Manipulation of immunometabolism by HIV-accessories to the crime?

Curr Opin Virol. 2016 Aug:19:65-70. doi: 10.1016/j.coviro.2016.06.014. Epub 2016 Jul 21.

Abstract

Evolutionary pressure has produced an 'arms race' between cellular restriction factors (limiting viral replication) and viral proteins (overcoming host restriction). The host factors SAMHD1 and SLFN1 patrol metabolic bottlenecks required for HIV replication. Conversely, the HIV accessory proteins Vpx, Vpu and Nef manipulate cellular metabolism to enable viral replication. Recent work identifying Vpu-mediated downregulation of the alanine transporter SNAT1 and Nef-mediated downregulation of the serine carriers SERINC3/5 has uncovered the importance of HIV manipulation of the amino acid supply. Interference with CD4(+) T-cell amino acid metabolism suggests a novel paradigm of viral immunomodulation, and signposts fundamental aspects of lymphocyte biology.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • CD4-Positive T-Lymphocytes
  • Down-Regulation
  • HIV Infections / virology
  • HIV-1 / immunology*
  • HIV-1 / physiology
  • Host-Pathogen Interactions*
  • Human Immunodeficiency Virus Proteins / immunology
  • Human Immunodeficiency Virus Proteins / metabolism
  • Humans
  • Metabolic Networks and Pathways*
  • Monomeric GTP-Binding Proteins / metabolism
  • SAM Domain and HD Domain-Containing Protein 1
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / metabolism
  • Viral Regulatory and Accessory Proteins / metabolism
  • Virus Replication

Substances

  • Human Immunodeficiency Virus Proteins
  • Viral Regulatory and Accessory Proteins
  • SAM Domain and HD Domain-Containing Protein 1
  • SAMHD1 protein, human
  • Monomeric GTP-Binding Proteins