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Hypervariable region 1 sequence stability during hepatitis C virus replication in chimpanzees.

S C Ray¹, Q Mao, R E Lanford

¹Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. sray@jhmi.edu

Journal of Virology

|March 9, 2000

Summary

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Hepatitis C virus (HCV) hypervariable region 1 (HVR1) variability is driven by immune selection pressure, not random mutations. Lower mutation rates in chimpanzees support this, indicating immune response shapes HCV evolution.

Area of Science:

Virology
Immunology
Genetics

Background:

The hepatitis C virus (HCV) envelope 2 (E2) gene includes hypervariable region 1 (HVR1), a site of significant genetic variation.
The driving force behind HVR1 variability remains debated: immune selection pressure versus random mutation accumulation.

Purpose of the Study:

To investigate whether genetic variability in HCV's HVR1 is primarily driven by immune selection or random mutation.
To test the hypothesis that immune pressure, not functional constraint, shapes HVR1 diversity.

Main Methods:

Examined HCV E2 gene sequences from a human inoculum and serially infected chimpanzees.
Utilized heteroduplex-single-stranded conformational polymorphism (SSCP) assays to analyze quasispecies complexity.
Sequenced unique clonotypes identified through SSCP analysis.

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Main Results:

HCV sequence diversity was significantly lower in chimpanzees compared to humans.
The majority clonotype sequence remained stable across eight serial passages in chimpanzees.
Rates of nonsynonymous (protein-altering) substitutions were reduced in chimpanzees.

Conclusions:

Nonsynonymous mutations in HCV HVR1 are indicative of selection pressure, specifically immune response.
The findings challenge the notion that HVR1 variability is merely a consequence of unconstrained replication.
Immune selection is a key factor shaping the genetic diversity of the hepatitis C virus.