The community engagement course and action network: strengthening community and academic research partnerships to advance health equity.

Background: Historically Black Colleges and Universities and Minority Serving Institutions are uniquely positioned to implement community-campus research partnerships based on a history of service, the pursuit of community trustworthiness and student demographics often similar to surrounding marginalized communities. The Morehouse School of Medicine Prevention Research Center collaborates with members of Historically Black Colleges and Universities, Minority Serving Institutes, and community organizations on the Community Engaged Course and Action Network. This network is the first of its kind and aims to strengthen members' ability to implement Community-Based Participatory Research (CBPR) principles and partnerships. Projects address public health priorities including mental health among communities of color, zoonotic disease prevention, and urban food deserts. Materials and methods: To assess the effectiveness of the network, a Participatory Evaluation framework was implemented to conduct process evaluation which included review of partnership structures, operations, project implementation processes, and preliminary outcomes of the research collaborations. A focus group of Community Engagement Course and Action Network members (community and academic) was also conducted to identify benefits and challenges of the network with emphasis on key areas for improvement to further enhance the relationships between partners and to facilitate their subsequent community-campus research. Results: Network improvements were tied to themes strengthening community-academic partnerships including sharing and fellowship, coalition building and collaboration, and greater connections and awareness of community needs through their current community-academic partnerships. The need to conduct ongoing evaluation during and after implementation, for determining the early adoption of CBPR approaches was also identified. Conclusion: Evaluation of the network's processes, infrastructure, and operation provides early lessons learned to strengthen the network. Ongoing assessment is also essential for ensuring continuous quality improvement across partnerships such as determining CBPR fidelity, assessing partnership synergy, and dynamics, and for quality improvement of research protocol. The implications and potential for advancing implementation science through this and similar networks are great towards advancing leadership in modeling how foundations in community service can advance to CBPR partnership formation and ultimately, health equity approaches, that are local defined and assessed.

Virulence-associated sequence duplication at the hemagglutinin cleavage site of avian influenza viruses.

Recent highly pathogenic (HP) field isolates of avian influenza (AI) virus from Mexico all possess an insertion of at least two basic amino acids (arg-lys) at the cleavage site of the hemagglutinin (HA) glycoprotein. One HP isolate has additional information which yields a 4 amino acid insert (arg-lys-arg-lys). We present here the nucleotide sequence of the HA gene of this unique isolate and compare it to recent H5N2 and other avian influenza isolates. The complete HA nucleotide sequence of the isolate and phylogenetic relationship suggest that it was derived in direct succession from a non-pathogenic strain isolated about 1 month earlier. The unique insertion sequence is a direct duplication of part of the purine-rich region preceding the arginine codon at the HA cleavage site. This evidence along with other data in this report provide compelling support for a proposed model explaining the mechanism of spontaneous, virulence-related insertions in type A influenza viruses.

Association of Venezuelan equine encephalitis virus subtype IE with two equine epizootics in Mexico.

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.

Re-emergence of vesicular stomatitis in the western United States is associated with distinct viral genetic lineages.

Phylogenetic analysis of partial phosphoprotein and glycoprotein gene sequences showed that a single genetic lineage of vesicular stomatitis virus (VSV) serotype New Jersey (NJ) caused the 1995 and 1997 outbreaks of vesicular stomatitis (VS) in the western United States. While distinct from VSV-NJ strains causing previous outbreaks in the western United States and those circulating in feral swine in the southeastern United States, this lineage was closely related to viral lineages circulating in the Mexican states of Guerrero, Veracruz, and Oaxaca in 1996, 1989, and 1984 respectively. In 1997 and 1998, VSV serotype Indiana 1 (IN1) re-emerged in the western United States after 30 years. Viruses causing these outbreaks grouped within a single genetic lineage distinct from VSV-IN1 isolates causing outbreaks in the western United States in 1929 and 1956 but closely related to a strain circulating in the state of Colima in central Mexico in 1997. Our data showed that sporadic VS outbreaks in the western United States are caused by genetically distinct viral lineages closer to those circulating in enzootic areas of central and southern Mexico than to those causing previous outbreaks in the United States. The genetic evidence and temporal distribution of outbreaks are not consistent with a pattern of long-term maintenance of VSV in the western United States.

Complejos inmunes circulantes en ovinos infestados con Fasciola hepatica / Circulating immune complex in sheep infected with Fasciola hepatica

Se determinó la presencia de complejos inmunes circulantes (CIC) en 38 sueros de ovinos infestados con Fasciola hepatica y 15 sueros de ovinos libres del parásito, por precipitación con polietilenglicol 6000 (PEG) al 4, 6, 8 y 10%. La cantidad de proteína precipitada fue mucho mayor en los ovinos parasitados que en los testigos en todas las concentraciones de PEG utilizadas, observándose la mayor diferencia con PEG al 10%. Para corroborar la presencia de CIC se precipitaron los sueros con PEG al 2.5% y se determinó el consumo de complemento (CC) de estos precipitados obteniéndose valores promedio de 57% en los ovinos con fasciolasis y de 29% en los ovinos testigos. Se determinaron los títulos de anticuerpos contra F. hepatica por hemoaglutinación pasiva (HP), difusión doble en agar (DD) e inmunoensayo en capa delgada (ICD). No hubo relación entre la presencia de CIC y los títulos determinados en las pruebas serológicas, excepto en ICD dondo los sueros en títulos más altos fueron los sueros que dieron mayor preciptación con PEG y mayor CC