On the boundary between economy and environment in life cycle assessment

Purpose

We investigate how the boundary between product systems and their environment has been delineated in life cycle assessment and question the usefulness and ontological relevance of a strict division between the two.

Methods

We consider flows, activities and impacts as general terms applicable to both product systems and their environment and propose that the ontologically relevant boundary is between the flows that are modelled as inputs to other activities (economic or environmental)—and the flows that—in a specific study—are regarded as final impacts, in the sense that no further feedback into the product system is considered before these impacts are applied in decision-making. Using this conceptual model, we contrast the traditional mathematical calculation of the life cycle impacts with a new, simpler computational structure where the life cycle impacts are calculated directly as part of the Leontief inverse, treating product flows and environmental flows in parallel, without the need to consider any boundary between economic and environmental activities.

Results and discussion

Our theoretical outline and the numerical example demonstrate that the distinctions and boundaries between product systems and their environment are unnecessary and in some cases obstructive from the perspective of impact assessment, and can therefore be ignored or chosen freely to reflect meaningful distinctions of specific life cycle assessment (LCA) studies. We show that our proposed computational structure is backwards compatible with the current practice of LCA modelling, while allowing inclusion of feedback loops both from the environment to the economy and internally between different impact categories in the impact assessment.

Conclusions

Our proposed computational structure for LCA facilitates consistent, explicit and transparent modelling of the feedback loops between environment and the economy and between different environmental mechanisms. The explicit and transparent modelling, combining economic and environmental information in a common computational structure, facilitates data exchange and re-use between different academic fields.

     

Hypervariable Region 1 Deletion and Required Adaptive Envelope Mutations Confer Decreased Dependency on Scavenger Receptor Class B Type I and Low-Density Lipoprotein Receptor for Hepatitis C Virus

Hypervariable region 1 (HVR1) of envelope protein 2 (E2) of hepatitis C virus (HCV) serves important yet undefined roles in the viral life cycle. We previously showed that the viability of HVR1-deleted JFH1-based recombinants with Core-NS2 of H77 (H77_ΔHVR1, genotype 1a) and S52 (S52_ΔHVR1, genotype 3a) in Huh7.5 cells was rescued by E2 substitutions N476D/S733F and an E1 substitution, A369V, respectively; HVR1-deleted J6 (J6_ΔHVR1, genotype 2a) was fully viable. In single-cycle production assays, where HCV RNA was transfected into entry-deficient Huh7-derived S29 cells with low CD81 expression, we found no effect of HVR1 deletion on replication or particle release for H77 and S52. HCV pseudoparticle assays in Huh7.5 cells showed that HVR1 deletion decreased entry by 20- to 100-fold for H77, J6, and S52; N476D/S733F restored entry for H77_ΔHVR1, while A369V further impaired S52_ΔHVR1 entry. We investigated receptor usage by antibody blocking and receptor silencing in Huh7.5 cells, followed by inoculation of parental and HVR1-deleted HCV recombinants. Compared to parental viruses, scavenger receptor class B type I (SR-BI) dependency was decreased for H77_{ΔHVR1/N476D/S733F}, H77_N476D/S733F, S52_ΔHVR1/A369V, and S52_A369V, but not for J6_ΔHVR1. Low-density lipoprotein receptor (LDLr) dependency was decreased for HVR1-deleted viruses, but not for H77_N476D/S733F and S52_A369V. Soluble LDLr neutralization revealed strong inhibition of parental HCV but limited effect against HVR1-deleted viruses. Apolipoprotein E (ApoE)-specific HCV neutralization was similar for H77, J6, and S52 viruses with and without HVR1. In conclusion, HVR1 and HVR1-related adaptive envelope mutations appeared to be involved in LDLr and SR-BI dependency, respectively. Also, LDLr served ApoE-independent but HVR1-dependent functions in HCV entry.