Persistent SARS-COV-2 infection in vaccinated individual with three doses of COVID-19 vaccine.

We describe a case of a 24-year-old Brazilian woman previously vaccinated with CoronaVac and a booster dose of Pfizer-BioNTech, with mild-to-moderate COVID-19, with persistent viral shedding. We evaluated viral load, antibody dynamics for SARS-CoV-2 and performed genomic analysis to identify the viral variant. The female remained positive for 40 days following symptom onset (cycle quantification mean: 32.54 ± 2.29). The humoral response was characterized by absence of IgM for the viral spike protein, increased IgG for the viral spike (1800.60 to 19558.60 AU/mL) and for the nucleocapsid (from 0.03 to 8.9 index value) proteins, and high titers of neutralizing antibodies (>488.00 IU/mL). The variant identified was the sublineage BA. 5.1. of Omicron (B.1.1.529). Our results suggest that even though the female produced an antibody response against SARS-CoV-2, the persistent infection can be explained by antibody decline and/or the immune evasion by the Omicron variant, illustrating the need to revaccinate or update vaccines.

Model-based inference from multiple dose, time course data reveals Wolbachia effects on infection profiles of type 1 dengue virus in Aedes aegypti.

Infection is a complex and dynamic process involving a population of invading microbes, the host and its responses, aimed at controlling the situation. Depending on the purpose and level of organization, infection at the organism level can be described by a process as simple as a coin toss, or as complex as a multi-factorial dynamic model; the former, for instance, may be adequate as a component of a population model, while the latter is necessary for a thorough description of the process beginning with a challenge with an infectious inoculum up to establishment or elimination of the pathogen. Experimental readouts in the laboratory are often static, snapshots of the process, assayed under some convenient experimental condition, and therefore cannot comprehensively describe the system. Different from the discrete treatment of infection in population models, or the descriptive summarized accounts of typical lab experiments, in this manuscript, infection is treated as a dynamic process dependent on the initial conditions of the infectious challenge, viral growth, and the host response along time. Here, experimental data is generated for multiple doses of type 1 dengue virus, and pathogen levels are recorded at different points in time for two populations of mosquitoes: either carrying endosymbiont bacteria Wolbachia or not. A dynamic microbe/host-response mathematical model is used to describe pathogen growth in the face of a host response like the immune system, and to infer model parameters for the two populations of insects, revealing a slight-but potentially important-protection conferred by the symbiont.