This article is discussing the ability of viruses to switch hosts causing new epidemic diseases. The author is suggesting the source of some new viral diseases such as SARS and H5N1, the barriers that prevent some of them from being successful in changing hosts, their mechanism of development and adaptation, the way they transfer between different hosts, and the role of reassortment and recombination in helping viruses to become more effective upon infecting new hosts.
The author suggests that the source of new epidemic viruses is previous animal viruses that infect domestic or wild animals. Unfortunately, we do not know a lot about them. This small fraction of knowledge gave an advantage to viruses to transmit between different species. One example is HIV/AIDS, which switched from a certain type of Chimpanzees to humans. This viral switch, which took about 70 years ago infected hundreds of millions of people and caused between 1.8 to 4.1 million to die annually. Another example is SARS CoV which switched from bats to humans. It infected thousands of people between 2002 and 2003, caused death to hundreds, and resulted in a total loss of $40 billion dollars. Also the author included a table containing a lot of viruses that switched hosts causing new epidemics. (Table 1).
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Then the author discussed the barriers that alter the transmission of the viruses between different hosts. The first barrier is the intensity of contact between the donor and the host. This is controlled by many factors such as demographics, geological, social, and behavior separation between both donor and recipient. The more contact between the different species, the more chances for viruses to be introduced to new hosts. So the intensity of contact is controlled by the size of the population of the recipient host. For example, human trade and travel helped in the transfer of a virus carrier called "Aedes Albopictus mosquito" and so exposing some viruses to new hosts.
One thing that critically helps to increase the contact of animal viruses with new hosts is "intermediate and amplifying hosts." A virus, which normally has little contact with the new host, may infect an intermediate host that has closer contact with the new host so as to increase the chances for that virus to infect more hosts. The author gave an example of Nipah virus epidemic in Malaysia. The reservoir of that virus is Fruit Bats, which were attracted to pig farms due to the planting of fruit orchards near these farms in Malaysia. This caused a spillover of the virus from the bats (less contact with humans) to pigs (more contact with humans), and amplifying the virus transmission to humans causing a large-scale outbreak.
The second barrier is the host barriers. These barriers can be divided into many levels starting with the entry level represented by the mucosal surface, and the unbroken skin followed by the blood and lymphatic system. The author gave an example where the presence of glycans or lectins in the blood will inactivate most invading viruses, e.g. Influenza viruses, because these viruses lack esterase or neuraminidase that are capable of destroying the glycans. Although humans lack the glycans in their blood, the intestinal bacteria has a kind of glycans called "Galactosyl(alpha1-3)galactose" which elicits our defensive mechanisms to produce antibodies against it. So once a virus is produced within our body, it will be recognized rapidly and destroyed by these antibodies.
After that the virus needs to adapt to the receptor binding step. This step demonstrates how specific the virus could be upon infecting other species. For example, SARS CoV is a virus that was derived from viruses that infect bats. These viruses were found to react differently with the ACE 2 receptor (the receptor for SARS virus) due to differences at a single protein called "S protein". FIG 3B shows the structure of protein S, while the FIG 3A shows the variation of protein S structure in 3 different SARS species: 2004 human epidemic, 2002 human epidemic, and palm civets SARS. One palm civet virus out of twenty examined had a Therionine amino acid at the position 487, which is found in all 2002 human epidemic viruses. This could suggest that both viruses are related and one of them switched into the other's host. The avian and mammalian influenza viruses can bind to different sialic acids or glycans linkages- which are found in the respiratory tracks of humans. This gives a great advantage for these influenza viruses to rapidly adapt to the new receptor in the new hosts. On the other hand, HIV-1 showed specificity to bind to CD4 receptors and CCR5 or CXCR4 co-receptors. If these receptors/co-receptors are absent, this virus cannot infect the host.
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The last host barrier could be some intracellular defense mechanisms against different aspects of the viral life cycle after entry. The author gave two examples. First, in case of HIV-1 and SIV- like viruses which lack the appropriate Vif protein, the cell can pack cytidine deaminases into new virions so that they cannot infect any new cells. Second, those viruses which depend on the capsid proteins for infection can be altered by the binding of TRIM5 alpha protein inside the cell to the infecting capsid protein causing the virus to dysfunction. Also interferon plays a very important role in the intracellular defense against viruses. For example, although murine noroviruses have a good ability for a wide range receptor binding, it is restricted by alpha and beta interferon after entry.
Afterwards, the author discussed the viruses' development through the evolutionary changes to adapt to the new host's environment. The author said that it is not necessary for the virus to have evolutionary changes in order to switch hosts, however, in case of limited host range mutations and evolutions may play a critical role in helping viruses to transmit easily between hosts. An example of a virus that does not have to mutate is canine distemper virus which naturally has a wide host range and can infect many of the mammalian species in addition to some marines. On the other hand, there are some viruses that are poorly adapted to the new host and need some evolutionary changes to help them to be better infectors. The author suggested that in order for viruses to have a better adaptation ability they need to have more genetic variation. This leads to conclusion that RNA viruses should have more capability to adapt to new hosts than DNA viruses, because RNA viruses do not have a proofreading mechanism and so they cannot fix their mistakes. Also, RNA viruses can replicate faster than DNA viruses. However, there is evidence that some RNA viruses (hantaviruses and arenaviruses) took a very long period of time to adapt to the new hosts.
The author stated that the mechanism of transmission of viruses between hosts is not well understood yet, but there should be at least three hosts during a transmission: the reservoir, the recipient, and the intermediate host (vector). The author provided three suggested ways that the HIV virus was transmitted from chimpanzees to humans (FIG 5). All of the three ways suggested that there was one or more intermediate between donor and recipient.
Another suggestion provided by the author for adaptation is Recombination (also known as reassortment in viruses with segmented genes). This could help the genetic variation within the virus, allowing it to have more ability to adapt to the new host. For example, H2N2 and H3N2 influenza A viruses were formed by the addition of an avian genome into H1N1 virus. FIG 5 and FIG 4 also demonstrate how HIV and SARS CoV could evolve due to recombination. On the other hand, the recombination process could delete some of the genes coding for optimal protein structures within viruses, preventing them from being effective. For example, Influenza A virus has a complex for replication consisting of three proteins (PA, PB1, PB2). Reassortment could disrupt this complex, resulting in less replication and therefore less adaptation.
Although the article focused on the barriers and the difficulties that could face viruses in order to switch to a new host, it did not give much information about the development of viruses and their mechanism of infection. The author provided many solutions and strategies to prevent viruses from causing more epidemics and outbreaks, but it would be much more effective if we increased our concerns and studies on animal viruses, so we can fight that cross-transmission at the origin point. The article was not interesting because most of the points suggested by the author were "not well understood". Also most of the studies and tables provided were not illustrated efficiently, which increased my confusion during reading.