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This study describes the genetic variability of within\u2010host <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> viral variants in acute infection and correlates it with host\u2010 and virus\u2010related traits and infection outcome. Next generation sequence data (Illumina, MiSeq platform) of viral genomes from 116 incident acute infections (within 180\u00a0days of infection) were analysed to determine all the single nucleotide polymorphism (<jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>) frequencies above a threshold of 0.1%. The variability of the <jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>s for the full open reading frame of the genome as well as for each protein coding region were compared using mean standardized Shannon entropy (<jats:styled-content style=\"fixed-case\">SE<\/jats:styled-content>) values calculated separately for synonymous and nonsynonymous mutations. The envelope glycoproteins regions (E1 and E2) had the highest <jats:styled-content style=\"fixed-case\">SE<\/jats:styled-content> values (indicating greater variability) followed by the <jats:styled-content style=\"fixed-case\">NS<\/jats:styled-content>5B region. Nonsynonymous mutations rather than synonymous mutations were the main contributors to genomic variability in acute infection. The mean difference of Shannon entropy was also compared between subjects after categorizing the samples according to host and virus\u2010related traits. Host <jats:italic><jats:styled-content style=\"fixed-case\">IFNL<\/jats:styled-content>3<\/jats:italic> allele <jats:styled-content style=\"fixed-case\">CC<\/jats:styled-content> polymorphism at rs12979860 (vs others) and viral genotype 1a (vs 3a) were associated with higher genomic variability across the viral open reading frame. Time since infection, host gender or continent of origin was not associated with the viral genomic variability. 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