Antigenic escape selects for the evolution of higher pathogen transmission and virulence

Sasaki, Akira; Lion, Sébastien; Boots, Mike

doi:10.1038/s41559-021-01603-z

Cited by 33 publications

(61 citation statements)

References 53 publications

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“…Our model with host heterogeneity in immune competency showed stable coupled traveling waves of pathogen antigenic variants and specific host immunity in the antigenic space with a constant speed (Fig. 1B) as in the previous models (Gog and Grenfell, 2002;Haraguchi and Sasaki, 1997;Sasaki, 1994;Sasaki et al, 2022). However, we found that the wave speed, which corresponds to the speed of the accumulation of antigenic mutants, i.e., the pathogen's speed of notorious evolutionary changes against host immunity and vaccination, sensitively depends on the host heterogeneity in immune competency (Fig.…”

Section: Antigenic Escape In a Heterogeneous Host Populationsupporting

confidence: 72%

“…where 𝜖 is a small positive constant and 𝛿(𝑥) is the Dirac delta function), the pathogen persists by continuously evading host immunity as a traveling wave in antigenic space (Fisher, 1937;Gog and Grenfell, 2002;Haraguchi and Sasaki, 1997;Kolmogorov, 1937;Sasaki, 1994;Sasaki et al, 2022;Weinberger, 1982) with a constant wave speed:…”

Section: Modelmentioning

confidence: 99%

“…Several theoretical studies have attempted to elucidate the complex evolutionary epidemiological dynamics in which pathogens continue to evade host immunity by repeatedly changing their antigenicity (Gog and Grenfell, 2002; Haraguchi and Sasaki, 1997; Marchi et al, 2021; Sasaki, 1994; Sasaki et al, 2022; Sasaki and Haraguchi, 2000). These studies have revealed the speed of antigenic escape (Haraguchi and Sasaki, 1997; Marchi et al, 2021; Sasaki, 1994) and predicted cross-immunity-driven discontinuous outbreaks in both time and antigenic space (Gog and Grenfell, 2002; Haraguchi and Sasaki, 1997; Sasaki et al, 2022). They also evaluated the joint evolution of pathogen virulence and antigenic escape (Sasaki et al, 2022).…”

Section: Introductionmentioning

confidence: 99%

“…These studies have revealed the speed of antigenic escape (Haraguchi and Sasaki, 1997; Marchi et al, 2021; Sasaki, 1994) and predicted cross-immunity-driven discontinuous outbreaks in both time and antigenic space (Gog and Grenfell, 2002; Haraguchi and Sasaki, 1997; Sasaki et al, 2022). They also evaluated the joint evolution of pathogen virulence and antigenic escape (Sasaki et al, 2022). However, few studies have examined the epidemiological dynamics of antigenic escape when heterogeneity in host traits, such as recovery rates, is present.…”

Section: Introductionmentioning

confidence: 99%

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Antigenic escape accelerated by the presence of immunocompromised hosts

Kumata

Sasaki

2022

Preprint

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The repeated emergence of SARS-CoV-2 escape mutants from host immunity has obstructed the containment of the current pandemic and poses a serious threat to humanity. Prolonged infection in immunocompromised patients has received increasing attention as a driver of immune escape, and accumulating evidence suggests that viral genomic diversity and emergence of immune-escape mutants are promoted in immunocompromised patients. However, because immunocompromised patients comprise a small proportion of the host population, whether they have a significant impact on antigenic evolution at the population level is unknown. We used an evolutionary epidemiological model combining antigenic evolution and epidemiological dynamics in host populations with heterogeneity in immune competency to determine the impact of immunocompromised patients on the pathogen evolutionary dynamics of antigenic escape from host immunity. We derived analytical formulae of the speed of antigenic evolution in heterogeneous host populations and found that even a small number of immunocompromised hosts in the population significantly accelerates antigenic evolution. Our results demonstrate that immunocompromised hosts play a key role in viral adaptation at the population level and emphasize the importance of critical care and surveillance of immunocompromised hosts.

