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Biology subjects

Park, S.-C.

Publications and source records attributed to Park, S.-C..

7 recordsLinked to original sources

Mutation-biased adaptation: The Yampolsky-Stoltzfus model revisited

The Yampolsky-Stoltzfus (YS) model provided the first formal demonstration that a bias in the introduction of new mutations can shape the direction of adaptive evolution, even when mutation rates are small relative to selection coefficients. Despite its foundational role, the model has been characterized almost entirely by simulation and closed-form solutions for its central quantity, the probability PA that a mutationally favored but less-fit genotype fixes ahead of a rarer, fitter alternative, have been available only in the limiting regimes of vanishing mutation supply and infinite population size. Here we derive closed-form approximations for PA across the intermediate regime of finite population size and appreciable mutation supply that lies between these two limits. Under strong selection between the competing mutants, we combine an establishment-probability argument with clonal interference theory to obtain an explicit expression for PA that accounts for both the ongoing input of the mutationally favored mutation and the frequency-dependent establishment probability of its competitor. Under weak selection between competing mutants, we derive a complementary expression based on the fixation of a mixed population under Kimura's classical formula. Both expressions agree closely with direct simulation of the underlying Wright-Fisher process, recover the known limiting cases, and remain consistent with one another over a substantial intermediate range of parameters. These results are expected to provide a basis for assessing how the strength of mutation bias affects adaptation in empirical data.

evolutionary biology↗

Evaluation of new adjuvants in enhancing the immune response to a candidate of Severe Fever with Thrombocytopenia Syndrome Virus vaccine.

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging zoonotic disease caused by the tick-borne bunyavirus SFTSV. SFTSV is primarily transmitted by Haemaphysalis longicornis ticks and can cause a hemorrhagic fever-like illness characterized by high fever, thrombocytopenia, leukopenia, and multiorgan failure, with reported case-fatality rates ranging from 10% to over 30%. Despite its growing public health relevance, no licensed vaccines or specific antiviral therapies are currently available. Here, we evaluated a beta-propiolactone-inactivated SFTSV vaccine candidate based on strain YL1, formulated with benchmark adjuvants (Addavax and Alhydrogel) or experimental innate immune agonists, including Sendai virus-derived defective interfering RNA (SDI), a RIG-I agonist, and imidazoquinoline-poly(ethylene glycol)-cholesterol conjugate (IMDQ-P-C), a TLR7/8 agonist, alone or in combination. Using an extended prime-boost regimen, we examined adjuvant-dependent modulation of humoral immunity, antigen-specific cellular recall, antibody cross-reactivity, and functional protection following passive serum transfer and live-virus challenge in IFNAR-/- mice. All adjuvanted formulations induced detectable humoral responses, with Addavax and SDI eliciting the highest virus-specific binding and neutralizing antibody titers. Antigen-specific analyses identified the nucleoprotein (NP) as the dominant target of vaccine-induced immune memory. NP elicited robust antibody response and the broadest cytokine recall profile following ex vivo stimulation. This response was broader than that induced by the whole inactivated virus and was characterized by mixed Th1-associated, Th2-associated, and proinflammatory-associated features that varied across adjuvant formulations. In contrast, the head domain of the Gn glycoprotein elicited limited cellular recall responses, consistent with its relatively weak humoral immunogenicity after both priming and boosting. Nevertheless, sera from SDI and Addavax-adjuvanted groups displayed cross-reactivity with Gn from a heterologous SFTSV strain, suggesting broader antibody recognition across viral genotypes. Functionally, sera from SDI and Addavax-immunized mice conferred partial protection following passive transfer into IFNAR-/- recipients, as reflected by reduced viral loads, delayed disease onset, and prolonged survival after lethal SFTSV challenge. Together, these findings support the immunogenicity and protective potential of a BPL-inactivated SFTSV vaccine platform and identify NP as a major target of vaccine-induced immune memory. They further highlight the importance of adjuvant selection in shaping the magnitude, antigenic focus, and functional quality of vaccine-induced antiviral immunity.

microbiology↗

Adjuvanted mucosal vaccination enhances protection and prevents influenza virus transmission in the guinea pig model.

