Geographic distribution of Venezuelan equine encephalitis virus subtype IE genotypes in Central America and Mexico

Phylogenetic analysis of 20 strains of Venezuelan equine encephalitis (VEE) virus subtype IE isolated from 1961 to 1996 in Mexico and throughout Central America showed that VEE virus subtype IE was monophyletic with respect to other VEE virus subtypes. Nonetheless, there were at least three distinct geographically separated VEE virus IE genotypes: northwestern Panama, Pacific coast (Mexico/Guatemala), and Gulf/Caribbean coast (Mexico/Belize). Strains from the Caribbean coast of Guatemala, Honduras, and Nicaragua may cluster with the Gulf/Caribbean genotype, but additional isolates from the region between Guatemala and Panama will be required to firmly establish their phylogenetic position. Viruses associated with two separate equine epizootics in Mexico in the 1990s were phlogenticaly related to nonepizootic viruses from neighbouring Guatemala and may represent the emergence or re-emergence of equine-virulent VEE virus subtype IE in Middle America.(AU)

The map1 gene of Cowdria ruminantium is a member of a multigene family containing both conserved and variable genes

Heartwater is an economically important disease of ruminants caused by the tick-transmitted rickettsia Cowdria ruminantium. The disease is present in Africa and the Caribbean and there is a risk of spread to the Americas, particularly because of a clinically asymptomatic carrier state in infected livestock and imported wild animals. The causative agent is closely related taxonomically to the human and animal pathogens Ehrlichia chaffeensis and Ehrlichia canis. A dominant immune response of infected animals or people is directed against variable outer membrane proteins of these agents known, in E. chaffeensis and E. canis, to be encoded by polymorphic multigene families. We demonstrate, by sequence analysis, the map1 encoding the major outer membrane protein of C. ruminantium is also encoded by a polymorphic multigene family. Two members of the gene family are located in tandem in the genome. The upstream member, orf2, is conserved, encoding only 2 amino acid substitution among six different rickettsial strains from diverse locations in Africa and the Caribbean. In contrast, the downstream member, map1, contains variable and conserved regions between strains. Interestingly, orf2 is more closely related in sequence to omplb of E. chaffeensis than to map1 of C. ruminantium. The regions that differ among orf2, map1, and omp1b correspond to previously identified variable sequences in outer membrane protein genes of E. chaffeensis and E. canis. These data suggest that diversity in these outer membrane proteins may arise by recombination among gene family members and offer a potential mechanism for persistence of infection in carrier animals.(AU)

Molecular evidence for the origin of the widespread Venezuelan equine encephalitis epizootic of 1969 to 1972

Venezuelan equine encephalitis (VEE) is a mosquito-borne pathogen that has caused encephalitis in equine species and humans during sporadic outbreaks in the western hemisphere. The last, and most widespread, VEE outbreak occurred in South America, Central America, Mexico and the U.S.A. (Texas) during 1969 to 1972. We have cloned and sequenced the genome of a virulent VEE subtype I-AB virus, strain 71-180, isolated in Texas in 1971. Thirty four nucleotide differences were detected between the genome of 71-80 virus and that of subtype I-AB Trinidad donkey (TRD) virus isolated during the 1943 VEE epizootic in Trinidad. Fifteen nucleotide changes occurred in the non-structural genes, 16 in the structural genes and three in the 3' non-coding region. Only six of the nucleotide diferences resulted in amino acid substitutions: one change in each of non-structural proteins nsP1 and nsP3, two in the E2 envelope glycoprotein, one in the 6K popypeptide and one in the E1 envelope glycoprotein. The close genetic relationship between 71-180 virus and TRD virus, commonly used for production of formalin-inactivated VEE vaccines, suggests that incompletely inactivated virulent vaccine virus may have been the source of this and other VEE outbreaks. Use of formalized virulent virus was discontinued during the 1969 to 1972 panzootic. No VEE epizootics have been reported since the introduction of the live attenuated TC-83 vaccine virus (AU)

Segregation of human T cell lymphotropic virus type I and II infections by antibody reactivity to unique viral epitopes

A recombinant protein of the human T cell lymphotropic virus type I (HTLV-I) gp46 outer membrane envelope, MTA-4 (residues 129-203), reacted by Western blot with sera from HTLV-I-infected individuals from the United States and Jamaica but not with 24 (10 percent) of 242 Japanese sera. A related gp46 recombinant protein, MTA-1 (residues 162-209), reacted with all 58 sera from HTLV-I-infected US and Jamaican individuals and 238 of 242 sera from infected Japanese (combined sensitivity of 99 percent). Neither recombinant showed reactivity to sera from HTLV-II-infected individuals or uninfected controls. The reactivity of recombinant proteins containing the region of HTLV-II gp46 analogous to MTA-1 was also evaluated by Western blot: GH2-K15 (residues 157-205) and GH2-K55 (residues 162-205) reacted with 88 (98 percent) and 89 (99 percent), respectively, of 90 sera from HTLV-II-infected individuals but not with sera from HTLV-I-infected individuals or uninfected controls. These recombinant proteins should permit the development of assays to unambiguously confirm and differentiate HTLV-I and HTLV-II infections. (AU)

Molecular cloning and complete nucleotide sequence of an adult T cell leukaemia virus/human T cell leukaemia virus type I (ATLV/HTLV-I) isolate of Caribbean origin:Relationship to other members of the ATLV/HTLV-I subgroup

We report the first complete nucleotide sequence of an adult T cell leukaemia virus/human T cell leukaemia virus type I (ATLV/HTLV) isolate from a British patient of Caribbean origin. Sequence comparisons of our proviral clone (HS-35) with other molecular clones are shown. We note the strong sequence conservation between isolates of Caribbean and Japanese origin (2.3 percent divergence), but demonstrate the higher homologies existing between isolates originating from similar geographical areas (approximately 1 percent divergence). Implications for the origin, evolution and dissemination of the ATLV/HTLV-I subgroup are discussed. Analysis of defective proviral clones isolated from the same genomic library is also reported,and suggests a pattern of proviral sequence deletions during the biogenesis of defective proviruses. (AU)

Hb F Kingston (G gamma 55 (D6) Met leads to Arg)

A fetal haemoglobin variant was noted in a healthy Jamaican infant of mixed African/Chinese extration. A two-dimensional chromatogram of the soluble tryptic peptides (Tp) showed 2 'new' ones. One was composed of the last 4 residues of the usually insoluble Tpgamma41-59. To permit a tryptic split this required a change of residue gamma 55 Met to Lys or Arg. The other new Tp contained arginine and was in the position expected for a Ty gamma41-55 (55 Arg). As the material was limited it could not be analysed. When after more than 6 years no example of Hb F Kingston had become available it was decided to describe the variant on the basis of the present evidence. (AU)

Haemoglobin Spanish Town alpha27 Glu replaced by Val (B8)

A new alpha chain variant Hb Spanish Town, a27 Glutamic acid-Valine, awas detected in the cord blood of a Jamaica Negro infant. In the mother the adult component (a2 Spanish TownB2) has an electrophoretic mobility between haemoglobins S and F at alkaline pH and measures 11.0-12.0 percent of the total haemoglobin. (Summary)

Hemoglobin F Port Royal (alpha2G gamma2 125 GLU leads to Ala)

A Gy-chain variant, Hb F Port Royal, with an electrophoretic mobility intermediate between Hb S and Hb C was found in a Jamaican-Negro infant, and made up to 14-15 percent of the total Hb F. A glycinamidation procedure was employed to aid in the determining the amino-acid residu substitution of gamma 123 Glu leads to Ala, and the presence of glycine in position 136. (AU)