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Virus Entry via the Alternative Coreceptors CCR3 and FPRL1 Differs by Human Immunodeficiency Virus Type 1 Subtype.

In English

Författare

  • R Nedellec
  • M Coetzer
  • N Shimizu
  • H Hoshino
  • V R Polonis
  • L Morris
  • Ulrika Mårtensson
  • J Binley
  • J Overbaugh
  • D E Mosier

Summary, in English

HIV-1 infects target cells by binding to CD4 and a chemokine receptor, most commonly CCR5. CXCR4 is a frequent alternative coreceptor (CoR) in subtype B and D HIV-1 infection, but the importance of many other alternative CoR remains elusive. We have analyzed HIV-1 envelope proteins (Env) from 66 individuals infected with the major subtypes of HIV-1 to determine if virus entry into highly permissive NP-2 cell lines expressing most known alternative CoR differed by HIV-1 subtype. We also performed linear regression analysis to determine if virus entry via the major CoR CCR5 correlated with use of any alternative CoR, and if this correlation differed by subtype. Virus pseudotyped with subtype B Env showed robust entry via CCR3 that was highly correlated with CCR5 entry efficiency. By contrast, viruses pseudotyped with subtype A and C Env were able to use the recently described alternative CoR FPRL1 more efficiently than CCR3, and use of FPRL1 was correlated with CCR5 entry. Subtype D Env was unable to use either CCR3 or FPRL1 efficiently, a unique pattern of alternative CoR use. These results suggest that each subtype of circulating HIV-1 may be subject to somewhat different selective pressures for Env-mediated entry into target cells, and suggest that CCR3 may be used as a surrogate CoR by subtype B while FPRL1 may be used as a surrogate CoR by subtype A and C. These data may provide insight into development of resistance to CCR5-targeted entry inhibitors and alternative entry pathways for each HIV-1 subtype.

Avdelning/ar

  • Drug Target Discovery

Publiceringsår

2009

Språk

Engelska

Sidor

8353-8363

Publikation/Tidskrift/Serie

Journal of Virology

Volym

83

Dokumenttyp

Artikel i tidskrift

Förlag

American Society for Microbiology

Ämne

  • Pharmacology and Toxicology

Status

Published

Forskningsgrupp

  • Drug Target Discovery

ISBN/ISSN/Övrigt

  • ISSN: 1098-5514