Can RNA Viruses Have Multiple Hosts

To better understand the evolutionary and molecular arguments an ecological perspective will help. West Nile Virus is a good example of an RNA virus associated with several hosts because of the research that has been done to track this virus. WNV is an Arbovirus (Arthropod born) that is carried in mosquitoes. It is a ss(+)RNA virus consisting of 11kb and a nucleocapsid. In the USA the Culex mosquito is the most common carrier of this virus (1,2). Female mosquitoes are the blood feeders in their species, as it is needed for their progeny. The most investigated infectious cycle starts with a Culex feeding on the blood of an infected bird. The female

At the molecular level these viruses are engineered in a way that loosely directs them toward a particular host. The hosts provide the essentials for survival, like permissiveness, replication and cellular machinery for propagating virion (6). More simply, there are special mechanisms that promote infection, spreading and persistence. The focus here will be on one of these minor yet essential molecular factors that promotes specificity. Like most viruses, RNA viruses follow special binding procedures that need to occur before infection can even begin. This process is known as receptor mediated endocytosis. Upon inoculation of WNV, the virus uses an protein to bind to a specific cite on the host cell. The binding proteins on the virus are highly conserved and similar in many species. Some only differ in location on the host cell membrane. A group of carbohydrate residues are located on a protein band of the host cell membrane that, with the help of co-receptors, signals the binding protein of the virus. This is the E protein and helps recognize the receptor and hide the virus from host immune responses. An integrin aids the process of integrating its genome into the host cell. Once in the cell, the viral RNA can go through its process of replication, transcription, translation and exiting from the cell. The highly conserved binding protein region of the WNV, and a complementary binging site on the host cell, suggest a degree of specificity between the virus and the host (6). In the case of WNV the binding sites of the horse, human and avian hosts are all very similar, indicating specificity for vertebrate cell membranes. Although the horse, human, and bird are of different species, they are all vertebrates that are closely related based on phylogenies. This is reason enough to infer that some latitude in host specificity could occur, assuming a potential for evolutionary relationships between WNV and vertebrate hosts (1,6,7).

This brings about the consideration that different WNV strains can be considered their own viral species. They have the ability to adapt and change into something that is similar to the original strain, but not the same. Because of the divergence from a common ancestral strain of a virus, the resulting viruses may carry some of the ability of the ancestors, but more specialized features to infect a particular host. Consider a hypothetical example to support this argument. A large vertebrate host like horses may have been a target in an ancestral strain of WNV. This will be considered “H” strain. As a selective pressure occurred the virus changed its host selection to avian vertebrates, resulting in a new mutant strain “A” strain. If this mutant is then repetitively exposed to the horse population, over time it could revert or mutate to be virulent in the horse host again. If the mutation occurred in a gene different from the original Horse-Bird mutation, it woul

Some topics in this essay:
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