No abstract

A previous study from our laboratory showed that a mutant of herpes simplex virus type 1 (HSV-1), strain KOS-321, carrying a deletion in the structural gene for glycoprotein C (gC) had reduced pathogenicity for the mouse central nervous system when compared to the wild-type virus (Kümel et al., 1985). In this study, eight additional gC negative (gC-) mutants derived from KOS-321 were shown to vary widely in their ability to induce lethal encephalitis in female DBA/2 mice following intracerebral inoculation. This variation in virulence showed no correlation with thymidine kinase activity. One less virulent gC- strain, gC-39, was further studied to determine whether the neurovirulent phenotype could be restored by rescue of the gC gene using standard marker rescue cotransfection procedures. The resulting progeny contained 2% gC+ recombinant virions and was tested for its ability to cause encephalitis. Although this progeny had increased virulence, it was not attributable to the acquisition of the gC gene since passive immunization of mice with a pool of anti-gC monoclonal antibodies had no effect on the development of encephalitis and only gC- viruses were isolated from diseased brain tissues. In agreement with these findings, individual plaque-purified gC positive (gC+) virus recombinants were shown not to have been restored to the wild-type virus level of neurovirulence. It is concluded that gC is not a virulence determinant in this mouse model of HSV-induced encephalitis and that cotransfection procedures can induce additional mutations that affect viral pathogenesis.

Abstract. In September 1995, a Michigan resident with no history of international travel was diagnosed with Plasmodium vivax infection, and local mosquito-borne transmission was suspected. An epidemiological investigation did not identify additional cases of local transmission, and there was no apparent link to the 12 imported malaria cases detected in the region. Potential sites of nighttime outdoor exposure included a campground in a swampy area, close to a racetrack frequented by international travelers, some of whom were known to come from countries with malaria transmission. Entomological investigation identified Anopheles spp. larvae and adults near the campsite. Summer temperatures 4.2ЊC above average would have contributed to shortened maturation time of P. vivax within the insect vector, increasing the likelihood of infectivity. These investigations indicated that this patient probably acquired P. vivax infection through the bite of a locally infected Anopheles spp. mosquito. Physicians need to consider malaria as a possible cause of unexplained febrile illness, even in the absence of international travel, particularly during the summer months.