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1. The evolution of post-infection mortality

   https://doi.org/10.1098/rspb.2024.1854  

   Saad-Roy, Chadi M; White, Andy; Boots, Mike (November 2024, Proceedings of the Royal Society B: Biological Sciences)

   COVID-19 infections have underlined that there can be substantial impacts on health after recovery, including elevated mortality. While such post-infection mortality (PIM) is clearly widespread, we do not yet have any understanding of its evolutionary dynamics. To address this gap, we use an eco-evolutionary model to determine conditions where PIM is evolutionarily favoured. Importantly, from a pathogen perspective, there are two potential ‘resources’: never-infected susceptibles and previously infected susceptibles (provided some reinfection is possible), and PIM only occurs in the latter. A key insight is that unlike classic virulence (i.e. during-infection mortality, DIM) PIM is neutral and not selected against in the absence of other trade-offs. However, PIM modulates characteristics of endemicity, and may also vary with other pathogen-specific components. If PIM is only correlated with transmission, recovery or DIM, it simply acts to modulate their impacts on the evolutionary outcome. On the other hand, if PIM trades off with the relative susceptibility to reinfection, there are important evolutionary implications that contrast with DIM. We find settings where a susceptibility–mortality trade-off (i.e. an increase in mortality leads to higher relative susceptibility to reinfection) can select against DIM but favour PIM. This provides a potential explanation for the ubiquity of PIM. Overall, our work illustrates that PIM can readily evolve in certain settings and highlights the importance of considering different sources of mortality. 

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2. ACE2 enhance viral infection or viral infection aggravate the underlying diseases

   https://doi.org/10.1016/j.csbj.2020.08.002  

   Teng, Shaolei; Tang, Qiyi (January 2020, Computational and Structural Biotechnology Journal)
3. The mutual interplay between calcification and coccolithovirus infection: Calcification and coccolithovirus infection

   https://doi.org/10.1111/1462-2920.14362  

   Johns, Christopher T.; Grubb, Austin R.; Nissimov, Jozef I.; Natale, Frank; Knapp, Viki; Mui, Alwin; Fredricks, Helen F.; Van Mooy, Benjamin A.; Bidle, Kay D. (September 2018, Environmental Microbiology)
4. The Effect of the Infection Rate on Oncolytic Virotherapy

   https://doi.org/10.11648/j.cbb.20200801.14  

   Kim, Dongwook; Kim, Haeyoung; Wu, Hui; Shin, Dong-Hoon (January 2020, Computational Biology and Bioinformatics)

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5. The durability of natural infection and vaccine-induced immunity against future infection by SARS-CoV-2

   Jeffrey P Townsend; Hayley B Hassler; Pratha Sah; Alison P Galvani; Alex Dornburg (July 2022, Proceedings of the National Academy of Sciences of the United States of America)

   The durability of vaccine-mediated immunity to SARS-CoV-2, the durations to breakthrough infection, and the optimal timings of booster vaccination are crucial knowledge for pandemic response. Here, we applied comparative evolutionary analyses to estimate the durability of immunity and the likelihood of breakthrough infections over time following vaccination by BNT162b2 (Pfizer-BioNTech), mRNA-1273 (Moderna), ChAdOx1 (Oxford-AstraZeneca), and Ad26.COV2.S (Johnson & Johnson/Janssen). We evaluated anti-Spike (S) immunoglobulin G (IgG) antibody levels elicited by each vaccine relative to natural infection. We estimated typical trajectories of waning and corresponding infection probabilities, providing the distribution of times to breakthrough infection for each vaccine under endemic conditions. Peak antibody levels elicited by messenger RNA (mRNA) vaccines mRNA-1273 and BNT1262b2 exceeded that of natural infection and are expected to typically yield more durable protection against breakthrough infections (median 29.6 mo; 5 to 95% quantiles 10.9 mo to 7.9 y) than natural infection (median 21.5 mo; 5 to 95% quantiles 3.5 mo to 7.1 y). Relative to mRNA-1273 and BNT1262b2, viral vector vaccines ChAdOx1 and Ad26.COV2.S exhibit similar peak anti-S IgG antibody responses to that from natural infection and are projected to yield lower, shorter-term protection against breakthrough infection (median 22.4 mo and 5 to 95% quantiles 4.3 mo to 7.2 y; and median 20.5 mo and 5 to 95% quantiles 2.6 mo to 7.0 y; respectively). These results leverage the tools from evolutionary biology to provide a quantitative basis for otherwise unknown parameters that are fundamental to public health policy decision-making. 

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