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Smallpox: The Main Site of Transmission is the OropharynxDepartment of Microbiology & Immunology, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-1019; sabaron{at}utmb.edu
Key Words: smallpox • transmission • shedding • oropharynx The threat of a bioterrorist attack with smallpox virus is real because immunity of our population is low (Cohen, 2001). In response to this threat, interruption of oral shedding may be an important area for study. Often unrecognized is that infected persons shed most smallpox virus from the epithelium of the naso-oropharynx and salivary glands (Dixon, 1962; Suvakovic and Kecmanovic, 1976; Fenner et al., 1988; Henderson et al., 1999; Smee et al., 2001; Whitby et al., 2002). The titer of infectious virus shed from the naso-oropharynx is 106-108 compared with 10- to 100-fold lower titers in the lungs and the skin during natural infection. The high levels of virus in the oropharynx result from virus multiplication in the mucosa after viremic dissemination into that site, which occurs at the same time as dissemination to the skin and lungs. Oropharyngeal shedding theoretically can be controlled by several measures, such as isolation procedures (Henderson et al., 1999), immunization (Hochstein-Mintzel et al., 1972), natural antiviral substances in saliva (Baron, 2001), antiviral drugs such as Cidofovir (Smee et al., 2001), antibody, and disinfection of air (Henderson et al., 1999). In addition, practical and immediate interruption of oropharyngeal shedding may be accomplished by topical antiviral agents such as microbicides (Baron et al., 2001). Decisive studies of the mechanisms of shedding and techniques to decrease oropharyngeal shedding of poxviruses were curtailed when smallpox was eliminated about 30 years ago (Henderson et al., 1999; Cohen, 2001). It may be reasonable to conclude that resumption of studies of oropharyngeal shedding of poxviruses and methods for interruption should be given high priority by scientists in the dental and infectious disease areas of research. Received for publication December 16, 2002. Accepted for publication December 17, 2002. REFERENCES
Journal of Dental Research, Vol. 82, No. 4,
252 (2003) This article has been cited by other articles:
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