US28 actions in HCMV infection: lessons from a versatile hijacker

Rev Med Virol. Jul-Aug 2005;15(4):269-82. doi: 10.1002/rmv.468.

Abstract

Mimicking host proteins is a strategy adopted by several herpesviruses to exploit the host cell for their own benefit. In this respect the human cytomegalovirus (HCMV) chemokine receptor homologue US28, has been extensively studied. Molecular pirates such as US28 can teach us about crucial events in HCMV infection and may either offer a potential target for antiviral therapy or provide an alternative strategy to immune suppression. Despite elaborate research into the chemokine binding affinity, signalling properties, intracellular trafficking and expression kinetics of US28, a solid hypothesis about the role of US28 in HCMV infection has not yet been proposed. It appears that US28 may behave as a molecular pirate that employs smart strategies for cell entry, host gene regulation and immune evasion. This review will elaborate on these aspects of US28 biology and discuss possible implications for HCMV infection.

Publication types

  • Review

MeSH terms

  • Arteriosclerosis / etiology
  • Chemokine CX3CL1
  • Chemokines, CX3C / metabolism
  • Cytomegalovirus / physiology*
  • Cytomegalovirus Infections / physiopathology*
  • Humans
  • Membrane Proteins / metabolism
  • Muscle, Smooth, Vascular / cytology
  • Muscle, Smooth, Vascular / virology
  • Myocytes, Smooth Muscle / physiology
  • Myocytes, Smooth Muscle / virology
  • Receptors, Chemokine / physiology*
  • Signal Transduction
  • Viral Proteins / physiology*
  • Virus Latency

Substances

  • CX3CL1 protein, human
  • Chemokine CX3CL1
  • Chemokines, CX3C
  • Membrane Proteins
  • Receptors, Chemokine
  • US28 receptor, Cytomegalovirus
  • Viral Proteins