Anna M Powell1, Zhenwu Luo2, Lisa Martin3, Zhuang Wan2, Lei Ma4, Guoyang Liao4, Yuxia Song5, Xiaochun Li5, J Michael Kilby3, Lei Huang6, Wei Jiang7. 1. Department of Obstetrics and Gynecology, Medical University of South Carolina, 29425, USA. 2. Department of Microbiology and Immunology, Medical University of South Carolina, Charleston 29425, USA. 3. Divison of Infectious Diseases, Department of Medicine, Medical University of South Carolina, Charleston 29425, USA. 4. Chief of No. 5 Biologicals Department, Institute of Medical Biology, Chinese Academy of Medical Sciences & Peking Union Medical College, Kuming 650118, China. 5. The Sixth People's Hospital of Xinjiang Uyghur Autonomous Region, Kashi East Road 100 North Lane Of Xinshi District, Xinjiang, Urumqi 830013, China. 6. The 302 Hospital of PLA, Treatment and Research Center for Infectious Diseases, Beijing 100039, China. Electronic address: huangleiwa@sina.com. 7. Department of Microbiology and Immunology, Medical University of South Carolina, Charleston 29425, USA; Divison of Infectious Diseases, Department of Medicine, Medical University of South Carolina, Charleston 29425, USA. Electronic address: jianw@musc.edu.
Abstract
BACKGROUND: Studies have shown that HIV infection is associated with an impaired influenza vaccine response. We examined the role of cellular phenotypes and function in influenza vaccine responsiveness in healthy controls and aviremic HIV-infected subjects on antiretroviral treatment (ART). METHODS: 16 healthy controls and 26 ART+ aviremic HIV+ subjects were enrolled in the current study. Blood was collected at pre-vaccination (D0), and on days 7-10 (D7) and 14-21 (D14) following the 2013-2014 seasonal influenza vaccine administrations. Subjects were classified as responders if neutralizing titers against H1N1 virus increased ⩾4-fold at D14 compared to D0. A serial analysis of B and CD4+ T cell frequencies and activation was performed on D0 and D7 by flow cytometry. RESULTS: 9 of 26 (34.6%) HIV-infected individuals and 7 of 16 (43.8%) healthy controls were classified as responders to influenza vaccines. Total B cell apoptosis (annexin V) was increased on D7 post-vaccination in non-responders but not in responders among both controls and HIV+ subjects. Surface CD80 expression on memory B cells and intracellular CD40L expression on memory CD4+ T cells were induced on D7 in responders of controls but not in non-responders. The CD80 and CD40L induction was not demonstrable in HIV-infected subjects regardless of responders and non-responders. Memory CD4+ T cell cycling tended to increase on D7 in the four study groups but did not achieve significance. All the other parameters were indistinguishable between responders and non-responders, regardless of HIV-infection status. CONCLUSION: The perturbation of activation and apoptotic induction on B cells or CD4+ T cells after seasonal influenza vaccination in non-responders and HIV-infected subjects may help understand the mechanism of impaired vaccine responsiveness.
BACKGROUND: Studies have shown that HIV infection is associated with an impaired influenza vaccine response. We examined the role of cellular phenotypes and function in influenza vaccine responsiveness in healthy controls and aviremic HIV-infected subjects on antiretroviral treatment (ART). METHODS: 16 healthy controls and 26 ART+ aviremic HIV+ subjects were enrolled in the current study. Blood was collected at pre-vaccination (D0), and on days 7-10 (D7) and 14-21 (D14) following the 2013-2014 seasonal influenza vaccine administrations. Subjects were classified as responders if neutralizing titers against H1N1 virus increased ⩾4-fold at D14 compared to D0. A serial analysis of B and CD4+ T cell frequencies and activation was performed on D0 and D7 by flow cytometry. RESULTS: 9 of 26 (34.6%) HIV-infected individuals and 7 of 16 (43.8%) healthy controls were classified as responders to influenza vaccines. Total B cell apoptosis (annexin V) was increased on D7 post-vaccination in non-responders but not in responders among both controls and HIV+ subjects. Surface CD80 expression on memory B cells and intracellular CD40L expression on memory CD4+ T cells were induced on D7 in responders of controls but not in non-responders. The CD80 and CD40L induction was not demonstrable in HIV-infected subjects regardless of responders and non-responders. Memory CD4+ T cell cycling tended to increase on D7 in the four study groups but did not achieve significance. All the other parameters were indistinguishable between responders and non-responders, regardless of HIV-infection status. CONCLUSION: The perturbation of activation and apoptotic induction on B cells or CD4+ T cells after seasonal influenza vaccination in non-responders and HIV-infected subjects may help understand the mechanism of impaired vaccine responsiveness.
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