of both the new host and the infected animal, puts us in the presence of animals that we might not have otherwise come in contact with. In the cause of H5N1 avian influenza, seasonal bird migration allowed the virus to cross geographical barriers. Human practices, like farming, may increase our risk of infection due to repeated exposure to viral carriers.

Once the virus has overcome geographical barriers, the virus must be able to infect the new host. However, different species may possess different immunities that the virus can not get around. Therefore, it is worth while for the virus to infect species that are closely related to the species it had already infected. For example, it is more plausible for SIV to cross over to humans because genetically we are so much alike. However, it is possible that similar species may have evolved from one another and may have inherited immunity from the virus altogether before ever being infected. The virus must also possess the right structure in order to infect the correct tissue. This may mean evolving in order to bind to a certain receptor. Influenza viruses are able to infect new host quickly, because they bind to sialic acids, which are found in a variety of hosts. However, HIV is very specific and requires CD4 receptors and a corrector in order to infect its host.

After the virus has infected the host cell, it must replicate. However, the new host may not be an ideal environment for replication and expression. In influenza virus, it has been observed that the rate of replication in a human host is reduced from its previous host. Other viruses may actually be blocked from the entire process. Proteins such as Trimα actual stop infection by binding to the capsid of intruding viruses. In order to effectively infect humans, HIV had to evolve to target this protein before it can undergo genome replication and expression.

The article states that one way to get around these multiple obstacles is to infect an alternative host before infecting the target host. By infecting an alternative host, the virus may be able to overcome geographical barriers, like in the case of bird migration. Infections in alternative hosts may also give the virus a head start on evolution so that it will be ready for the target host, especially if the target host is very similar to the alternative host.

However, it is not just enough to infect the new host. Once the virus has infected the new host, it must evolve in order to infect others within the population. Influenza viruses in humans affect the respiratory tract, but do not in other animals. However, because it affects the respiratory tract of humans, it is able to be easily transmitted from person to person. Other viruses such as HIV rely on the actual behaviors, like sex, of a population to spread. If the virus can not be effectively transmitted through out a population, then it will not become an epidemic. The virus must also evolve in order to keep the host healthy enough to infect others. This is known as the “viral-fitness trade off” (Parrish, et al., 2008). If the virus causes too much harm to the host too quickly, it is unlikely that the host will be able to infect many others.

Lastly, the article describes the viral mechanism for host switching. The author describes that the changes that allow viruses to switch host may not be evolutionary factors at all. RNA viruses do not have the proofreading capabilities that DNA viruses do and ssDNA viruses are extremely diverse even along identical strains. Also genetic recombination may play a large part in the rapid emergence of new viruses. Viruses that infect the same animal at once may combine to form new viruses like the SARS CoV virus, which is the combination of the bat CoV virus and another unknown virus.

The article concludes by offering suggestions in ways to protect humans from emerging viral epidemics. Although we are unable to be certain which zoonotic virus will be the next human epidemic, by monitoring and treating animals through vaccination, we may greatly reduce our personal risk. Also, by researching existing human viruses, we are able to see patterns in their evolution in order to predict the future patterns of new viruses so that we may prepare ourselves.

While I personally agree with the fact that the emergence of new viruses due to species cross over is an important topic, I believe that the author is a bit more dramatic and pessimistic than necessary. Although the author discusses the heavy impact of epidemic zoonotic viruses such as HIV and influenza viruses, he neglects to discuss any zoonotic viruses that have crossed over and have caused no reason for alarm. By reading this article, it seems like every zoonotic virus that crosses over is an epidemic while that may not be the case. However, I do agree with the author in that the epidemic viruses that have crossed over must be researched in order to distinguish a pattern to stop further epidemics. Although we may not be able to stop the viruses from crossing over, we will be able to understand them, and possibly reduce their emergence. By monitoring animals, we will be able to monitor emerging viral diseases. I agree with the author in that we will not be able to monitor all animals. However, I believe that heavily monitoring animals that we are typically in contact with, such as domestic and even entertainment animals (i.e. zoo and safari animals), will help to reduce the amount of emerging diseases.


Parrish, C., Holmes, E. M., Park, E., Burke, D., Calisher, C., Laughlin, C., et al. (2008). Cross-
species virus transmission and the emergence of new epidemic diseases. Microbiology and Molecular Bilogy Reviews (72) , 457-470.

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