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Section: Antigenic Escape In a Heterogeneous Host Populationsupporting

confidence: 72%

Section: Modelmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Antigenic escape accelerated by the presence of immunocompromised hosts

Kumata

Sasaki

2022

Preprint

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“…This could be seen with a reduction in the host’s physical level of activity or their death. Therefore, it is predicted that compromised moderate levels of virulence should be in sync with the pathogen’s evolution (Alizon et al 2009a , b ; Goldhill and Turner 2014 ; Sasaki et al 2022 ).…”

Section: Introductionmentioning

confidence: 99%

From HIV to COVID-19, Molecular mechanisms of pathogens’ trade-off and persistence in the community, potential targets for new drug development

et al. 2022

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Background On the staggering emergence of the Omicron variant, numerous questions arose about the evolution of virulence and transmissibility in microbes. Main body of the abstract The trade-off hypothesis has long speculated the exchange of virulence for the sake of superior transmissibility in a wide array of pathogens. While this certainly applies to the case of the Omicron variant, along with influenza virus, various reports have been allocated for an array of pathogens such as human immunodeficiency virus (HIV), malaria, hepatitis B virus (HBV) and tuberculosis (TB). The latter abide to another form of trade-off, the invasion–persistence trade-off. In this study, we aim to explore the molecular mechanisms and mutations of different obligate intracellular pathogens that attenuated their more morbid characters, virulence in acute infections and invasion in chronic infections. Short conclusion Recognizing the mutations that attenuate the most morbid characters of pathogens such as virulence or persistence can help in tailoring new therapies for such pathogens. Targeting macrophage tropism of HIV by carbohydrate-binding agents, or targeting the TMPRSS2 receptors to prevent pulmonary infiltrates of COVID-19 is an example of how important is to recognize such genetic mechanisms.

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Blood‐derived product therapies for SARS‐CoV‐2 infection and long COVID

Wu,

Yang,

et al. 2023

MedComm

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Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) is capable of large‐scale transmission and has caused the coronavirus disease 2019 (COVID‐19) pandemic. Patients with COVID‐19 may experience persistent long‐term health issues, known as long COVID. Both acute SARS‐CoV‐2 infection and long COVID have resulted in persistent negative impacts on global public health. The effective application and development of blood‐derived products are important strategies to combat the serious damage caused by COVID‐19. Since the emergence of COVID‐19, various blood‐derived products that target or do not target SARS‐CoV‐2 have been investigated for therapeutic applications. SARS‐CoV‐2‐targeting blood‐derived products, including COVID‐19 convalescent plasma, COVID‐19 hyperimmune globulin, and recombinant anti‐SARS‐CoV‐2 neutralizing immunoglobulin G, are virus‐targeting and can provide immediate control of viral infection in the short term. Non‐SARS‐CoV‐2‐targeting blood‐derived products, including intravenous immunoglobulin and human serum albumin exhibit anti‐inflammatory, immunomodulatory, antioxidant, and anticoagulatory properties. Rational use of these products can be beneficial to patients with SARS‐CoV‐2 infection or long COVID. With evidence accumulated since the pandemic began, we here summarize the progress of blood‐derived product therapies for COVID‐19, discuss the effective methods and scenarios regarding these therapies, and provide guidance and suggestions for clinical treatment.

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Antigenic escape selects for the evolution of higher pathogen transmission and virulence

Cited by 33 publications

References 53 publications

Antigenic escape accelerated by the presence of immunocompromised hosts

Antigenic escape accelerated by the presence of immunocompromised hosts

From HIV to COVID-19, Molecular mechanisms of pathogens’ trade-off and persistence in the community, potential targets for new drug development

Blood‐derived product therapies for SARS‐CoV‐2 infection and long COVID

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