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Enhancing effects of adjuvanted 2009 pandemic H1N1 influenza A vaccine on memory B-cell responses in HIV-infected individuals

Ho, Jasona,*; Moir, Susana,*; Wang, Weia; Posada, Jacqueline Ga; Gu, Wenjuanb; Rehman, Muhammad Tc; Dewar, Robinc; Kovacs, Colind; Sneller, Michael Ca; Chun, Tae-Wooka; Follmann, Dean Ab; Fauci, Anthony Sa

doi: 10.1097/QAD.0b013e328342328b
Basic Science

Objective: To assess the humoral immune response to low-dose AS03-adjuvanted and standard-dose nonadjuvanted 2009 pandemic H1N1 influenza A vaccine in HIV-infected aviremic individuals receiving antiretroviral therapy and in uninfected individuals.

Design: A three-arm study.

Setting: Two clinics: one at the National Institutes of Health in Bethesda, Maryland, USA; and the other at the Maple Leaf Medical Clinic in Toronto, Ontario, Canada.

Participants: HIV-infected and HIV-uninfected adults.

Intervention: Single intramuscular 15 μg dose of the monovalent inactivated 2009 pandemic H1N1 influenza A vaccine without adjuvant or 3.75 μg dose of the same strain with adjuvant AS03.

Main outcomes: Immunogenicity, as measured by hemagglutination inhibition (HAI) antibody titers and vaccine-specific memory B-cell responses.

Results: A total of 74 participants were enrolled. Twenty-one HIV-infected individuals received the low-dose adjuvanted 2009 pandemic H1N1 influenza A vaccine. Twenty-nine HIV-infected and 24 HIV-uninfected individuals received the standard-dose nonadjuvanted vaccine. There were no significant differences in antibody responses at 9 weeks postvaccination among the three groups studied. However, the IgG memory B-cell response against the vaccine was significantly higher in the HIV-infected group that received the low-dose adjuvanted vaccine when compared to the HIV-infected and uninfected groups that received the standard-dose nonadjuvanted vaccine. Conclusions remained unchanged after regression adjustment for age, gender, CD4+ T-cell count, and baseline HAI titer.

Conclusion: These data suggest that adjuvants could be used to expand coverage through dose sparing and improve humoral immune responses in immunocompromised individuals.

aNational Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, USA

bBiostatistics Research Branch, USA

cApplied and Developmental Research Directorate, Science Applications International Corporation-Frederick, National Cancer Institute-Frederick, Frederick, Maryland, USA

dMaple Leaf Medical HIV Research Collaborative Inc, Toronto, Ontario, Canada.

*J.H. and S.M. contributed equally to the writing of the article.

Received 26 August, 2010

Revised 26 October, 2010

Accepted 1 November, 2011

Correspondence to Susan Moir, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10, Room 6A02, 9000 Rockville Pike, Bethesda, MD 20892, USA. Tel: +1 301 402 4559; fax: +1 301 480 0643; e-mail: smoir@niaid.nih.gov

© 2011 Lippincott Williams & Wilkins, Inc.