Academic journal article Bulletin of the World Health Organization

Interrupting the Transmission of Wild Polioviruses with Vaccines: Immunological Considerations

Academic journal article Bulletin of the World Health Organization

Interrupting the Transmission of Wild Polioviruses with Vaccines: Immunological Considerations

Article excerpt

Introduction

In May 1988, the 41st World Health Assembly established the goal of global eradication of poliomyelitis by the year 2000. Specific targets include both the elimination of paralytic disease caused by wild poliovirus and the elimination of the wild virus itself.

Progress has been rapid in eliminating disease due to wild poliovirus. In 1993, a total of 143 countries/territories reported to WHO no cases of poliomyelitis associated with the wild virus. Areas that are free of poliomyelitis now include North America, South America, Japan, and Australia. In addition, disease-free zones appear to be emerging in southern Africa, North Africa, Europe, the Middle East, and the Western Pacific.

The eradication of poliomyelitis is often compared with that of smallpox. However, in contrast to infection with variola virus, most persons infected with poliovirus remain asymptomatic and can excrete the virus for several months. Outbreaks of poliomyelitis in Finland (2), the Netherlands (3, 4), and Oman (5) suggest that wild polioviruses can replicate in well-immunized persons who have no clinical disease, spread to other persons, and eventually induce paralytic poliomyelitis in susceptible individuals.

This review examines the immunological considerations relevant to interrupting the asymptomatic transmission of wild polioviruses with vaccines. Summarized are published studies from two eras. First, to review the mechanisms of spread of poliovirus and the immune response of individuals to infection with wild and vaccine viruses, particular attention has been paid to studies conducted in the 1950s and 1960s. Second, to gain insight into recent transmission patterns of polioviruses, selected lessons from recent poliomyelitis outbreaks are reviewed.

Mechanisms of person-to-person

spread of polioviruses

By the mid 1960s, the pathology of poliomyelitis had been well described (6). The course of poliovirus infection can be divided into the following steps: implantation and replication of the virus at the primary portals of entry (the oropharyngeal mucosa and the intestinal mucosa); spread of the virus to the tonsils and deep cervical nodes in the oropharyngeal region and to Peyer's patches and the mesenteric lymph nodes in the lower alimentary tract; entry of the virus into the bloodstream, resulting in viraemia; and establishment of infection in the central nervous system.

Poliovirus can implant and replicate independently in the throat or the intestine (7). Virus is shed from the nasopharynx for up to 3-4 weeks after infection and can be isolated from the throat for about a week, with peak levels of [10.sup.5] - [10.sup.6] [TCID.sub.50] per swab (8). Large amounts of virus are shed in the faeces for up to 5-6 weeks (9). Once excreted, poliovirus can survive outside the human body for weeks at room temperature and for many years at -20[degrees]C (10).

There are two routes of spread of poliovirus - faecal-oral and nasopharyngeal - and their importance varies, depending on the level of sanitation and the population density. Where sewerage systems are well developed and water remains uncontaminated, the faecal-oral mode of spreading will be reduced. For countries where the level of sanitation is high, the main route of poliovirus infection is droplets or aerosol from the nasopharynx; whereas, for countries with a low level of sanitation, infection is mainly by the faecal-oral route (11). However, to some extent this classification is artificial, since in all countries infant stools are an important source of faecal-oral spread and in all countries coughing and sneezing can spread polioviruses.

Immunity and the role of different

classes of antibodies

Natural infection with poliovirus initiates a complex process that eventually results in both humoral and mucosal immunity. Both humoral and mucosal immunity are important in protecting the individual against paralytic poliomyelitis. …

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