Jose G. Estrada-Franco

West Nile virus in Mexico: evidence of widespread circulation since July 2002.

West Nile virus (WNV) antibodies were detected in horses from five Mexican states, and WNV was isolated from a Common Raven in the state of Tabasco. Phylogenetic studies indicate that this isolate, the first from Mexico, is related to strains from the central United States but has a relatively high degree of sequence divergence.

Human Trypanosoma cruzi Infection and Seropositivity in Dogs, Mexico

Seroanalysis of parasite circulation in dogs can help identify T. cruzi infection in humans.

Genome sequence and attenuating mutations in West Nile virus isolate from Mexico.

The complete genome sequence of a Mexican West Nile virus isolate, TM171-03, included 46 nucleotide (0.42%) and 4 amino acid (0.11%) differences from the NY99 prototype. Mouse virulence differences between plaque-purified variants of TM171-03 with mutations at the E protein glycosylation motif suggest the emergence of an attenuating mutation.

Introductions of West Nile Virus Strains to Mexico

Complete genome sequencing of 22 West Nile virus isolates suggested 2 independent introductions into Mexico. A previously identified mouse-attenuated glycosylation variant was introduced into southern Mexico through the southeastern United States, while a common US genotype appears to have been introduced incrementally into northern Mexico through the southwestern United States.

Use of a Recombinant Envelope Protein Subunit Antigen for Specific Serological Diagnosis of West Nile Virus Infection

ABSTRACT Serological diagnosis of West Nile virus (WNV) infection is complicated by extensive antigenic cross-reactivity with other closely related flaviviruses, such as St. Louis encephalitis virus. Here we describe a recombinant, bacterially expressed antigen equivalent to structural domain III of the WNV envelope protein that has allowed clear discrimination of antibody responses to WNV from those against other related flaviviruses in indirect enzyme-linked immunosorbent assays using standardized control antisera and field-collected samples.

Genetic determinants of Venezuelan equine encephalitis emergence.

Following a period of inactivity from 1973-1991, Venezuelan equine encephalitis (VEE) reemerged during the past decade in South America and Mexico. Experimental studies of VEE virus (VEEV) infection of horses with virus strains isolated during these outbreaks have revealed considerable variation in the ability of equine-virulent, epizootic strains to exploit horses as efficient amplification hosts. Subtype IC strains from recent outbreaks in Venezuela and Colombia amplify efficiently in equines, with a correlation between maximum viremia titers and the extent of the outbreak from which the virus strain was isolated. Studies of enzootic VEEV strains that are believed to represent progenitors of the epizootic subtypes support the hypothesis that adaptation to efficient replication in equines is a major determinant of emergence and the ability of VEEV to spread geographically. Correlations between the ability of enzootic and epizootic VEEV strains to infect abundant, equiphilic mosquitoes, and the location and extent of these outbreaks, also suggest that specific adaptation to Ochlerotatus taeniorhynchus mosquitoes is a determinant of some but not all emergence events. Genetic studies imply that mutations in the E2 envelope glycoprotein gene are major determinants of adaptation to both equines and mosquito vectors.

Venezuelan Equine Encephalitis Virus, Southern Mexico

Evidence of enzootic and endemic Venezuelan equine encephalitis virus circulation in southern Mexico since the 1996 epizootic was obtained from serosurveys and virus isolations.

Equine amplification and virulence of subtype IE Venezuelan equine encephalitis viruses isolated during the 1993 and 1996 Mexican epizootics.

To assess the role of horses as amplification hosts during the 1993 and 1996 Mexican Venezuelan equine encephalitis (VEE) epizootics, we subcutaneously infected 10 horses by using four different equine isolates. Most horses showed little or no disease and low or nonexistent viremia. Neurologic disease developed in only 1 horse, and brain histopathologic examination showed meningeal lymphocytic infiltration, perivascular cuffing, and focalencephalitis. Three animals showed mild meningoencephalitis without clinical disease. Viral RNA was detected in the brain of several animals 12-14 days after infection. These data suggest that the duration and scope of the recent Mexican epizootics were limited by lack of equine amplification characteristic of previous, more extensive VEE outbreaks. The Mexican epizootics may have resulted from the circulation of a more equine-neurotropic, subtype IE virus strain or from increased transmission to horses due to amplification by other vertebrate hosts or transmission by more competent mosquito vectors.

West Nile Virus Infection of Birds, Mexico

Birds of 2 of 3 passerine species died after experimental infection with 2 strains from Mexico.

The continuous spread of West Nile virus (WNV): seroprevalence in asymptomatic horses

West Nile virus (WNV) was probably introduced in southern and northern Mexico from the USA in two independent events. Since then, WNV activity has been reported in several Mexican states bordering the USA and the Gulf of Mexico, but disease manifestations seen there in humans and equids are quite different to those observed in the USA. We have analysed WNV seroprevalence in asymptomatic, unvaccinated equids from two Mexican states where no data had been previously recorded. WNV IgG antibodies were detected in 31.6% (91/288) of equine sera from Chiapas and Puebla states (53.3% and 8.0%, respectively). Analysis by plaque reduction neutralization test (PRNT) showed good specificity (99.4%) and sensitivity (84.9%) with the ELISA results. Further analyses to detect antibodies against three different flaviviruses (WNV, St Louis encephalitis virus, Ilheus virus) by haemagglutination inhibition (HI) tests on a subset of 138 samples showed that 53% of the 83 HI-positive samples showed specific reaction to WNV. These data suggest continuous expansion of WNV through Mexico.