Influenza virus infects the respiratory mucosa, highlighting the importance of mucosal immunity for early protection and transmission control. Here, we evaluated whether intranasal (IN) vaccination with recombinant trimeric hemagglutinin protein from A/Michigan/45/2015 (triHA) formulated with a combined mucosal adjuvant, nanoemulsion plus IVT, an RNA-based RIG-I agonist (NE/IVT), could protect guinea pigs against heterologous A/Netherlands/602/2009 challenge and reduce viral transmission. To compare mucosal and parenteral immunization, IN triHA/NE/IVT was benchmarked against IN triHA alone, IM triHA/AddaVax (IM triHA/Advx), and standard IM quadrivalent inactivated influenza vaccine (QIV). We also tested whether IN triHA/NE/IVT could boost IM QIV- primed immunity and included animals previously infected with A/Michigan/45/2015 to model pre-existing infection- induced immunity. Transmission was assessed by co-housing naive sentinels with vaccinated, challenged donors. IN triHA/NE/IVT induced systemic humoral responses comparable to IM triHA/Advx while generating superior nasal mucosal IgA responses. Unexpectedly, IM triHA/AddaVax also induced detectable, albeit lower, mucosal IgG and IgA, contrasting with prior mouse data and highlighting species-specific differences. IN triHA/NE/IVT boosting after IM QIV enhanced serum IgG and mucosal IgA compared with QIV prime-boost alone and increased cross-neutralizing activity against antigenically distinct A/Victoria/4897/2022. Both IN triHA/NE/IVT and IN Michigan/15 prior- infection prevented detectable viral shedding after challenge, and naive sentinels co-housed with IN triHA/NE/IVT- vaccinated donors remained seronegative. Together, these findings support NE/IVT as a potential mucosal platform capable of inducing robust systemic and mucosal immunity and boosting IM vaccine-primed responses.

microbiology↗

Disease modulation by TIV vaccination during secondary pneumococcal infections in influenza-infected mice.

Secondary bacterial infections can significantly worsen the clinical course of influenza virus infections and are a leading cause of morbidity and mortality during seasonal influenza epidemics. Despite being a vaccine-preventable disease, influenza-related complications from secondary bacterial infections are an important cause of death, particularly among the elderly population. Streptococcus pneumoniae (Spn) is the most common agent responsible for influenza-related secondary bacterial infections. Influenza virus vaccination serves as an effective prophylactic strategy for preventing influenza and reducing the burden of influenza-associated pathology, including secondary bacterial infection. However, whether the protective effects of influenza virus vaccination differ in the context of a secondary Spn infection at the level of the host response remains poorly characterized. Here, we present a preclinical mouse model to examine the impact of influenza vaccination in scenarios involving single infections with influenza A virus H1N1 (NC99) or Spn serotype 1; simultaneous infection with both NC99 and Spn (coinfection), or NC99 infection followed by Spn infection seven days later (superinfection). A single dose of trivalent inactivated Influenza vaccine (TIV) is able to decrease infection lethality in both secondary bacterial infection scenarios. Protection is associated with reduction in both viral and bacterial titers, decreased production of pro-inflammatory cytokines, protection of alveolar macrophages, prevention of exacerbated lung neutrophil recruitment, modulation of neutrophil activation status and induction of lung eosinophil recruitment and activation. These findings underscore the importance of influenza vaccination in modulating disease progression and preventing morbidity and mortality associated with secondary bacterial infections.

microbiology↗

A combination TLR7/8 and RIG-I agonist adjuvant reverts asthmatic allergic sensitization and prevents aggravated influenza infection in OVA-sensitized mice.

