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1.
Clin Microbiol Infect ; 29(4): 540.e9-540.e15, 2023 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-36423864

RESUMEN

OBJECTIVES: To characterize the timing and genotype distribution of symptomatic and asymptomatic sapovirus infections and re-infections in a Nicaraguan birth cohort. METHODS: Infants (N = 444) were enrolled at 10-14 days of life and observed weekly until 2 years of age. Stool samples were collected for each acute gastroenteritis (AGE) episode, and routine stool samples were collected monthly. Stool samples were tested for sapovirus using RT-qPCR, and positive samples were genotyped. RESULTS: A total of 348 children completed 2 years of AGE weekly surveillance; 93 (26.7%) of them experienced sapovirus AGE. Most infections occurred after 5 months of age and mainly during the second year of life (62.4%, 58/93) and early in the rainy season. Sapovirus screening in all stools from a subset of 67 children who consistently provided samples showed sapovirus infections in 91 of 330 (27.6%) AGE episodes and in 39 of 1350 (2.9%) routine stools. In this subset, the median age at the first sapovirus AGE was 11.2 months (95% CI, 9.3-15.9 months); 38 of 67 (57%) children experienced re-infections, 19 symptomatic and 19 asymptomatic. On average, sapovirus re-infections were reported 7.2 months after symptomatic and 5.3 months after asymptomatic infections. Genogroup GI (64%, 69/108) was the most common detected. Sapovirus GI.1 was more frequently detected in AGE stool samples than in routine stool samples (47.2%, 43/91 vs. 25.6%, 10/39; p 0.005), and re-infection with the same genotype was uncommon. DISCUSSION: The first sapovirus infections occurred at approximately 11 months of age, whereas the median time to symptomatic re-infection was 7.2 months. Re-infections with the same sapovirus genotype were rare during 2 years of life suggesting genotype-specific protection after natural infection.


Asunto(s)
Infecciones por Caliciviridae , Sapovirus , Lactante , Niño , Humanos , Reinfección , Sapovirus/genética , Cohorte de Nacimiento , Infecciones Asintomáticas/epidemiología , Infecciones por Caliciviridae/epidemiología , Infecciones por Caliciviridae/diagnóstico , Filogenia , Genotipo , Heces
2.
J Anim Ecol ; 89(10): 2367-2377, 2020 10.
Artículo en Inglés | MEDLINE | ID: mdl-32688437

RESUMEN

Co-infections by multiple parasites are common in natural populations. Some of these are likely to be the result of sequential rather than simultaneous infections. The timing of the co-infections may affect their competitive interactions, thereby influencing the success of the parasites and their impact on the host. This may have important consequence for epidemiological and eco-evolutionary dynamics. We examined in two ecological conditions the effect of sequential co-infection on the outcome of infection by two microsporidians, Vavraia culicis and Edhazardia aedis, that infect the mosquito Aedes aegypti. The two parasites have different transmission strategies: V. culicis is transmitted horizontally either among larvae or from adults to larvae, while E. aedis can be transmitted horizontally among larvae or vertically from females to their eggs. We investigated how the timing and order of the co-infection and how the host's food availability affected the parasite's transmission potential (the percentage of individuals that harboured transmissible spores) and the host's juvenile survival, its age at emergence and its longevity. The outcome of co-infection was strongly affected by the order at which the parasites arrived. In co-infections, V. culicis had greater horizontal transmission if it arrived early, whereas the transmission potential of E. aedis, either vertical or horizontal, was not affected by the competitor V. culicis. The availability of food determined the duration of infection leading to variation in mortality and in the transmission potential. For both parasites low food decreased juvenile survival, delayed emergence to adulthood and increased horizontal transmission potential. High food increased juvenile survival and the probability of emergence with higher vertical transmission for E. aedis. Overall, our results suggest that early infection favours transmission and that (a) V. culicis plastically responded to co-infection, (b) E. aedis was not affected by co-infection but it was more susceptible to factors extending or decreasing the time it spent in the host (time of infection and food). Our results emphasize the complexity of the impact of co-infection on host-parasite interactions. In particular, the timing and order of sequential co-infections can result in different within-host dynamics and modify infection outcomes.


Asunto(s)
Coinfección , Microsporidios , Parásitos , Animales , Coinfección/veterinaria , Femenino , Interacciones Huésped-Parásitos
3.
Front Microbiol ; 8: 2152, 2017.
Artículo en Inglés | MEDLINE | ID: mdl-29163436

RESUMEN

Synchronous viral infection facilitates the study of viral gene expression, viral host interactions, and viral replication processes. However, the protocols for achieving synchronous infections were hardly ever tested in proper temporal resolution at the single-cell level. We set up a fluorescence-based, time lapse microscopy assay to study sources of variability in the timing of gene expression during herpes simplex virus-1 (HSV-1) infection. We found that with the common protocol, the onset of gene expression within different cells can vary by more than 3 h. We showed that simultaneous viral genome entry to the nucleus can be achieved with a derivative of the previously characterized temperature sensitive mutant tsB7, however, this did not improve gene expression synchrony. We found that elevating the temperature in which the infection is done and increasing the multiplicity of infection (MOI) significantly promoted simultaneous onset of viral gene expression among infected cells. Further, elevated temperature result in a decrease in the coefficient of variation (a standardized measure of dispersion) of viral replication compartments (RCs) sizes among cells as well as a slight increment of viral late gene expression synchrony. We conclude that simultaneous viral gene expression can be improved by simple modifications to the infection process and may reduce the effect of single-cell variability on population-based assays.

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