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Franceschi, V. B.

Publications and source records attributed to Franceschi, V. B..

3 recordsLinked to original sources

Untangling the effects of within-host and between-host natural selection in viruses with applications to evolution of HIV-1 co-receptor usage

The fitness of a pathogen can be characterised at multiple levels corresponding to different stages of its life cycle, including replication within target cells (replicative capacity), immune evasion, and the capacity to infect new hosts (transmissibility). Pathogens evolve towards greater fitness within hosts, which can potentially compromise transmissibility. Typically, epidemiological studies for measuring pathogen fitness compute a single selection coefficient for pathogen variants that encompasses all stages of the pathogen life cycle. To address this problem, we develop a population-genetic model and software for the inference of multi-level selection coefficients which represent relative within-host fitness and transmissibility. Our approach builds on population genetic models previously applied to macro-evolution, whereby speciation and extinction rates are state-dependent. We relate the state-dependence in speciation and extinction rates to competing within- and between-host selection. Evolution of beneficial phenotypes within hosts may occur rapidly (higher speciation), but reduce rates of dispersal between hosts (higher extinction). This new coalescent-based method also accounts for highly nonlinear-population dynamics and variable sampling through time making it suitable for epidemiological studies. We derive the equilibrium proportion of a variant with multi-level selection under mutation-selection balance and show how this can be used in combination with the coalescent to greatly increase accuracy and precision of estimated selection coefficients. We characterise the accuracy of this method using a variety of birth-death and coalescent simulations before analysing a real dataset of HIV-1 genetic sequences from a large population-based sample of 4056 people living with HIV in Zambia. We quantified the multi-level relative fitness underlying HIV-1 co-receptor switching. In accordance with previous observations, we estimate that the relative transmissibility of X4-tropic virus is 9%, while within-host switching to X4-tropism is approximately seven-fold higher than switching to R5-tropism, indicating a strong within-host and between-host tradeoff of co-receptor usage. Our methods are available in an open-source R package musseco, providing a general-purpose tool for inferring multi-level selection coefficients for epidemiological sequence data. Author SummaryThe fitness of a pathogen can be characterised at each stage of its life cycle. However, epidemiological studies measuring pathogen fitness typically estimate a single value encompassing the entire life cycle. Pathogens evolve towards greater fitness within hosts, but this can compromise the capacity to infect new hosts. Our new method quantifies relative fitness at both levels. This method accounts for rapidly changing pathogen populations and variable sampling through time making it suitable for epidemiological studies. We tested our method using simulations and demonstrate its application by analysing real HIV-1 genetic sequences from people living with HIV in Zambia. This method sheds new light on long-standing questions about the relative fitness of HIV-1 variants which utilise different host-cell co-receptors. Using our new method, we estimate that the capacity of X4 variants to infect new people is just 9% of that of R5 variants, while within-host switching from R5 to X4 usage is seven times greater than the reverse switch. This indicates a strong within-host and between-host trade-off in co-receptor usage.

evolutionary biology↗

Molecular evolution and structural analyses of the spike glycoprotein from Brazilian SARS-CoV-2 genomes: the impact of the fixation of selected mutations

The COVID-19 pandemic caused by Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has reached by July 2021 almost 200 million cases and more than 4 million deaths worldwide since its beginning in late 2019, leading to enhanced concern in the scientific community and the general population. One of the most important pieces of this host-pathogen interaction is the spike protein, which binds to the human Angiotensin-converting enzyme 2 (hACE2) cell receptor, mediates the membrane fusion and is the major target of neutralizing antibodies against SARS-CoV-2. The multiple amino acid substitutions observed in this region, specially in the Receptor Binding Domain (RBD), mainly after almost one year of its emergence (late 2020), have enhanced the hACE2 binding affinity and led to several modifications in the mechanisms of SARS-CoV-2 pathogenesis, improving the viral fitness and/or promoting immune evasion, with potential impact in the vaccine development. In this way, the present work aimed to evaluate the effect of positively selected mutations fixed in the Brazilian SARS-CoV-2 lineages and to check for mutational evidence of coevolution. Additionally, we evaluated the impact of selected mutations identified in some of the VOC and VOI lineages (C.37, B.1.1.7, P.1, and P.2) of Brazilian samples on the structural stability of the spike protein, as well as their possible association with more aggressive infection profiles by estimating the binding affinity in the RBD-hACE2 complex. We identified 48 sites under selective pressure in Brazilian spike sequences, 17 of them with the strongest evidence by the HyPhy tests, including VOC related mutation sites 138, 142, 222, 262, 484, 681, and 845, among others. The coevolutionary analysis identified a number of 28 coevolving sites that were found not to be conditionally independent, such as the couple E484K - N501Y from P.1 and B.1.351 lineages. Finally, the molecular dynamics and free energy estimates showed the structural stabilizing effect and the higher impact of E484K for the improvement of the binding affinity between the spike RBD and the hACE2 in P.1 and P.2 lineages, as well as the stabilizing and destabilizing effects for the positively selected sites.

evolutionary biology↗

E484K as an innovative phylogenetic event for viral evolution: Genomic analysis of the E484K spike mutation in SARS-CoV-2 lineages from Brazil

The COVID-19 pandemic caused by SARS-CoV-2 has affected millions of people since its beginning in 2019. The propagation of new lineages and the discovery of key mechanisms adopted by the virus to overlap the immune system are central topics for the entire public health policies, research and disease management. Since the second semester of 2020, the mutation E484K has been progressively found in the Brazilian territory, composing different lineages over time. It brought multiple concerns related to the risk of reinfection and the effectiveness of new preventive and treatment strategies due to the possibility of escaping from neutralizing antibodies. To better characterize the current scenario we performed genomic and phylogenetic analyses of the E484K mutated genomes sequenced from Brazilian samples in 2020. From October, 2020, more than 40% of the sequenced genomes present the E484K mutation, which was identified in three different lineages (P1, P2 and B.1.1.33) in four Brazilian regions. We also evaluated the presence of E484K associated mutations and identified selective pressures acting on the spike protein, leading us to some insights about adaptive and purifying selection driving the virus evolution.

evolutionary biology↗