Allergen-specific immunotherapy (AIT) is the only disease-modifying treatment currently available to treat allergy. However, it has limitations, as most allergens are poorly immunogenic, resulting in an AIT process that can take years. Therefore, adjuvant selection becomes critical to achieve a more efficacious therapy. Our group has developed and tested an amphiphilic TLR7/8 agonist (IMDQ) and a RIG-I agonist (SDI) that used alone, or in combination, have demonstrated strong adjuvant activity for influenza and SARS-CoV-2 vaccines in preclinical models. Here we describe the effect of these adjuvants in the sensitization of preclinical models with the ovalbumin (OVA) asthmatic allergic model via an in-depth humoral and cellular immune profiling. We assess their immune skewing and tolerance inducing capacities in previously sensitized preclinical models with different genetic backgrounds (C57BL/6 vs. BALB/c mice). Moreover, we evaluate their effect in an unrelated antigenic challenge with influenza. Finally, we investigate the role of IgG subclasses and T-cell subpopulations in the protection against OVA challenge conferred by the combination of IMDQ and SDI. We demonstrate that OVA-immunization in combination with IMDQ+SDI prevents allergic sensitization via the induction of a balanced Type 1/Type 2 response. Furthermore, it can revert the allergic phenotype in mice previously sensitized with OVA-Alum, through reducing lung eosinophilia, as well as IL-4 and IL-5 production. However, this was dependent on genetic background. IMDQ+SDI sensitization also led to reduced morbidity of a secondary influenza challenge in OVA-sensitized mice. Finally, we demonstrated that IgG2c, by itself, cannot protect from allergic sensitization and that both CD4+ and CD8+ T-cells are needed for IMDQ+SDI prevention of eosinophil recruitment and activation upon intranasal OVA-challenge.

immunology↗

Recombination and mutational robustness in neutral fitness landscapes

Mutational robustness quantifies the effect of random mutations on fitness. When mutational robustness is high, most mutations do not change fitness or have only a minor effect on it. From the point of view of fitness landscapes, robust genotypes form neutral networks of almost equal fitness. Using deterministic population models it has been shown that selection favors genotypes inside such networks, which results in increased mutational robustness. Here we demonstrate that this effect is massively enhanced by recombination. Our results are based on a detailed analysis of mesa-shaped fitness landscapes, where we derive precise expressions for the dependence of the robustness on the landscape parameters for recombining and non-recombining populations. In addition, we carry out numerical simulations on different types of random holey landscapes as well as on an empirical fitness landscape. We show that the mutational robustness of a genotype generally correlates with its recombination weight, a new measure that quantifies the likelihood for the genotype to arise from recombination. We argue that the favorable effect of recombination on mutational robustness is a highly universal feature that may have played an important role in the emergence and maintenance of mechanisms of genetic exchange. Author summaryTwo long-standing and seemingly unrelated puzzles in evolutionary biology concern the ubiquity of sexual reproduction and the robustness of organisms against genetic perturbations. Using a theoretical approach based on the concept of a fitness landscape, in this article we argue that the two phenomena may in fact be closely related. In our setting the hereditary information of an organism is encoded in its genotype, which determines it to be either viable or non-viable, and robustness is defined as the fraction of mutations that maintain viability. Previous work has demonstrated that the purging of non-viable genotypes from the population by natural selection leads to a moderate increase in robustness. Here we show that genetic recombination acting in combination with selection massively enhances this effect, an observation that is largely independent of how genotypes are connected by mutations. This suggests that the increase of robustness may be a major driver underlying the evolution of sexual recombination and other forms of genetic exchange throughout the living world.

evolutionary biology↗

Genotypic complexity of Fisher’s geometric model

Fishers geometric model was originally introduced to argue that complex adaptations must occur in small steps because of pleiotropic constraints. When supplemented with the assumption of additivity of mutational effects on phenotypic traits, it provides a simple mechanism for the emergence of genotypic epistasis from the nonlinear mapping of phenotypes to fitness. Of particular interest is the occurrence of reciprocal sign epistasis, which is a necessary condition for multipeaked genotypic fitness landscapes. Here we compute the probability that a pair of randomly chosen mutations interacts sign-epistatically, which is found to decrease with increasing phenotypic dimension n, and varies non-monotonically with the distance from the phenotypic optimum. We then derive expressions for the mean number of fitness maxima in genotypic landscapes composed of all combinations of L random mutations. This number increases exponentially with L, and the corresponding growth rate is used as a measure of the complexity of the landscape. The dependence of the complexity on the model parameters is found to be surprisingly rich, and three distinct phases characterized by different landscape structures are identified. Our analysis shows that the phenotypic dimension, which is often referred to as phenotypic complexity, does not generally correlate with the complexity of fitness landscapes and that even organisms with a single phenotypic trait can have complex landscapes. Our results further inform the interpretation of experiments where the parameters of Fisher's model have been inferred from data, and help to elucidate which features of empirical fitness landscapes can be described by this model.

evolutionary biology↗