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Showing papers by "Scott C. Weaver published in 1998"


Journal ArticleDOI
TL;DR: Two outbreaks of encephalitis consistent with an etiology of Venezuelan equine encephalitis (VEE) virus occurred in equines on the Pacific coast of southern Mexico in 1993 (Chiapas State) and in 1996 (Oaxaca State).
Abstract: Two outbreaks of encephalitis consistent with an etiology of Venezuelan equine encephalitis (VEE) virus occurred in equines on the Pacific coast of southern Mexico in 1993 (Chiapas State) and in 1996 (Oaxaca State). In Chiapas, there were 125 cases, of which 63 were fatal and in Oaxaca, there were 32 cases and 12 fatalities. Virus was isolated from two horses from each outbreak, including three brain isolates and one from blood. Virus isolates (93-42124, ISET-Chi93, Oax131, and Oax142) were shown by indirect immunofluorescence, hemagglutination inhibition, monoclonal antibody ELISA, and nucleotide sequencing to be VEE virus, subtype IE, a type previously thought to be equine-avirulent. Genetic characterization and phylogenetic analysis indicated that the outbreak viruses were identical or nearly identical to one another and that they were closely related to equine-avirulent IE strains from Guatemala and the Gulf coast of Mexico. In a plaque-reduction neutralization test, sera collected from healthy horses in Chiapas and Oaxaca reacted significantly better with isolate 93-42124 than with Guatemala IE isolate 68U201, suggesting that subtle genetic changes may have resulted in alteration of neutralization domains. It is not clear whether these differences may also influence equine virulence. However, renewed VEE virus subtype IE activity in Mexico, and its apparent conversion to equine virulence, underscores the need for increased surveillance, additional laboratory and epidemiologic studies in VEE-endemic regions, and possibly new vaccines.

74 citations


Journal ArticleDOI
TL;DR: E1 gene nucleotide sequences of 63 rubella virus isolates from North America, Europe, and Asia isolated between 1961 and 1997 were compared phylogenetically, indicating evolution in response to vaccination programs.
Abstract: E1 gene nucleotide sequences of 63 rubella virus isolates from North America, Europe, and Asia isolated between 1961 and 1997 were compared phylogenetically. Two genotypes were evident: Genotype I contained 60 viruses from North America, Europe, and Japan, and genotype II contained 3 viruses from China and India. The genotype I isolates prior to 1970 grouped into a single diffuse clade, indicating intercontinental circulation, while most post-1975 viruses segregated into geographic clades from each continent, indicating evolution in response to vaccination programs. The E1 amino acid sequences differed by no more than 3%; thus, no major antigenic variation was apparent. Among 4 viruses from congenital rubella syndrome that occurred following reinfection, only one amino acid substitution occurred in several important epitopes, indicating that antigenic drift is not important in this phenomenon. However, 2 viruses isolated from chronic arthritis exhibited changes in these epitopes. Isolates of the RA 27/3 vaccine strain were readily identifiable by nucleotide sequence.

61 citations


Book ChapterDOI
01 Jan 1998
TL;DR: Phylogenetic studies of the two recent, northern South American VEE outbreaks have further supported the hypothesis of evolution and emergence of epidemic/epizootic IAB/IC viruses from enzootic ID-like progenitors.
Abstract: Venezuelan equine encephalomyelitis (VEE) viruses are positive-strand, unsegmented RNA viruses in the genus Alphavirus of the family Togaviridae. The first phylogenetic analyses of the VEE complex, based on partial nsP4, El, and 3' untranslated sequences, indicated that IAB, IC, and ID viruses are closely related and have a recent common ancestor. This work also suggested that epidemic/epizootic VEE viruses evolved from ID progenitors on more than one occasion. Several hypotheses for VEE emergence were proposed, including (i) maintenance of IAB and/or IC viruses in continuous, cryptic transmission cycles; (ii) maintenance of IAB and/or IC viruses in latent equine or other animal infections; (iii) reemergence of epizootic viruses following administration of incompletely inactivated vaccine preparations; (iv) maintenance of IAB and/or IC viruses as minority subpopulations within enzootic virus populations; and (v) periodic emergence of epizootic viruses via mutations of enzootic strains. Phylogenetic studies of the two recent, northern South American VEE outbreaks have further supported the hypothesis of evolution and emergence of epidemic/epizootic IAB/IC viruses from enzootic ID-like progenitors. Current phylogenetic trees, obtained from reverse transcription-polymerase chain reaction products of 857 nucleotides derived from the E3 and E2 genes, identify three distinct monophyletic groups or lineages of epizootic/ epidemic VEE viruses. The most important gaps remaining in one's understanding of epidemic/epizootic VEE emergence concern the viral determinants of virulence and the pathogenesis changes that lead to high-viremia-facilitated transmission among equines and other large mammals.

50 citations


Journal ArticleDOI
TL;DR: A novel Rickettsia species of undetermined pathogenicity was detected in Ixodes scapularis and DNA sequencing showed the highest nucleotide sequence similarities with R. australis for the 17 kDa gene, R. helvetica for gltA, and R. montana for rompA.
Abstract: A novel Rickettsia species of undetermined pathogenicity was detected in Ixodes scapularis. DNA sequencing showed the highest nucleotide sequence similarities with R. australis for the 17 kDa gene, R. helvetica for gltA, and R. montana for rompA. The new organism, provisionally designated as genotype Cooleyi, is highly divergent in three conserved genes from recognized Rickettsia species.

44 citations


Journal ArticleDOI
TL;DR: The recent Iquitos VEE viral isolates were the first Panama-genotype VEE ID virus strains identified outside of the Republic of Panama, and were more closely related to Panamanian ID strains than to isolates previously obtained in Iquito, Peru, or in Colombia and Venezuela.
Abstract: Venezuelan equine encephalitis (VEE) virus was isolated in 1993, 1994, and 1995 from human cases of acute, undifferentiated, febrile illness in the Peruvian Amazon Basin. Two virus isolates were recovered in 1994 from Peruvian soldiers at a jungle outpost near Pantoja in northern Peru, and 10 isolates were obtained from military personnel and civilians in 1993-1995 in Iquitos, an urban center in northeastern Peru. The genetic relationship of these isolates to other VEE virus strains was determined by sequencing 856-867 nucleotide reverse transcription-polymerase chain reaction fragments derived from the PE2 glycoprotein gene. The sequences were compared with those of other VEE virus strains, including representatives of the IAB, IC, ID, IE, II, and IIIC subtypes. The two Pantoja isolates were most closely related to subtype IC and ID viruses previously isolated in Colombia and Venezuela, and to the ID viruses isolated during the 1970s in Iquitos. All of the recent Iquitos isolates were similar to one another, but they were more closely related to Panamanian ID strains than to isolates previously obtained in Iquitos, Peru, or in Colombia and Venezuela. The recent Iquitos VEE viral isolates were the first Panama-genotype VEE ID virus strains identified outside of the Republic of Panama.

35 citations