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Evolution of hypervariable region 1 of hepatitis C virus in primary infection

A Manzin1, L Solforosi, E Petrelli

  • 1Istituto di Microbiologia, Università di Ancona, Ancona, Italy. manzin@popcsi.unian.it

Journal of Virology
|June 17, 1998
PubMed

Insights

Hepatitis C virus (HCV) hypervariable region 1 (HVR-1) evolution during primary infection suggests an oligoclonal event. Host selective pressure drives distinct viral genetic adaptations for persistence.

Area of Science:

  • Virology
  • Immunology
  • Genetics

Background:

  • Hepatitis C virus (HCV) infection remains a significant global health concern.
  • Understanding viral evolution during acute infection is crucial for developing effective treatments.
  • The hypervariable region 1 (HVR-1) of the HCV E2 envelope protein is a key target for host immune responses.

Purpose of the Study:

  • To investigate the dynamics of intrahost HCV variability during primary infection.
  • To determine the role of host selective pressure in driving HCV genetic evolution.
  • To analyze HVR-1 sequence variations in sequential samples from patients with acute hepatitis C.

Main Methods:

  • Analysis of HVR-1 sequences from 20 clones per time point in sequential samples from three patients.
  • Amplification, cloning, and purification of plasmid DNA from transformed cells.
  • Intrasample and intersample evolutionary analyses including Ka, Ks, Ka/Ks ratio, and genetic distances.

Main Results:

  • Low genetic distances in early HVR-1 samples, decreasing further after seroconversion, indicating an oligoclonal origin of primary HCV infection.
  • Differential levels and dynamics of host selective pressure observed across the three cases.
  • Intersample analysis confirmed individual HCV genetic evolution patterns, highlighting varied contributions of neutral evolution and selective forces.

Conclusions:

  • Primary HCV infection is likely an oligoclonal event.
  • Host selective pressure plays a significant role in shaping viral genetic diversity during acute infection.
  • HCV adaptation for in vivo persistence involves diverse evolutionary routes, reflecting viral fitness in individual host environments.

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