The most common causes of mutation in proliferating viruses are thought to be errors in polymerase transcription and endogenous damage to nucleic acid bases. Coxsackievirus is an RNA virus and best online essay writer lacks the proofreading capability that is a feature of DNA replication. Because of the lack of RNA replicases with proofreading ability, RNA viruses are susceptible to high mutation rates. The high mutation rate of RNA viruses results in the continuous generation of virus mutants, producing a dynamic and changing viral population.

Thus, any increase in viral replication may be expected to enhance the evolution of new viral mutants. Two possibilities may account for the increased viral titers in the deficient mice. Virus may have escaped from normal immune clearance mechanisms, thus allowing a higher and more persistent degree of replication. A second alternative although not mutually exclusive is that cardiac cell membranes may have been compromised such that virus was able to replicate to higher titers in oxidatively stressed cardiac cells versus normal cardiac cells.

Another possible explanation for the change in viral genotype may be that the oxidative stress status of the host directly affected the virus. The reactive oxygen species ROS generated due to the nutritional deficiency may have damaged the viral RNA, which is similar to what occurs when ROS damages DNA. This damage may have resulted in the mutations.

This possibility is currently being explored in this laboratory. Thus, the work with Coxsackievirus and host Se deficiency demonstrates that not only can the nutritional deficiency affect the host, but effects on the pathogen must be considered as well. This work demonstrates that once the benign virus has mutated, as a result of replication in a nutritionally deficient host, it can now infect and cause disease even in best online essay writer of normal nutriture.

The work has implications for troops deployed in the field. It may be possible that if a few soldiers are oxidatively stressed, as a result of a nutritional deficiency or severe physical activity, a viral pathogen could mutate into a potentially morevirulent pathogen and infect other soldiers who may or may not be oxidatively stressed. It would seem prudent to ensure that any food products provided for the troops contain a balance of nutrients to limit oxidative stress. Clearly, trace elements have been shown to be important for immune system functioning.

A deficiency in Cu, Zn, or Se has immunosuppressive effects on the host, which can lead to increased susceptibility to infectious disease. The usual model for understanding the effect of nutrition on infectious disease is diagrammed as follows:However, this author's work with Se and CVB3 demonstrates that host nutrition can affect not only the host but the pathogen as well. Therefore, the following model is proposed:This model takes into account not only best online essay writer effect that host nutriture has on the immune response but also the effect of host nutriture on the viral pathogen.

This model more accurately represents the relationship between nutrition and infectious disease. A number of studies, many of which have been cited in this paper, have examined the effect of trace elements on immune function. These studies are important, in that they indicate which immune parameters are sensitive to these nutrients. However, these studies are limited in that most do not correlate immune dysfunction with an actual increase in illness. For example, if a mild deficiency in Zn decreases T-cell proliferative responses by 20 percent, is this enough to increase susceptibility to infectious disease.

It is entirely possible that some of the immune changes induced by nutritional status will not result in increased incidence or duration of illness. The immune system has many redundant pathways, and measurements of one particular aspect of this systemmay not provide a true picture of the host's ability to respond to infection. This author recommends that any food supplement tested in military personnel for its effect on immune function should also be ranked for protection against illness.

Effects can be self-reported although this is the least reliable measure or medical personnel can record and monitor symptoms. Additionally, sampling of throat or nasal washes for common respiratory viruses could be obtained. Thus, a more ''real world'' indication of immune function-the ability to resist infection-can be determined. The combined effect of selenium deficiency and viral infection on the myocardium of mice. The effect of copper deficiency on the immune response in mice. Benign human enterovirus becomes virulent in selenium-deficient mice.

Vitamin E deficiency intensifies the myocardial injury of Coxsackievirus B3 infection of mice. Increased virulence of a human enterovirus Coxsackievirus B3 in selenium-deficient mice. Rapid genomic evolution of a non-virulent Coxsackievirus B3 in selenium-deficient mice results in selection of identical virulent isolates. Oxidative decay of DNA.

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