313 research outputs found
Letter from Dr. Beaty to Dr. Koch
Letter Thanking Dr Koch for agreeing to give lecture Fibrolysis and Fibrotherapy on Oct 25, 1999 at San Francisco AOA Convention
Letter from Dr. Beaty to Dr. Koch
Thanks Dr Koch for agreeing to give lecture Fibrolysis and Fibrotherapy on Oct 25, 1999 at San Francisco AOA Convention
Dengue virus type 2: replication and tropisms in orally infected Aedes aegypti mosquitoes
BACKGROUND: To be transmitted by its mosquito vector, dengue virus (DENV) must infect midgut epithelial cells, replicate and disseminate into the hemocoel, and finally infect the salivary glands, which is essential for transmission. The extrinsic incubation period (EIP) is very relevant epidemiologically and is the time required from the ingestion of virus until it can be transmitted to the next vertebrate host. The EIP is conditioned by the kinetics and tropisms of virus replication in its vector. Here we document the virogenesis of DENV-2 in newly-colonized Aedes aegypti mosquitoes from Chetumal, Mexico in order to understand better the effect of vector-virus interactions on dengue transmission. RESULTS: After ingestion of DENV-2, midgut infections in Chetumal mosquitoes were characterized by a peak in virus titers between 7 and 10 days post-infection (dpi). The amount of viral antigen and viral titers in the midgut then declined, but viral RNA levels remained stable. The presence of DENV-2 antigen in the trachea was positively correlated with virus dissemination from the midgut. DENV-2 antigen was found in salivary gland tissue in more than a third of mosquitoes at 4 dpi. Unlike in the midgut, the amount of viral antigen (as well as the percent of infected salivary glands) increased with time. DENV-2 antigen also accumulated and increased in neural tissue throughout the EIP. DENV-2 antigen was detected in multiple tissues of the vector, but unlike some other arboviruses, was not detected in muscle. CONCLUSION: Our results suggest that the EIP of DENV-2 in its vector may be shorter that the previously reported and that the tracheal system may facilitate DENV-2 dissemination from the midgut. Mosquito organs (e.g. midgut, neural tissue, and salivary glands) differed in their response to DENV-2 infection
Presencia del virus del oeste del Nilo en el noreste de México
Objetivo. Detectar la presencia del virus del oeste del
Nilo (VON) en aves, equinos y seres humanos en el noreste de México. Material y métodos. Se buscó en diferentes localidades del noreste de México la presencia de anticuerpos antivirus del oeste del Nilo (anti-VON) en suero de 33 aves, 24 caballos y 237 personas mediante pruebas de ELISA durante el periodo de julio de 2003 a julio de 2006. En los
sueros humanos se buscó también el RNA-VON mediante RT-PCR. Resultados. Se encontraron tres aves seropositivas y 15 equinos. En el hombre, 40% de los sueros fue positivo para anticuerpos IgG y ninguno para anticuerpos IgM. Conclusiones.
El VON se encuentra activo en México y se suma
a otras enfermedades emergentes transmitidas por vectores que representan un reto a la investigación y a los programas de prevención
PUBLIC HEALTH Assessment of Ecologic and Biologic Factors Leading to Hantavirus Pulmonary Syndrome, Colorado, U.S.A
Aim. To understand the ecologic parameters of Sin Nombre virus (SNV; family Bunyaviridae, genus Hantavirus) infections in the deer mouse (Peromyscus maniculatus), environmental variables impacting the rodent populations, and the conditions under which SNV is amplified. This may help us understand the antecedents of human risk for developing hantavirus pulmonary syndrome (HPS) as a consequence of SNV infection. Method. Each 6 weeks, we trapped, measured, tagged, bled, and released rodents at three widely spaced sites in Colorado, USA: Fort Lewis (1994Lewis ( -2001, Molina (1994Molina ( -2001, and Pinyon Canyon Maneuver Site (1995)(1996)(1997)(1998)(1999)(2000)(2001). The ELISA method was used to test rodent blood samples for IgG antibody to SNV antigen. Results. Where rodent species richness was high, the prevalence of infection of deer mice (as determined by the presence of antibody) with SNV was low, and vice versa. There was a higher prevalence of antibody to SNV in male than in female rodents, and seasonal differences were observed in acquisition of SNV between male and female deer mice. Long-lived infected deer mice served as transseasonal, over-winter reservoirs for the virus, providing the mechanism for its survival. Conclusion. Prevalence of rodent infection appears to be associated with fluctuations in deer mouse populations and, indirectly, with timing and amount of precipitation and the resulting biologic events (a "trophic cascade"). Together with information regarding transseasonal maintenance of SNV, seasonal differences in acquisition of SNV between sexes, group foraging, and various other factors may expand our understanding of the risk factors for acquiring HPS. Taken together and applied, we anticipate developing methods for preventing this disease as well as diseases caused by other rodent-borne viruses
Natural history of Sin Nombre virus in western Colorado.
A mark-recapture longitudinal study of immunoglobulin G (IgG) antibody to Sin Nombre virus (SNV) in rodent populations in western Colorado (1994-results summarized to October 1997) indicates the presence of SNV or a closely related hantavirus at two sites. Most rodents (principally deer mice, Peromyscus maniculatus, and pinyon mice, P. truei) did not persist on the trapping webs much beyond 1 month after first capture. Some persisted more than 1 year, which suggests that even a few infected deer mice could serve as transseasonal reservoirs and mechanisms for over-winter virus maintenance. A positive association between wounds and SNV antibody in adult animals at both sites suggests that when infected rodents in certain populations fight with uninfected rodents, virus amplification occurs. At both sites, male rodents comprised a larger percentage of seropositive mice than recaptured mice, which suggests that male mice contribute more to the SNV epizootic cycle than female mice. In deer mice, IgG antibody prevalence fluctuations were positively associated with population fluctuations. The rates of seroconversion, which in deer mice at both sites occurred mostly during late summer and midwinter, were higher than the seroprevalence, which suggests that the longer deer mice live, the greater the probability they will become infected with SNV
Population Dynamics Of A Diverse Rodent Assemblage In Mixed Grass-Shrub Habitat, Southeastern Colorado, 1995–2000
We followed seasonal and year-to-year population dynamics for a diverse rodent assemblage in a short-grass prairie ecosystem in southeastern Colorado (USA) for 6 yr. We captured 2,798 individual rodents (range, one to 812 individuals per species) belonging to 19 species. The two most common species, deer mice (Peromyscus maniculatus) and western harvest mice (Reithrodontomys megalotis), generally had population peaks in winter and nadirs in summer; several other murid species demonstrated autumn peaks and spring nadirs; heteromyids were infrequently captured in winter, and populations generally peaked in summer or autumn. Interannual trends indicated an interactive effect between temperature and precipitation. Conditions associated with low rodent populations or population declines were high precipitation during cold periods (autumn and winter) and low precipitation during warm periods (spring and summer). Severity of adverse effects varied by species. Heteromyids, for example, were apparently not negatively affected by the hot, dry spring and summer of 2000. Cross-correlations for the temporal series of relative population abundances between species pairs (which are affected by both seasonal and interannual population dynamics) revealed positive associations among most murids and among most heteromyids, but there were negative associations between murids and heteromyids. These results have important implications for those attempting to model population dynamics of rodent populations for purposes of predicting disease risk
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