The genetic interaction between HIV and the antibody repertoire

Strauli, Nicolas; Fryer, Emily; Pham, Olivia; Abdel‐Mohsen, Mohamed; Facente, Shelley N.; Pilcher, Christopher D.; Pennings, Pleuni S.; Pillai, Satish K.; Hernández, Ryan D.

doi:10.1101/646968

Cited by 5 publications

(7 citation statements)

References 76 publications

(94 reference statements)

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“…Instead, in the context of the “red-queen phenomenon” ( 58 ), a constant escape and chase, it may be that [as others have observed ( 33 , 35 )] sequential viral/host coevolution is not particularly relevant for early HIV pathogenesis. A surprisingly similar message arose from a deep analysis of HIV and antibody repertoires sequenced from the same individuals ( 40 ).…”

Section: Discussionmentioning

confidence: 84%

See 1 more Smart Citation

Evolution during primary HIV infection does not require adaptive immune selection

Swan

Rolland

Herbeck

et al. 2022

Proc. Natl. Acad. Sci. U.S.A.

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Modern HIV research depends crucially on both viral sequencing and population measurements. To directly link mechanistic biological processes and evolutionary dynamics during HIV infection, we developed multiple within-host phylodynamic models of HIV primary infection for comparative validation against viral load and evolutionary dynamics data. The optimal model of primary infection required no positive selection, suggesting that the host adaptive immune system reduces viral load but surprisingly does not drive observed viral evolution. Rather, the fitness (infectivity) of mutant variants is drawn from an exponential distribution in which most variants are slightly less infectious than their parents (nearly neutral evolution). This distribution was not largely different from either in vivo fitness distributions recorded beyond primary infection or in vitro distributions that are observed without adaptive immunity, suggesting the intrinsic viral fitness distribution may drive evolution. Simulated phylogenetic trees also agree with independent data and illuminate how phylogenetic inference must consider viral and immune-cell population dynamics to gain accurate mechanistic insights.

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Section: Discussionmentioning

confidence: 84%

“…Yet, bNAbs can arise quickly without many mutations (38) and in infants (39). Recently, Strauli et al analyzed data of unprecedented detail on both HIV and antibody repertoire sequences, ultimately finding that HIV/Ab coevolution is at minimum hard to detect, if not rare entirely (40).…”

mentioning

confidence: 99%

Evolution during primary HIV infection does not require adaptive immune selection

Swan

Rolland

Herbeck

et al. 2022

Proc. Natl. Acad. Sci. U.S.A.

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“…The open access database of Strauli et al [32] is available from from the Sequence Read Archive (SRA), BioProject ID PRJNA543982 at: https://www.ncbi.nlm.nih.gov/bioproject/?term= PRJNA543982.…”

Section: Data Accessibilitymentioning

confidence: 99%

Inspecting the interaction between human immunodeficiency virus and the immune system through genetic turnover

Mazzolini

Mora

Walczak

2023

Phil. Trans. R. Soc. B

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Chronic infections of the human immunodeficiency virus (HIV) create a very complex coevolutionary process, where the virus tries to escape the continuously adapting host immune system. Quantitative details of this process are largely unknown and could help in disease treatment and vaccine development. Here we study a longitudinal dataset of ten HIV-infected people, where both the B-cell receptors and the virus are deeply sequenced. We focus on simple measures of turnover, which quantify how much the composition of the viral strains and the immune repertoire change between time points. At the single-patient level, the viral–host turnover rates do not show any statistically significant correlation, however, they correlate if one increases the amount of statistics by aggregating the information across patients. We identify an anti-correlation: large changes in the viral pool composition come with small changes in the B-cell receptor repertoire. This result seems to contradict the naïve expectation that when the virus mutates quickly, the immune repertoire needs to change to keep up. However, a simple model of antagonistically evolving populations can explain this signal. If it is sampled at intervals comparable with the sweep time, one population has had time to sweep while the second cannot start a counter-sweep, leading to the observed anti-correlation. This article is part of the theme issue ‘Interdisciplinary approaches to predicting evolutionary biology’.

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“…The open access database of Strauli et al [32] is available om the Sequence Read Archive, SRA, under the BioProject ID PRJNA543982. https://www.ncbi.nlm.nih.gov/bioproject/?term=PRJNA543982.…”

Section: S1 Dataset Descriptionmentioning

confidence: 99%

“…To our knowledge, only one dataset of this kind has been made public, where a portion of the HIV envelope gene and B-cell receptors have been both deeply sequenced in time for different patients [32]. We base our analysis on this dataset and define simple macroscopical observables for the evolution of the two populations, which quantify genetic turnover and selective pressure.…”

Section: Introductionmentioning

confidence: 99%

Inspecting the interaction between HIV and the immune system through genetic turnover

Mazzolini

Mora

Walczak

2022

Preprint

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Chronic infections of the human immunodeficiency virus (HIV) create a very complex co-evolutionary process, where the virus tries to escape the continuously adapting host immune system. Quantitative details of this process are largely unknown and could help in disease treatment and vaccine development. Here we study a longitudinal dataset of ten HIV-infected people, where both the B-cell receptors and the virus are deeply sequenced. We focus on simple measures of turnover, which quantify how much the composition of the viral strains and the immune repertoire change between time points. At the single-patient level, the viral-host turnover rates do not show any statistically significant correlation, however they correlate if the information is aggregated across patients. In particular, we identify an anti-correlation: large changes in the viral pool composition come with small changes in the B-cell receptor repertoire. This result seems to contradict the naive expectation that when the virus mutates quickly, the immune repertoire needs to change to keep up. However, we show that the observed anti-correlation naturally emerges and can be understood in terms of simple population-genetics models.

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The genetic interaction between HIV and the antibody repertoire

Cited by 5 publications

References 76 publications

Evolution during primary HIV infection does not require adaptive immune selection

Evolution during primary HIV infection does not require adaptive immune selection

Inspecting the interaction between human immunodeficiency virus and the immune system through genetic turnover

Inspecting the interaction between HIV and the immune system through genetic turnover

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