Genetic resistance factor for HIV-1 and immune response to varicella zoster virus

• Published in: The Lancet (British edition) Vol. 357; no. 9253; pp. 360 - 361
• Main Authors: Wiencke, John K, Kelsey, Karl T, Zuo, Zheng-fa, Weinberg, Adriana, Wrensch, Margaret R
• Format: Journal Article
• Language: English
• Published: London Elsevier Ltd 03.02.2001; Lancet; Elsevier Limited
• Subjects: Biological and medical sciences; Blood; Chickenpox - genetics; Chickenpox - immunology; Female; General aspects; Genetic Predisposition to Disease; Genetics; Health care; HIV; Human immunodeficiency virus; Humans; Immune response; Immune system; Infectious diseases; Male; Medical sciences; Middle Aged; Polymorphism, Genetic; Receptors, CCR5 - immunology; Studies; Viral diseases; Viruses; Human; Varicella zoster virus; Immune response; HIV-1 virus; Herpesviridae; Alphaherpesvirinae; Cytokine; Retroviridae; Structure gene; Lentivirus; Infection; Virus; Chemokine; Resistance; Immunology; Viral disease; Deletion; Genetics; Human immunodeficiency virus; Mutation
• ISSN: 0140-6736; 1474-547X
• DOI: 10.1016/S0140-6736(00)03646-1

A 32 bp deletion in the chemokine receptor CCR5 gene modulates HIV-1 infection. However, whether this CCR5 gene variation modifies immunity to common herpesvirus infections is unknown. We investigated whole blood IgG concentrations of 157 normal adult blood donors. Also we assessed whether the 32 bp deletion of CCR5 (Δ32 CCR5) was associated with circulating IgG to four herpesviruses: varicella zoster virus, Epstein-Barr virus, cytomegalovirus, and herpes simplex virus type 1 and type 2. Individuals who carried Δ32 CCR5 were 9·2 times more likely to be seronegative for varicella zoster virus than non-carriers (95% CI 2·9–29·1), but no differences were seen for the other herpesviruses studied. Variation in CCR5 may modulate humoral immunity to varicella zoster virus.