Reproductive toxicology. Diethylphthalate.

Poliomyelitis has afflicted humankind since antiquity, and for nearly a century now, we have known the causative agent, poliovirus. This pathogen is an enterovirus that in recent history has been the source of a great deal of human suffering. Although comparatively small, its genome is packed with sufficient information to make it a formidable pathogen. In the last 20 years the Global Polio Eradication Initiative has proven successful in greatly diminishing the number of cases worldwide but has encountered obstacles in its path which have made halting the transmission of wild polioviruses a practical impossibility. As we begin to realize that a change in strategy may be crucial in achieving success in this venture, it is imperative that we critically evaluate what is known about the molecular biology of this pathogen and the intricacies of its interaction with its host so that in future attempts we may better equipped to more effectively combat this important human pathogen. Background The word poliomyelitis, the medical term used to describe the effect of poliovirus (PV) on the spinal cord, is derived from the Greek words for gray (polio) and marrow (myelon). The first known clinical description of poliomyelitis is attributed to Michael Underwood, a British physician, who in 1789 reported observing an illness which appeared to target primarily children and left those afflicted with residual debility of the lower extremities. In subsequent years, additional cases of poliomyelitis would be reported. Initial outbreaks in Europe were documented in the early 19th century and outbreaks in the United States were first reported in 1843. However, it was not until the early 20th century that the number of paralytic poliomyelitis cases reached epidemic proportions. In 1938, in efforts to support care for patients with poliomyelitis as well as fund research to combat the illness, the National Foundation for Infantile Paralysis (now the March of Dimes) was established. The number of paralytic cases in the United States, estimated to have been in excess of 21,000, peaked in 1952. Fortunately, on April 12, 1955, the March of Dimes declared that the Salk polio vaccine was both safe and effective. Then, in 1963, the development of a second vaccine, the Sabin polio vaccine, was announced. With the introduction of effective vaccines, the incidence of poliomyelitis rapidly declined. Indeed, in the United States, the last case of poliomyelitis due to infection with wild type (wt) virus was reported in 1979. Less than a decade later, in 1988, the World Health Organization (WHO) launched a global campaign to eradicate PV. Since initial descriptions of poliomyelitis were first documented to the present time, innumerable milestones have been reached in understanding the molecular biology of PV and the pathogenesis of poliomyelitis. Such advances have certainly led to the more effective management of Published: 10 July 2007 Virology Journal 2007, 4:70 doi:10.1186/1743-422X-4-70 Received: 27 May 2007 Accepted: 10 July 2007 This article is available from: http://www.virologyj.com/content/4/1/70 © 2007 De Jesus; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.