Immune System Deficiencies Do Not Alter SARS-CoV-2 Evolutionary Rate but Favour the Emergence of Mutations by Extending Viral Persistence.

Immune System Deficiencies Do Not Alter SARS-CoV-2 Evolutionary Rate but Favour the Emergence of Mutations by Extending Viral Persistence.

Publication date: Mar 13, 2024

During the COVID-19 pandemic, immunosuppressed patients showed prolonged SARS-CoV-2 infections, with several studies reporting the accumulation of mutations in the viral genome. The weakened immune system present in these individuals, along with the effect of antiviral therapies, are thought to create a favourable environment for intra-host viral evolution and have been linked to the emergence of new viral variants which strongly challenged containment measures and some therapeutic treatments. To assess whether impaired immunity could lead to the increased instability of viral genomes, longitudinal nasopharyngeal swabs were collected from eight immunocompromised patients and fourteen non-immunocompromised subjects, all undergoing SARS-CoV-2 infection. Intra-host viral evolution was compared between the two groups through deep sequencing, exploiting a probe-based enrichment method to minimise the possibility of artefactual mutations commonly generated in amplicon-based methods, which heavily rely on PCR amplification. Although, as expected, immunocompromised patients experienced significantly longer infections, the acquisition of novel intra-host viral mutations was similar between the two groups. Moreover, a thorough analysis of viral quasispecies showed that the variability of viral populations in the two groups is comparable not only at the consensus level, but also when considering low-frequency mutations. This study suggests that a compromised immune system alone does not affect SARS-CoV-2 within-host genomic variability.

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Concepts Keywords
Genomes COVID-19
Host Humans
Immunocompromised immunocompromised subjects
Longer intra-host
Viral Mutation
Pandemics
Quasispecies
SARS-CoV-2
SARS-CoV-2 genomic variability
viral quasispecies

Semantics

Type Source Name
pathway REACTOME Immune System
disease MESH COVID-19 pandemic
disease IDO host
disease MESH immunocompromised patients
disease MESH infections
disease VO frequency
disease MESH Infectious Diseases
disease VO population
pathway KEGG Viral replication
disease IDO infectivity
drug DRUGBANK Coenzyme M
disease VO time
disease IDO infection
disease VO protocol
disease VO efficient
disease MESH clinical progression
disease IDO assay
disease VO gene
disease VO manufacturer
drug DRUGBANK Aspartame
disease IDO quality
drug DRUGBANK Methylergometrine
drug DRUGBANK Nonoxynol-9
disease MESH mutation frequency
drug DRUGBANK Pidolic Acid
disease MESH malignancies

Original Article

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