Archana Thomas1, Erika Hammarlund1, Lina Gao2, Susan Holman3, Katherine G Michel4, Marshall Glesby5, Maria C Villacres6, Elizabeth T Golub7, Nadia R Roan8, Audrey L French9, Michael H Augenbraun3, Mark K Slifka1. 1. Division of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University, Beaverton, Oregon, USA. 2. Biostatistics Shared Resource, Knight Cancer Institute, Biostatistics & Bioinformatics Core, Oregon National Primate Research Center, Oregon Health & Science University, Portland, Oregon, USA. 3. Division of Infectious Diseases, Department of Medicine, SUNY Downstate Health Sciences University, Brooklyn, New York, USA. 4. Department of Medicine, Georgetown University Medical Center, Washington, DC, USA. 5. Division of Infectious Diseases, Department of Medicine, Weill Cornell Medical College of Cornell University, New York, New York, USA. 6. Department of Pediatrics, Keck School of Medicine of USC, Los Angeles, California, USA. 7. Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, USA. 8. Department of Urology, University of California, San Francisco, San Francisco, California, USA. 9. Department of Medicine, Cook County Health and Hospitals System, Chicago, Illinois, USA.
Abstract
BACKGROUND: It is unclear whether human immunodeficiency virus (HIV) infection results in permanent loss of T-cell memory or if it affects preexisting antibodies to childhood vaccinations or infections. METHODS: We conducted a matched cohort study involving 50 pairs of HIV-infected and HIV-uninfected women. Total memory T-cell responses were measured after anti-CD3 or vaccinia virus (VV) stimulation to measure T cells elicited after childhood smallpox vaccination. VV-specific antibodies were measured by means of enzyme-linked immunosorbent assay (ELISA). RESULTS: There was no difference between HIV-infected and HIV-uninfected study participants in terms of CD4+ T-cell responses after anti-CD3 stimulation (P = .19) although HIV-infected participants had significantly higher CD8+ T-cell responses (P = .03). In contrast, there was a significant loss in VV-specific CD4+ T-cell memory among HIV-infected participants (P = .04) whereas antiviral CD8+ T-cell memory remained intact (P > .99). VV-specific antibodies were maintained indefinitely among HIV-uninfected participants (half-life, infinity; 95% confidence interval, 309 years to infinity) but declined rapidly among HIV-infected participants (half-life; 39 years; 24-108 years; P = .001). CONCLUSIONS: Despite antiretroviral therapy-associated improvement in CD4+ T-cell counts (nadir, <200/μL; >350/μL after antiretroviral therapy), antigen-specific CD4+ T-cell memory to vaccinations or infections that occurred before HIV infection did not recover after immune reconstitution, and a previously unrealized decline in preexisting antibody responses was observed.
BACKGROUND: It is unclear whether human immunodeficiency virus (HIV) infection results in permanent loss of T-cell memory or if it affects preexisting antibodies to childhood vaccinations or infections. METHODS: We conducted a matched cohort study involving 50 pairs of HIV-infected and HIV-uninfected women. Total memory T-cell responses were measured after anti-CD3 or vaccinia virus (VV) stimulation to measure T cells elicited after childhood smallpox vaccination. VV-specific antibodies were measured by means of enzyme-linked immunosorbent assay (ELISA). RESULTS: There was no difference between HIV-infected and HIV-uninfected study participants in terms of CD4+ T-cell responses after anti-CD3 stimulation (P = .19) although HIV-infected participants had significantly higher CD8+ T-cell responses (P = .03). In contrast, there was a significant loss in VV-specific CD4+ T-cell memory among HIV-infected participants (P = .04) whereas antiviral CD8+ T-cell memory remained intact (P > .99). VV-specific antibodies were maintained indefinitely among HIV-uninfected participants (half-life, infinity; 95% confidence interval, 309 years to infinity) but declined rapidly among HIV-infected participants (half-life; 39 years; 24-108 years; P = .001). CONCLUSIONS: Despite antiretroviral therapy-associated improvement in CD4+ T-cell counts (nadir, <200/μL; >350/μL after antiretroviral therapy), antigen-specific CD4+ T-cell memory to vaccinations or infections that occurred before HIV infection did not recover after immune reconstitution, and a previously unrealized decline in preexisting antibody responses was observed.
Authors: Kehmia Titanji; Angelo De Milito; Alberto Cagigi; Rigmor Thorstensson; Sven Grützmeier; Ann Atlas; Bo Hejdeman; Frank P Kroon; Lucia Lopalco; Anna Nilsson; Francesca Chiodi Journal: Blood Date: 2006-04-27 Impact factor: 22.113
Authors: Dina Alzhanova; David M Edwards; Erika Hammarlund; Isabel G Scholz; Daniëlle Horst; Mary J Wagner; Chris Upton; Emmanuel J Wiertz; Mark K Slifka; Klaus Früh Journal: Cell Host Microbe Date: 2009-11-19 Impact factor: 21.023