Key result
Wild boars persistently infected with the CSFV Cat01 strain were protected from superinfection by the virulent CSFV Margarita strain, evidenced by the absence of clinical signs and Margarita RNA.
Why the study?
Does persistent infection with CSFV Cat01 strain prevent superinfection by the virulent CSFV Margarita strain in wild boars?
Does persistent infection with CSFV Cat01 strain prevent superinfection by the virulent CSFV Margarita strain in wild boars?
Postnatal persistent infection with a low-virulence CSFV strain completely protects wild boars from superinfection by a highly virulent strain, demonstrating superinfection exclusion in vivo.
Answers are grounded in this paper and cite their sources.
Demonstrates superinfection exclusion in a large-animal model; leaves open translation to other hosts or human persistent infections.
Two groups with three wild boars each were used: Group A (animals 1 to 3) served as the control, and Group B (animals 4 to 6) was postnatally persistently infected with the Cat01 strain of CSFV (primary virus). The animals, six weeks old and clinically healthy, were inoculated with the virulent strain Margarita (secondary virus). For exclusive detection of the Margarita strain, a specific qRT-PCR assay was designed, which proved not to have cross-reactivity with the Cat01 strain. The wild boars persistently infected with CSFV were protected from superinfection by the virulent CSFV Margarita strain, as evidenced by the absence of clinical signs and the absence of Margarita RNA detection in serum, swabs and tissue samples. Additionally, in PBMCs, a well-known target for CSFV viral replication, only the primary infecting virus RNA (Cat01 strain) could be detected, even after the isolation in ST cells, demonstrating SIE at the tissue level in vivo. Furthermore, the data analysis of the Margarita qRT-PCR, by means of calculated ΔCt values, supported that PBMCs from persistently infected animals were substantially protected from superinfection after in vitro inoculation with the Margarita virus strain, while this virus was able to infect naive PBMCs efficiently. In parallel, IFN-α values were undetectable in the sera from animals in Group B after inoculation with the CSFV Margarita strain. Furthermore, these animals were unable to elicit adaptive humoral (no E2-specific or neutralising antibodies) or cellular immune responses (in terms of IFN-γ-producing cells) after inoculation with the second virus. Finally, a sequence analysis could not detect CSFV Margarita RNA in the samples tested from Group B. Our results suggested that the SIE phenomenon might be involved in the evolution and phylogeny of the virus, as well as in CSFV control by vaccination. To the best of our knowledge, this study was one of the first showing efficient suppression of superinfection in animals, especially in the absence of IFN-α, which might be associated with the lack of innate immune mechanisms.
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Muñoz‐González et al. (2016) studied Classical Swine Fever Virus (CSFV) infection (n=6). CSFV Margarita strain inoculation vs. Naive wild boars (Group A) was evaluated on Superinfection by virulent CSFV Margarita strain (clinical signs and RNA detection). Wild boars persistently infected with the CSFV Cat01 strain were protected from superinfection by the virulent CSFV Margarita strain, evidenced by the absence of clinical signs and Margarita RNA.
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